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How come the role of the Apis mellifera is determined by nutrition rather than chromosomes?
Prior to making my question I browsed on similiar question such as this one but it doesn't specifically addressed my doubt in the sense that it is related with a different species and on a concept not mentioned in that question. More specifically on whether does nutrition may influence genetics on the sex determination or not?.
My doubt arises as I'm learning about Partheneogenesis and genetic determination of the sex. Upon reading this entry in Wikipedia, it explains that a queen bee of the Apis mellifera is determined during the development of the larva. The article doesn't state anything about the chromosomes of the larva. It just states that the queen will develop into that by feeding it from royal jelly, from which I believe it has some sort of protein that may influence the development of such larva giving it their characteristics.
But this topic is letting me confused. Does this means that for example a male bee can become into the queen?.
This article explains that some insects produce haploid males from unfertilized eggs by I believe Partheneogenesis. But if the bee doesn't mate, how is the sex determined?. I believe that it will produce only females (as his genetic sex determining chromosome is ZW?) and as such will yield only females, but if the queen does successfuly mate with a male may produce males which in turn can also lay eggs (by Partheneogenesis) and those eggs will all be males?.
From this I'm getting the conclusion that it can occur that some individuals may be all females or all males?.
How come is it possible for an haploid organism get into full develpment isn't it necessary to be diploid?. Do they become into diploid at some moment?.
Can someone help me to clear out this doubt?. This topic has left me confused, so an answer which would help me the most is some sort of explanation on the concepts of partheneogenesis and sex determination in the bees.

Where did you read that bees have ZW sex determination system?

The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Unresearched questions may be subject to down-voting and closure. ——— Searching for "sex determination in bees" leads to multiple pages such that should help you.

@BagiM I concluded this from reading at the wikipedia page on Partheneogenesis but of course I could be wrong, hence the necessity of an answer which could clear this doubt.

@tyersome I'm sorry but I disagree. If you read with attention I started my question by saying that I made an initial effort into looking for answers in Wikipedia. Not only this but I also browsed for similar questions on this community, but yet I'm unable to understand. Thus I require some sort of answer which could address my doubts.

You say you made an effort, but I'm suggesting you can (and should) do more — e.g. by doing some reading based on the previous comments and correcting the mistakes in your post. ———— This is not a forum or tutorial service; it is a Q&A site where specific questions relating to biology get specific answers. Please take the [tour] and carefully read through the [help] to learn more about the site, including what is on-topic and what is not, and [ask] a good question.

I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful. Wikipedia is also generally a good starting point and you can then check their references. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

So you have read the sentence: "Among species with the haplo-diploid sex-determination system, such as hymenopterans (ants, bees and wasps) and thysanopterans (thrips), haploid males are produced from unfertilized eggs." And you concluded the sex determination system in bees is ZW???


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Is a pampa an example of ecological succession?
I'm not very sure if a pampa is an example of an ecological succession.
The reason of my doubt is due I've remember hearing that a Pampa is formed when a Valley which has had a river on it, no longer has it due the river changed its course and left the place without water.
But is it okay for this reason to imply that the Pampa (biome) is the result of an ecological succession?. The wikipedia entry doesn't give much details.
But it constrains the term for only the lands located in Brazil and Uruguay. It does not give any indication why some other places such as in Bolivia and Peru also use the term. Given these, could it be confused with a Mediterranean forest or with a Chaparral?.
Are those of the same origin?. Can someone help me here?. I'm confused about these.

This is a difficult question to answer. I would say that is uncommon (though not improper) to think of questions of ecological succession at the biome scale. In this case, the pampa is probably a good example of a climax community (if we exclude human-caused changes). After the rivers changed course there would have been a lot of bare substrate. Over time different plant species would establish and then  be replaced by other plant species. After thousands of years you would get to the somewhat stable state of the pampa biome. It is important to note that this biome is maintained by fire and grazing (Vignolio et al 2003). Fire/grazing prevent trees and shrubs from establishing in high densities and maintains the open grasslands of the pampa. In general, every place in the world that has natural life would be the result of ecological succession. Succession is a process that happens as life establishes and ecological communities change.
As for why other places are also called pampas, the word "pampa" apparently comes from a Quechua word for plains, that was then adopted into Spanish. Since Peru and Bolivia both have Quechua speaking populations, it seems reasonable that this work was applied to plains areas in those countries.
Edit in response to comments
Comment about biome scale
The reason behind the scale comment is that typically we observe succession for a given habitat. Part of this stems from the origin of the succession ideas, where Frederic Clements posited that climate was the major driving factor of successional trajectories (Clements 1916). This would actually fit well with the biome view of succession, however in order for this model to explain all the variation we see in the world (eg. why a tree grows in location X but not location Y 4 metres away), you devolve into splitting the world into infinitesimally small micro-climates. Henry Gleason proposed a more individualistic model, which suggested that climate was just one influence, and that each plant species responds to a myriad of different environmental cues (Gleason 1927). The sum of these responses results in the community at a given location. This seems to fit better with our current understanding of succession but is not without problems. In a Gleasonian model, any variation can be expected to result in a different community. Since it would be strange for the pampas region to be homogeneous over 1.2 million km2, there are likely distinct communities within the biome, each developing as a result of factors like soil moisture, soil chemistry, climate, wind exposure, and herbivore use. One can still talk about succession at a biome scale, but at that scale we would be thinking about what factors lead the pampas region to become a grassland, rather than what factors lead grass X, tree Y and forb Z to coexist next to each other.
Factors maintaining grassland type ecosystems are fairly uniform globally. You need some sort of event that will kill woody vegetation but not kill grasses and forbs. Fire and grazing are natural examples (Briggs et al. 2002), but mowing would also maintain grassland (Fidelis et al. 2012). Earthquakes are unlikely to maintain grassland as trees and shrubs are likely to survive earthquakes.
Comment about global pampas
Yes, and no. There are other wet grasslands in the world that would have similar moisture regimes and productivity levels seen in the pampas of South America. However, these are likely not called pampas. Temperate grasslands in Canada and the US are typically called prairies or plains, while the same kind of system is called a steppe in Eurasia. Ecologically they are very similar in function, though they may have very different species present. Perelman, Burkart, and Leon (2003) use prairie and steppe to refer to different sub-communities of the Pampa. Perhaps the closest analogue would be the Great Plains of North America. There is no other area called the Great Plains, but since the great plains are made up of prairie, steppe, and savannah (Oesterheld et al. 1999), there are many other areas globally that exhibit similar ecological function. This can get confusing, as there are cultural usages of these terms to refer to places, and there are ecological uses of these terms to refer to grassland sub-types.
I am not sure I understand how you are relating chaparral/Mediterranean forest to this. Both of those ecosystems will have much higher presence of trees and shrubs than pampas/prairie/steppes (Hanes 1971, Palahi 2008). Chaparrals tend to be dominated by evergreen drought tolerant shrubs, while Mediterranean forests will have more trees present. All of these systems are influenced naturally by fire and drought, so they are similar that way.
Sources
Briggs, John M., Alan K. Knapp, and Brent L. Brock. "Expansion of woody plants in tallgrass prairie: a fifteen-year study of fire and fire-grazing interactions." The American Midland Naturalist 147.2 (2002): 287-294.
Clements, Frederic Edward. Plant succession: an analysis of the development of vegetation. No. 242. Carnegie Institution of Washington, 1916.
Fidelis, Alessandra, et al. "Short‐term changes caused by fire and mowing in Brazilian Campos grasslands with different long‐term fire histories." Journal of Vegetation Science 23.3 (2012): 552-562.
Gleason, Henry Allan. "Further views on the succession‐concept." Ecology 8.3 (1927): 299-326.
Hanes, Ted L. "Succession after fire in the chaparral of southern California." Ecological monographs 41.1 (1971): 27-52.
Oesterheld, M., et al. "Grazing, fire, and climate effects on primary productivity of grasslands and savannas." Ecosystems of the world (1999): 287-306.
Palahi, M., et al. "Mediterranean forests under focus." International forestry review 10.4 (2008): 676-688.
Vignolio, Osvaldo R., et al. "Effects of fire frequency on survival, growth and fecundity of Paspalum quadrifarium (Lam.) in a grassland of the Flooding Pampa (Argentina)." Austral Ecology 28.3 (2003): 263-270.

Gee I had to wait for almost three months to get a reply from somebody. But it is nice that it finally happened!. Regarding your answer you mention that it is uncommon to think questions at the biome scale. Why is this?. Does this means that ecological succession is more used at higher scales?. Such as communities?. I'm okay with the second part of your answer. But I wonder, if other events but fire also maintain the pampa biome?, would earthquakes account?.

Regarding the last part of your answer, it isn't very clear to me if there are other places in the world which do have pampas? This stems from the confusion of the term with mediterranean forest and chaparral, are all of these the same? and do they exist in Asia for example?.

I'm already accepting your answer, but it would be very nice if you could add an additional details from my comments into your answer. Sorry for the late reply by the way.

Responded to your questions. See above.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

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Why is sickle cell trait expressed in half of all cells rather than all cells containing half-sickled haemoglobin
If sickle cell trait is due to be heterozygous with respect to a single gene mutation on the haemoglobin β-globin chain, why is it the case that ~50% of RBCs are sickled rather than half of the haemoglobin in every RBC containing haemoglobin-S β-globin chains?
Is it due to some form of monoalleic expression that occurs by chance or are all the proteins in one RBC formed from one random allele during erythropoiesis?

Welcome to SE Biology. I am not sure that I understand what you say or that it is correct.  What do you mean by the "trait  is due to be heterozygous"? The heterozygotes are carriers and do not suffer sickling. Only the red cells of homozygotes sickle. Likewise your statement about only half the blood cells sickling. Presumably that is just statistical chance as the oxygen concentration decreases and nothing to do with expression. Could you please clarify and support your statements with links to references. Then we may be able to help sort it out for you.

Sickle cell carriers (heterozygous) don't have sickle cells, but do have altered blood cells

"The sickle cell trait" affects people who are homozygous for the HbS allele. These individuals only have hemoglobin S (after all fetal and embryonic hemoglobin genes are switched off). Hemoglobin S forms large crystal aggregates under conditions of low oxygen tension, and cause red cells to sickling and then to lyse. Anemia is most often severe and lethal.
Heterozygous subjects (HbA/HbS) form both hemoglobin A (normal) and hemoglobin S in approximately equal quantities, and suffer only a mild form of anemia, that may be even unnoticed.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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Where can I find the data on the geographical distribution of the species of Drosophila within various areas of the world?
Let X denote an arbitrary geographic area where drosophilas occur in the wild. I will need the answers to the questions of the following type:

What is the three most occurring species of the genus Drosophila within X?

Where can I find the data on the geographical distribution of Drosophila species within various areas of the Earth?

@user1136: I don't see how TaxoDros can help to answer a "What are the three most occurring species of the genus Drosophila in this particular country?" question. I have not found any source that contains such information.

Source: pinterest.com
I have been unable to find data on a global scale, for now here's a map on the USA.

Pinterest.com is not a source. It is a (closed) shop for stolen goods. And a map of the US doesn’t answer the question.

First, I don't see how your highly subjective opinion lacking any basis can be following the Community Lines. Second, I advise reading the picture description in order to avoid wasting your time in such comments.

— My opinion is based on the many images stolen from websites I run and which were marked up with Pinterest’s own code to flag that they shouldn’t be copied to Pinterest. I had to request their removal, which Pinterest honoured. I was able to identify them by searching for reference to my website, and presumably you could have identified the source of the image you posted. Asking readers who may be partially sighted to read text rendered as graphics is discriminatory, but in this case clearly does not answer the question as posted.  My comment explained my down-vote.


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What organism is this?
This is something I found growing under my kitchen’s sink. It looks like a growing potato and it’s really hard (tried to pull it down using a hard cardboard but in vain). I think a knife may work but I want to know what this is and if I should be taking any precaution.

I’ve put up a video of it as well here:
https://photos.app.goo.gl/JLqJrxeqnboRn9bg8

That looks to me to be non-biological but rather the result of using an expanding foam filler product to fill in gaps, as might occur in the wallboard where a sink is mounted.  Here's an example of such a product:


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How to find the enhancer region of a specific gene?
I am new to these concepts in biology and need some help understanding. My main concern is how to find the enhancer of my gene of interest, specifically the sequence of the enhancer. I am working on a project where I will be attempting to use CRISPR- mediated deletion of the promoter region and enhancer region in my gene of interest FOXN2, in MCF7 Tamoxifen resistant breast cancer cells. I already have the sequence for the promoter region from UCSC's GenomeBrowser, but I'm not sure if the enhancer region sequence can just be looked up on there or anywhere else. Do I need to do a protocol to find the enhancer region myself? I have seen many things about ChIP-Seq and that I may need to do that to get data to find my enhancer but I am just not sure. I plan to use the sequences of the enhancer and promoter region of my gene of interest to create gRNA for CRISPR. Thank you to anyone who can help.

Encode is a good resource for browsing cis-regulatory elements in the human and mouse genomes.  Here is the page listing candidate cis-regulatory elements proximal to the human FOXN2 gene.

Remember that genes can have several enhancer and repressor regions and they can be spread more or less all over the genome if you're unlucky. FOXN2 seems to be reasonably well-known though, so there should be information on this out there.

There are several ways to identify enhancers:
(1) Chip seq / chip-chip recognize transcription factor binding sites,
(2) Enhancer specific factors can also be used to identify enhancers, such as EP300, the binding sites of EP300 are often used to predict enhancers;
(3) RNA polymerase II can bind thousands of enhancers, so POLR2A2a, the largest subunit of RNA polymerase II, can also be used to search for enhancer sites;
(4) The high sensitive site of deoxyribonuclease I (DHS) represents the open chromatin region, many of which are covered with enhancers;
(5) A large number of active regulatory elements, including enhancers, can be identified by formaldehyde assisted separation regulatory elements (face) combined with sequencing;
(6) Some histone modification patterns reflect different chromatin states, such as the binding of h3k4me1 and h3k27ac, which are widely used for enhancer labeling;
(7) Enhancer sequence can be transcribed, and the transcriptional enhancer RNA (enrna) is also a marker of enhancer activation;
(8) The method of chromosome 3D conformation (e.g. 5C and Chia pet, capture-c) can also provide the information of enhancer promoter interaction.

Welcome and thanks for your interesting contribution. Can you add some sources to your answer, preferably references to journal papers? But also a wiki link here and there can help other users a lot to background read on your material. Cheers.


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Analysis of post transplantation lineage tags
I'm having some trouble understanding some bits of a study, mostly about the Sleeping Beauty system and TARIS model, from this paper: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4408613/
I understand the concept, but not how it works technically. Can anyone explain it for me?

I can't find a reference to a "TARIS model" in the paper you linked, but we can break down the molecular circuitry of this lineage tag tracking system step-by-step.

The authors use a type of Tet expression system in order to tightly control the expression of a hyperactive Sleeping Beauty (HSB) transposase.  In the absence of doxycycline, the reverse tetracycline-controlled transactivator M2-rtTA does not bind the TetO operator. Jackson Labs has a very good summary of Tet-On (and Tet-Off) systems:

... rtTA is a fusion protein comprised of the TetR repressor and the VP16 transactivation domain; however, a four amino acid change in the tetR DNA binding moiety alters rtTA's binding characteristics such that it can only recognize the tetO sequences in the [tetracycline-responsive promoter element (TRE)] of the target transgene in the presence of the Dox effector. Thus, in the Tet-On system, transcription of the TRE-regulated target gene is stimulated by rtTA only in the presence of Dox.

In the presence of doxycycline, the transactivator drives expression of HSB from the constituent promoters of the TetO operator.  HSB contains DNA binding motifs that specifically recognize the direct repeats (white triangles) and a catalytic domain that excises the direct repeats and the DNA they flank, which contains a transcription stop signal (Tn-STOP).
Excision of the Tn-STOP signal allows for expression of DsRed driven by a strong synthetic promoter (CAGGS, first described here).  The excised sequence is then inserted somewhere else in the genome.
Because successful Tn-STOP excision is concurrent with transcription of DsRed, red fluorescing cells can be selected and prepared for NGS.  HSB transposition is "random", so two different transposition events are unlikely to target the same insertion locus.  The specific insertion site can then be used as a molecular fingerprint to identify the progenitor stem cell after replication and differentiation.


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What if all virus suddenly disappear?
Exactly as the question says:
Let's say that all the viruses suddenly disappear (it doesn't matter the cause, just evaporate!): what would happened with the life on Earth?
I know: if this question says "bacteria", that would be a cataclysm, but with virus?
Note: let me know if this is not a correct space for this question. Thanks!

As a new user to SE Biology it would be courteous to our community if you read to the end of the [Tour] where you would see that questions that are primarily opinion-based are not suitable for this site. This is expanded in the Help on questions to avoid asking, which specifically refers to the case: "you are asking an open-ended, hypothetical question: “What if ______ happened?".

I think it's a very interesting question because viruses have a major impact on many fields of global populations, climate and chemistry.

Viruses are the fungus of the bacterial world, they also naturally control invasive invertebrate, plant and pest populations, and have an effect on geochemistry and climate. https://www.google.com/search?q=main+effects+of+viruses+on+planet+earth&oq=main+effects+of+viruses+on+planet+earth&aqs=chrome..69i57j33i160.6752j0j4&sourceid=chrome&ie=UTF-8

ha - i'd say. more like its a viral world and the bacteria and fungi just live in it :)

I'm okay with speculative questions — they are often re-writeable into typical SE questions.
My short answer is that we guess but we don't really know.  Viruses do keep many bacterial and microbial populations in check.  They cause disease too but I'm guessing that they also transport information from one point in the ecosystem.  I remember some of the research into cholera showed that disease causing genes in Vibrio cholerae are transmitted by phage (a bacterial virus).  So that suggests that benign bacteria have reserves of phenotypes which they can pull out of the virosphere when they need to change their stripes.
How often does this sort of thing happen? We know so little about the estimated millions of bacterial species, much less how they might effect the microbial ecosystem.
I feel something would happen but it's really hard to say what.  Would viruses come back? there are quite a few viruses embedded in genomes, which reactivate at interval.  It's easier to imagine the earth scrubbed of all life before viruses would be gone!  Just sayin'

Their disappearance will not be much impactful because these are damaging to cells only, but we can also see this situation from another angle.
Many viruses act as 'bacteria eaters' such as bacteriophages. Most of these viruses are the main factors in slowing down the exponential reproduction rate of bacteria.
A typical bacteria duplicates every 25 minutes. On the other hand, the viral reproduction rate is extremely high. For instance, during the "lytic cycle", T-4 bacteriophage even reduces the number of bacteria in a bacterial population.
Moreover, the disappearance of all viruses will be dramatically beneficial for humans, as viruses are the main causative agents of many of dangerous diseases.Mian examples include influenza, small pox, AIDS, hepatitis, measles and mumps.

Welcome to SE Biology. This is an objective question and answer site, not a discussion site, so it would be better to ignore this sort of "What if?" sort of question. See my comment on the actual question for a more detailed explanation of this.


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A question about dna triplex
Short DNA triplex strands have been identified in various organsims. But, would injecting a single strand of DNA or RNA (with its bases complementary to the bases of DNA found in the major groove of a certain gene ) cause it to form a DNA triplex   at that gene?

Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. ——— We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). In particular, are you sure you understand how triplexes form? The third strand interacts with the others through Hoogsteen base pairs, which is different from complementary (Watson-Crick) base pairing ... Thanks!

@tyersome Yes i understand this, I meant is triplex formation a spontaneous interaction that occurs at physiological state when the needed strand is present?

Possibly, yes, but there are complications.
There are other conditions that help create the energetically-favorable conditions for bases to bind in a way to form a triplex, including acidity and presence of magnesium ions.
The region of DNA where your gene of interest lies (or its regulatory regions, depending on what you're trying to do) would need to be unpacked, as well. DNA is usually packaged into chromatin. Histone complexes, which wrap up DNA, provide some measure of protection of the major groove. To make a triplex, you'd need biochemical conditions that unwrap histones and support triplex formation, generally.
Use of RNA, specifically, could be complicated if it is or could be processed into a short- or microRNA element, which could be consumed in downregulating the population of mRNA molecules (which, in turn, ultimately regulates gene expression). It isn't helpful if it gets used up before it binds to your triplex of interest.
There is some pharmaceutical interest in TFOs (triplex-forming oligonucleotides) as a drug-delivery mechanism.
If some gene is broken and implicated in a genetic disease, say, and its DNA or nearby regulatory regions can be made accessible, perhaps a TFO can be administered that would help turn up or down the expression of that gene's protein product.
Papers on TFOs could probably point you to other engineering problems that researchers have encountered and would need to overcome in order to create an effective medicine.


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A question about dicumarol
I know that dicumarol was discovered in moldy sweet clover as it caused hemorrhage in cattles, but if someone had thromboembolic disorders causing uncontrolled thrombosis,would it be fine to eat moldy sweet clover (in case of absence of any means of modern life) especially that it contains other microorganisms?


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A question about L-Citrulline
I know that L-Citrulline enters in the second step of urea cycle in the liver mitochondria and I wonder if a person takes an overdose of L-Citrulline wouldn't that cause mild hyperammonemia or at least cause an increase in the glutamine amino acid?


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Phenotype of a possible gene mutation
I have noticed multiple cases where patients had similar body characteristics :

decreased ability to gain weight (slim)

they are capable of sleep only 6 hours or less with normal functioning (although they prefer long sleep)

increased susceptibility to ligaments and connective tissue damages

CVS morbidities: example angina

I think its a good opportunity to ask here what could this mutation be and how would someone search for such characteristics in gene mutation databases.
I searched a lot using ordinary way and found a possible match ( ADRB1 receptor mutation) it causes the affected person ability to sleep less hour and CVS symptoms but i can't confirm if that's the case with the first and third characteristics.

Sounds a lot like the symptom of Marfan syndrome.

@bob1, marfan syndrome would have a different presentation  (you will notice their long extermities and eyesight problems ) not quiet like this case.


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A question about microbes growing media
I was told in my microbiology course that blood agar can be put in GasPak system (anearobic) to grow strict anaerobes, but why would someone use blood-dependent bacteria in this experiment as these blood-dependent bacteria will be aerobes or at least facultative

Maybe they wish to select against aerobes in a mixed species sample? The blood is just for nutrients.

You can put any media in a GasPak or other anaerobic system depending the type of anaerobic growth you are looking for. Sometimes blood is simply added to media to meet nutritional requirements of an organism. I use Columbia Blood agar often as a general purpose anaerobic medium. In a collection of 100+ obligate anaerobes I am working with, around half grow well on columbia agar with 5% sheeps blood, and many of those will not grow on Columbia without this blood amendment. As an added bonus, I can easily spot certain common contaminants growing on my plates by their hemolysis paterns.

Blood agar is prepared by heating the blood so that there will be lysis of RBC. Blood agar is mostly used to grow pathogenic organisms such as Haemophilus influenzae and Neisseria gonorrhoeae which cannot grow on other media.Neisseria gonorrhoeae can grow in the absence of oxygen. Haemophilus influenzae which is a facultative anaerobe also can carry out anaerobic respiration when there is no oxygen.Blood agar is very important to grow fastidious organisms, i.e the organism which is capable to lyse the RBC.

I think you are describing chocolate agar. https://en.wikipedia.org/wiki/Chocolate_agar


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What is the technical term for when a clade on a phylogenetic tree does not have an extended branch? (see image)

As we see with ZCA2, ECA2 & XCA2 these branches are compressed and do not extend as TCA does. Is there a technical term for this and what usually causes it?

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). For example, have you looked at the autogenerated "Related" posts associated with your question? This post seems like it could be relevant. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

The phenomenon where you have different "evolutionary clocks" of selection is called heterotachy. The branches are therefore heterotachic or simply long branches —long branch attraction is a problem with Bayesian inference for which many arguments have been had, so there is a lot of literature on it.


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What is the simplest way to demonstrate the germicidal property of UV light?
This is intended for a high school project. I am familiar with the one that studies growth of e coli over time in a petri dish but I a bit concerned about as to how safe a demonstration of this nature might be. also no idea as how one may obtain such e coli sample safely.

Welcome to Biology.SE! ——— Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

You can make homemade bacterial growth medium.
https://www.madaboutscience.com.au/shop/science-extra/post/grow-bacteria-on-homemade-agar-plates/
Basically it is just nutrient jello: beef stock, sugar, gelatin to make a firm surface.  It would be nice to have all your cultures in uniform plates or cups.  You could order petri dishes or use what you have available.  I would consider an ice cube tray or you could cut off disposable Red Solo cups to make dishes.
Then forget e.coli.  Inoculate the dishes with random things in the environment.  Everything has microbial life.   Fingerprints from various people are fine. Tongueprints would be a good variation - the jello is not poisonous.   A paw print from an animal would be fun.  A stick from the yard.  A snail.  Label each one with a label you can see from above - maybe a piece of paper on the table next to it.
Each of these prints will grow a mixed bunch of germs and fungi.  You might want to keep them cool because they will grow fast.  Take pictures periodically over time.  Keep them covered so they don't dry out.
Each type of dish (for example, Ted's tongue print) will have one dish in the dark (under foil) one in the light and one under UV light.  If you make big dishes you could have a half and half: light side and dark side.
Count colonies that can be seen at each time period.  That is your hard number and you can graph it over time.  The lines will diverge which will be a great visual.
In addition to the inhibitory effect of UV you can discuss how it differs.  Suppose there are orange colonies which do not seem to be inhibited by UV in the same way as everything else.  You could smear some of the orange on a microscope and look it is.  Is it some resistant organism?  You could discuss the variety of colonies that appear depending on the inoculum.


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CD spectra of Porin molecules?
Can anyone please help me how will the CD spectra or graph of porin molecule look like. Porin molecule has 14 beta plated structures joined by some random coil, but it's very confusing to draw it. Can anyone please help me?

Welcome to Biology.SE! First, please define abbreviations (i.e. CD). Second, we encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). For example, if I search with your title I get numerous hits to papers including this.——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and edit your question accordingly. Thanks!

CD (circular dichroism) spectrum of porin will look like CD spectra of most beta-sheet-reach proteins. You can look, for example, paper on PorB protein (Minetti et al, JBC, 1998) where authors present CD spectra of one of porines:
Circular dichroism spectra of recombinant PorB class 3 protein as a function of SDS. Standard solutions of PorB rclass 3 protein (1.0 mg/ml) dialyzed against a buffer comprised of 10 mM sodium phosphate and 0.05% zwittergent 3-14 and incubated with varying concentrations of SDS (0-1%) at 25.0 °C for 24 h prior to spectroscopic analysis. Far UV CD spectra are recorded for rclass 3 in the absence of SDS (solid circles) and at the following SDS concentrations: 0.15% (open triangles), 0.25% (solid squares), 0.30% (open diamonds), 0.40% (solid triangles), 0.45% (open circles), 0.50% (solid diamonds), and 1.0% (open squares).


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Insect Identification question: Is this a flea? If yes, what kind?
I live in the pacific northwest and I found these insects in the carpet and comforter. I suspect them to be flea based on my image search. But I would like to confirm. Can you also tell me what kind of flea is this?
1
2
3
My apologies for the grainy pictures. These are my attempts at capturing the photo from the microscope's eye piece using my smart phone.

This may be indistinguishable, thus better images may need to be taken.

It does look very much like a flea though.


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Creating animal models
I was wondering how a scientist in a lab may know which type of animal model to use. I have been looking at the effect of a protein on a disease. And have thought about the ways that’s i know this has been done in other research-
- deletion of gene which encodes for protein
- insert GFP by Gene for protein leaving gene intact
- or insert gfp by gene for protein deleting the gene
However I cannot seem to understand how a scientist decides to choose a certain model?

Hi Beth and welcome to Bio.SE! Could you link the paper you are describing in the experiments, and narrow down the question? Currently, it sounds like you are asking a very broad question about animal experimental design and then describing a molecular biology experiment.

If you look at the definition of a model organism as this can be found on the Nature Homepage, this clarifies quite a lot:

An organism suitable for studying a specific trait, disease, or
  phenomenon, due to its short generation time, characterized genome, or
  similarity to humans; examples are a fly, fish, rodent or pig, whose
  biology is well known and accessible for laboratory studies.

So you want an organism, that:

can be bred in large numbers
has a sufficiently short generation time, so you can analyze several generations of it
is well characterized
sufficiently close to the organism you want to learn more about (mostly: Humans), so the findings can be transfered
can be mutated and has your gene/protein/etc. of interest
has been sequenced completely

Besides this general considerations, practical ones also play a role. If you don't have a fish facility on hand, you will most likely not start using zebrafish as your animal model.
There are certainly more requirements, see one of the references.
References:

Requirements and selection of an animal model.
Selecting appropriate animal models and strains: Making the best use
of research, information and outreach
Basic Principles in Selecting Animal Species for Research Projects


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qPCR to detect viral load
In an experiment qPCR was used to determine viral load. Alongside this conventional PCR was also performed and ran on an agarose gel. However I do not understand why both methods would have been used, any insight would be greatly appreciated?

Can you please add some more information about the experiment? Or add a link to the reference where you found the description of the experiment. Otherwise this question will be hard to answer, since there may be many reasons to do a conventional PCR.

It was an experiment we did in the lab. We performed qPCR on samples from 2 patients to test them for HIV. I understand why qPCR was used however I do not understand why we were also asked to perform Conventional PCR alongside this.

How did the two experiment differ or what did you do with the samples (besides letting the samples from the conventional PCR run on a gel)? Which qPCR machine did you use?

qPCR primers are typically designed to amplify a single, small (<200 bp) amplicon.  Most modern qPCR machines allow the user to perform a melt curve analysis at the end of the experiment to determine if there is more than one amplicon species.  If you are using an older device without this capability, conventional PCR and gel electrophoresis could be used to determine primer specificity.  As for why the experimenter didn't just load the qPCR product into a gel, perhaps they forgot.


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Eagles carrying off a goat to its nest: How heavy is the young goat? How strong is the eagle? Here is my guess:
I posted a related question, here, trying to identify the exact subspecies of animals. In the documentary El Hombre y la Tierra, a golden eagle carries off some sort of juvenile(?) goat.
The Japanese golden eagle male weighs as little as 5.5 lbs, while the largest subspecies female weighs around 14 lbs. However, the largest species lives in Central Asia, and this footage is from Iberia, I believe. Therefore, it is more likely the subspecies is the one that lives in North Western Europe (I presume they reach south to the Iberian Peninsula), which weighs 7.7 lbs and 11 lbs on average for males and females respectively.
The question is how heavy a juvenile goat is likely to weight. The goat in the video does not look much smaller than the adults, though it is a little hard to tell. The Iberian ibex, which the goat supposedly is a member of, ranges in weight from 65 to 265 lbs.
If we estimated the goat to be a fraction of that lower estimate, say a quarter, that would be 16.25 lbs. If we took the 11 lb estimate for the golden eagle, that would mean it carried 147% of its body weight back to its nest. Wow!

The goat attacking the eagle in picture 2 must be an adult, either a male or a female. It does not seem much larger than the goat that was carried off in the first picture, however. This might mean the eagle carried off a goat significantly heavier than itself!
I would appreciate your input on my investigation into this matter. I feel this would be worth academic study.
Thank you.
PS: It was a lot of work to research and post this, so please don't delete it. I will repost it somewhere else if this is outside the scope of this stack exchange. Thank you for your understanding.

You may find this link to be of interest ...

@tyersome That is very interesting, thank you for sharing it!

The weight of the eagle is not the deciding factor, it is its lifting power of flight ie the “wing” power... which has to overcome the total body weight...


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what is this insect? just curious
Thank you for replying my question..and sorry for my broken english (https://i.sstatic.net/5GXs5.jpg)

@PriyanshuDas Answers should be posted as answers, not comments. Additionally, from How do I write a good answer? in the [help], Answer well-asked questions. Not all questions can or should be answered here. - we should encourage questions to be improved rather than answering ones that do not fit the guidelines.

Welcome to Biology.SE. See this page: https://biology.stackexchange.com/tags/species-identification/info for information on what we expect for species ID questions. Also please embed your image in your question rather than posting it as a link.


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Violation of Conservation of energy In food chain?
Food chains use a unidirectional transfer of energy. Plants absorb energy from the sun,  then the energy goes on to next tropic level and so on. But in this system, energy source is the Sun.
When any organism dies, it’s decomposition doesn’t contribute energy back to the sun (as the nuclear process in the sun keeps on generating energy).
So my question is - doesn’t it violate the law of conservation of energy? As energy is not flowing back to the sun? Here Sun is the ultimate source of energy as it just keeps on creating energy, so energy isn’t conserved?

The Sun doesn't create energy; it converts energy from one form to another - in particular, it makes light. The physical details need not concern us here: what matters is that the Sun's fuel supply is gradually depleted (over billions of years), producing light. What interests biologists is that photosynthesis harnesses some of this light energy, and each trophic level receives, on average, about 10% of the one below it.

I agree with you, But if we look at a food chain, Sun is a source of energy. At the end of the chain the energy doesn't go back to the sun. That is the reason for my question...

@neefg Conservation doesn't require energy to go back to where it started. If you use a hob to boil water, the oven never gets back the thermal energy.


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Why are humans rarely preyed on?
I did a bit of research and noted that some animals such as alligators can indeed digest humans. However, in a lot of cases, they actively avoid humans (bears, alligators, boas). Intellectually, yes humans are responsible for a lot of stuff (e.g. guns and habitat destruction), but on an animal's level, we're just a walking sack of meat with legs and arms.
This question sort of hinges on the idea that it would take too long a while for evolution to tell animals to avoid humans such that they're doing it now (feel free to tell me otherwise with an explanation as to how).

Tell that to Tanzanians. Predatory animals don't avoid humans.

First, I think you have a major misconception about prey selection being entirely evolutionary and driven by instinct.  Animals learn. Mammals, in particular, learn from their parents and/or other pack members, as well as from personal experience.  So wolves, lions, or other large predators develop a culture of humans not being good prey.
Second, many predatory animals tend to be opportunistic hunters.  They want to acquire their dinner at minimum cost to themselves.  They don't want to risk injury by engaging in a stand-up fight with something of comparable size.  Adult humans are pretty large creatures.
Third, and perhaps the most important, is that humans have learned to deal with large predators.  Even before the invention of modern weapons, they learned to avoid places where the predators might lurk.  For instance, if you visit Florida or parts of northern Australia, you're well-advised not to go swimming.  Even so, there are about 1000 deaths per year from crocodiles & alligators: https://en.wikipedia.org/wiki/Crocodile_attack

Its also worth noting humans have put some extremely strong pressure against predators that seem humans as prey and live near humans, Its worth noting predators that attack humans are wither hard to kill (semi or fully aquatic) live in places humans rarely live, or are extinct or close to it. humans have wiped out dozens of large predator species.

In support of learned behavior, animals that attack or kill humans (e.g. grizzlies) are hunted and destroyed, because, well, they tend to repeat that behavior once learned. If they weren't destroyed, there might be a whole lot more predators of humans around.

@anongoodnurse: The learning works the other way, too.  Consider dogs and skunks.  Most of my dogs have had a skunk encounter when fairly young.  Almost all of them learned not to repeat it. (Except my current dog, who needed two.  But then, he's not the smartest puppy in the litter.  Still chases bears, despite a rather unpleasant experience with one.) So even if the predator is just driven off, rather than killed by humans, it learns that there are easier meals to be had.


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Is the frequency at which a species mutate affected by natural selection?
As per natural selection, is it safe to assume that some species will have it genetically encoded so that they produce a certain 'perfect' rate of mutation so that they can adapt to an environment that changes quickly?
Another way to put this; does every type of organisms have  roughly the same amount of mutations each time they reproduce (relative to the size of their DNA)? If so, is/can/could this be governed by natural selection?

Does this answer your question? Has there been any observation of species adapting the evolution process?

Drake's rule
Let $L$ be the size of the genome. Let $\mu$ be the average per nucleotide mutation rate, then the genome-wide mutation rate $U$ is $U=L \mu$. There is a general relationship between the genome size of an organism and the nucleotide mutation rate that makes that the genome-wide mutation rate is often approximatively 1. There is of course several orders of magnitude of variation around this value of 1 among organisms.
This rule is called Drake's rule after the name of the author who first discovered it (Drake, 1991).
To my knowledge, this relationship is not fully well understood. Because you are looking for an adapted mutation rate in your question, I would like to highlight that I would not go about assuming this is adaptive. I could imagine that some molecular genetic constraint of the replication process could be causing this type of relationship between $L$ and $\mu$.
You will probably want to read this post about Drake's rule.
Mutation rate in humans
In humans, the average mutation rate is estimated to be around $\mu=2.5 \cdot 10^{-8}$ (Nachman and Crowell, 2000; see also this post), with a genome size of about $L=3 \cdot 10^9$, leading to an estimate of the genome-wide mutation rate of 80.
Interestingly, the mutation rate is in fathers is age-dependent. See the post Gender and age-specific mutation rate in plants.


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Do kids under a certain age not hear the warning beeps that smoke detectors make when they are running out of battery power?
I've always been very annoyed by those regular single beeps that smoke detectors start doing increasingly often as the batteries start to run out, to warn (and annoy) the user to replace the batteries. They drive me insane.
Lately, I've been observing how a bunch of kids seem to sit in a room and just ignore those beeps completely, even after I point it out and ask them to really listen. They can't hear them. I seriously believe that they just don't physically hear them. Kind of like those dog whistles.
Is this backed up by science? Do kids under a certain age literally not hear those "low battery" warning beeps? Is this maybe per design, even? If so, why? Isn't it important that as many humans as possible are annoyed by this so that they replace the old batteries with new ASAP?
It's really frustrating to me when they don't even hear it, but I hear it very well. I hate it so much.

Hi Leonard, I don't think this question in its current form is a good fit for Biology.SE. If you can add a reference to a notable claim then I think this question could be migrated to Skeptics.SE and answered there.


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Crossover Value and Genetic Mapping
In my textbook and most of the sources I have checked, it is stated that recombination frequency in eukaryotes give us knowledge on the location of the loci. I don't understand the direct correlation between the distance between the genes we are investigating and the recombination frequency. Assume that the recombinant gamete frequency of is around 35%, why does it mean that those genes would be located on the opposite ends of the chromosome? Do all crossover events take place with a single break on one chromosome? I have searched the crossing over mechanism for a bit and have seen diagrams in which two breaks occured and the DNA chunk acquired seemed to be transplanted, although it was in general a tad too complex for my understanding. If you have a link to a clearer and more concise explanation of the mechanism, it would be much appreciated! Please forgive my ignorance if that's a very basic question, I'm just a high school student.

Welcome to Biology.SE! For this question, you should be able to find answers quite easily from reliable sources and as such this question seems to fit this sites criteria for "homework". I encourage you to start with the basics — see my next comment for suggestions. That will allow you to ask more focused questions and make you have the background to understand the type of answers you are likely to get here. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful. Wikipedia is also generally a good starting point and you can then check their references. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

As a silly example:
Let's say that you are traveling along a road where you know there are bandits and thieves. You want to finish your journey quickly, and spend very little time on the road, because the more time you spend on the road, the more likely it is that you are robbed and they take your money away. If there are more thieves around one day, you still want to spend as little time on the road as possible, it's just that the risk is higher.
Using this logic, you can then try to figure out how far away two cities are on the road by how likely you are to be robbed by thieves while traveling between them.
Just substitute "chromosome" for "road", "crossover" for "robbed by thieves". You measure how far away two loci are by how likely there is to be a crossover between them.
It may help to think of it in a different way. There is nothing preventing multiple crossovers, but having more crossovers saturates with increasing distance. Here is one plot of how you can think of linkage (I just generated this, it's not mathematically accurate, only for demonstrating simple point):

Figure 1.
Basically, the closer two loci are, the less likely it is that there will be a crossover between them. So if you compare three loci, two of which (A, B) are close when the third (C) is far away, you will see few AxB crossovers/recombinants but many AxC and AxB crossovers/recombinants. This is because the probability of crossovers is fairly uniform across the genome. The more distance, the more opportunities for crossover.
Another confusing feature is that the maximum number of recombinants (usually) is 50%, because at that point the two loci are assorting independently, e.g. completely unlinked and behave as if they are on different chromosomes. However, two loci can be "unlinked" and still be on the same chromosome, they are just quite far apart then.
This is not really changed by multiple crossovers. The same principle of "loci further away" --> "weaker linkage between loci" is the same no matter how many crossovers occur in a chromosome. More crossovers just means that the map is "expanded", because everything is more weakly linked than with fewer crossovers per chromosome.
Update:
It may help to be very specific about what we mean by "same chromosome" vs. "different chromosomes". Recombination happens between two molecules that can be considered the "same chromosome" even if they are different molecules. We call them "homologous chromosomes" because they pair and recombine. On the other hand, when we talk about 23 chromosomes in human cells, those are "different chromosomes", but they are actually 23 pairs of homologous chromosomes, so there are in total 46 chromosome molecules, which can be arranged in 23 homologous pairs. For each pair, we get one from each parent ("paternal" and maternal").
Recombination only occurs between homologous chromosomes.
So when recombination happens, the locus doesn't transfer to a different chromosome. It stays on the "same" chromosome, it's just a different version of the same chromosome. See this image (Figure 2):

Figure 2.
You can think of a chromosome as a collection of loci in some linear order. This will arrangement will be the same (or close enough, for our purposes) for each chromosome of a homologous pair. It may have different versions of the locus on each chromosome of the pair. We call these different versions "alleles", which in Figure 2 are labeled "A" and "a" for locus A or "B"/"b" for locus B. So we start with types AB and ab, but if recombination happens then we would observe types Ab and aB. The loci didn't move between chromosomes, they just exchanged alleles.
In terms of how loci "split", think of them as two chains of the same length. When recombination happens you cut one link of each chain, exchange pieces, and rejoin the chains. See Figure 3:

Figure 3. single recombinant: a single recombination event occurred between maternal and paternal chromosomes at coordinate x = 1.0 to yield a recombinant. Double recombinant: two recombination events occur, at x = 0.8 and x = 1.0

Thank you a lot for the detailed answer sir, the analogy did help a lot! What I can't fully grasp is how a crossover incident between two loci guarantees that they would end up in different chromosomes. For example, for A, B and C genes located in that order on a chromosome, if a crossover happens on the gene B, does it automatically mean that A and C would be split?

@TarıkAkçin if there is only a break at B, then yes A and C would always be on different chromosomes. However, it's entirely possible that there could be more breaks between  A and B or B and C and whether A and C ended up on the same chromosome would depend on whether the total number of breaks between A and C was odd or even.. The probability of additional breaks depends on the distance between A, B, and C. In human chromosomes there is always at least one crossover, and typically between 2 and 4.

@TarıkAkçin see update to answer.

@TarıkAkçin and to directly answer your comment question, the answer is "yes" as long as the number of breaks is odd, and "no" if it's even. I am hunting for a good image that shows this.

@TarıkAkçin I gave up and made it myself. see figure 3.

There are two main question: (a) dependence of the frequency of recombination with the distance that separates genes and (b) do all crossover events take place with a single break on one chromosome?
Let's give some context. In gametogenesis, chromosome crossover takes place in every tetrad in prophase I. Tetrads are constituted by a pair of homologous chromosomes which are paired by a particular complex (synaptonemal complex). Such complex allows one chromosome to be very close to the other. This intimacy permits chromosome crossover to occur between non-sister chromatids and sister chromatids. This interchange is random and can potentially take place in any place of the chromatids and it begins with the breakage of the two chromatids in a common site, so there are two breaks per event (question b). It must be said that there are generally multiple chromosome crossover events per tetrad.
Even though chromosome crossovers can potentially take place at any site, the probability of such events occurring is proportional to the distance that separates two genes, which implies that genes that are separated by a great distance (one in the p-arm and the other in the q-arm, for example) are more likely to be split apart than any pair of genes which are closer to each other. The classical explanation is that there are physical impediments to the formation of chiasmata when genes are close to each other, such that the chromosome crossovers between neighboring genes is unfavorable, while the formation of chiasmata when the genes are far away lacks such physical impediments, and is therefore more favorable (question a).

    https://i.sstatic.net/2LbJT.png. A non-sister chromatid with three distinct genes (A, B and C). In addition, 1,2,3 and 4 are other genes.
A more intuitive way of understanding such dependence is by considering that chromosome crossover is random. Let's consider a non-sister chromatid, like the one in the figure above, whose genes A and C are far from each other. In order for recombination to take place between A and C, there would have a break in the space between the two genes. Because this distance is big, such break could take place in 1, 2, 3 or 4 (and many more), in the other hand, if we consider a recombination between the genes A and B, the only possible way to achieve this is by a break in 1. Because crossover is random, since there are a lot more possible sites of breakage between distant genes, it is more likely that one of these many places is selected as the site of crossover. Crudely speaking, it is analogous to the throw of a dice. The probability of getting a 2, 3, 4, 5 or 6 on a single throw is much bigger that the probability of getting a 1, simply because there are more possible outcomes in consideration.
Regarding the mechanism, it all depends in the depth you want to cover, nevertheless, I would advise to read the section of chromosome crossover in Introduction to genetic analysis by Griffith


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Why are plasmids called plasmids?
I knew from this website (https://www.etymonline.com/word/plasmid) that the word "plasmid" is a combination of "plasma" + "id" , where "id" means: belonging to or connected to.
But I don't understand how plasmids are connected to plasma even though they exist inside the bacteria cell cytoplasm not inside the blood/plasma

even though they exist inside the bacteria cell cytoplasm

Plasma has several meanings in biology.  Cytoplasm is a type of plasma.
A quick trip to Wikipedia tells us that the term plasmid was first used by Joshua Lederberg in Cell Genetics and Hereditary Symbiosis.  It seems that he coined the term plasmid to reconcile the many terms used to describe extrachromosomal DNA, at the time.

These discussions have left a plethora of terms adrift: pangenes, bioblasts,
  plasmagenes, plastogenes, chondriogenes, cytogenes and proviruses, which have lost
  their original utility owing to the accretion of vague or contradictory connotations. At the risk of adding to this list, I propose plasmid as a generic term for any extrachromosomal hereditary determinant. The plasmid itself may be genetically simple or complex. On occasion, the nuclear reference of the general term gene will be emphasized as chromogene...


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How does excessive acute inflammation damage tissue (eg, in sepsis or cytokine release syndrome)?
While inflammation is necessary to recruit immune cells to sites of infection in order to clear the etiological agent of disease, excessive inflammation has often been implicated in many of the poor outcomes associated with systemic infection, specifically end-stage organ failure (eg, in sepsis).
However, what is not clear to me is what the effector mechanisms of excessive inflammation are which mediate the tissue damage necessary to cause the organ damage. It's very clear to me that excessive signaling through neutrophils can, through positive feedback loops, create a large amount of systematically circulating inflammatory cytokines. But what's less clear to me is what the link is between extremely high levels of cytokines and the ultimate tissue damage associated with excessive inflammation. Presumably, it cannot be due to the direct effector functions of humoral responses or cell-based responses, as both antibodies as well as TCRs are exquisitely specific to foreign antigens. One common explanation is excessive fluid accumulation in tissue due to enhanced vascular permeability - a classic feature of the inflammatory cascade and necessary to allow leukocytes to enter the tissue space. But are there other effector mechanisms by which excessively high pro-inflammatory cytokine levels cause tissue damage?
In short then, while I understanding the pathogen --> inflammatory cytokine secretion stage, what I don't understand well is the inflammatory cytokine secretion --> ?? --> organ damage.
Sources:

https://en.wikipedia.org/wiki/Sepsis
https://en.wikipedia.org/wiki/Cytokine_release_syndrome

You can assume there are no effective antibodies. See immune response to respiratory virus: balancing virus clearance and immunopathology. This paper explains how cell suicide with in the same time call for phagocytes to clear the nearly dead cell is the normal way to eliminate infected cells and hence the virus. The inflammation enhances those processes but supposedly in a tightly controlled way.


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Are there any examples of viruses that have jumped from reptile to human?
I know that there are plenty of examples of zoonosis occurring from reptiles to humans that involve bacterial pathogens, (e.g. Salmonella) but are there any instances of viruses being transferred from reptiles to humans?
If applicable, for this question, I am only interested in reptilian viruses "jumping" from reptiles to humans, not the capacity of reptiles to serve as reservoirs for non-reptilian viruses that could potentially infect humans.

By reptiles, do you mean non-avian Reptilia?

Yes, thank you for the clarification.


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Does a tubular sodium reabsorption cause a stimulation of β2-adrenergic receptors?
I read the study "The Role of Aldosterone in Obesity-Related Hypertension" and there is one thing I didn't understand. They write: "According to norepinephrine-induced tubular sodium reabsorption, stimulation of β2-adrenergic receptors leads to activation of the Na–Cl cotransporter through suppression of the serine-threonine protein kinase WNK4 in the distal tubule." Is According to meant like due to? So does a tubular sodium Reabsorption cause a Stimulation of β2-adrenergic receptors?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4886496/

You've got it backwards. "norepinephrine-induced tubular sodium reabsorption" is the whole process. The β2-adrenergic receptors respond to norepinephrine (this is the "norepinephrine-induced" bit). The receptors then suppress WNK4 in the distal tube ("tubular"), which causes the Na-Cl cotransporter to activate, which in turn causes sodium reabsorption.
This was probably a poorly phrased sentence on the part of the writers, but the sentence follows the same logic as "According to the First Law of Thermodynamics, energy cannot be created or destroyed". The description of the process is just complicated by multiple clauses.


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Is it possible nowadays to artificially create an organism just by inserting organism's DNA into an artificial environment?
Let's say we have a DNA of a bacteria and we want to recreate the bacteria just from this DNA. Is it possible nowadays to get this DNA and insert it into some artificial solution so that from this DNA a bacteria coulb be grown?

Please note that this is not simply an answer site, but instead a site that promotes self-learning with some expert help. Consequently, questions that show little or no prior research effort are off-topic on this site as are "homework" questions unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Please take the [tour] and consult the [help] starting with [ask] for details.

There may be technical issues that make certain genomes easier to transplant than others, but it can and has been done. Craig Venter's lab used such a transplantation technique to discover what minimum set of genes are required for viability in an engineered bacteria.

Actually what I'm really interested about is a possibility to create an organism just from DNA using just just some artificial solution neccesary for organism's growth etc. Or is it always necessary nowadays to transplant this DNA into some living organism?

What is in your artificial solution? Nuclear proteins? TFs? Ribosomes? ATP? Floating balls of lipid bilayers? By the time you build this artificial solution that has what you need to get the necessary biochemistry going, you would effectively have the constituents of a cell, minus your DNA of interest.

Short answer-NO.
Long answer-NO, too. We are far from having the technology to do such feats of engineering no matter what some ill-informed pretenders say. We have the technology to create artificial genomes which could be integrated into real cells and good progress is made on creating artificial chromosomes, e. g. bodies containing the genetic information needed to sustain an organism, but we are far from being able to artificially create one.
And there is also the problem of infinite regress which no one seems to bother about but it's out there. It's essentially the notion of which component comes first in order to jump start a metabolism - whether you first put the genetic apparatus or the metabolism which is required to support it or you jumpstart them both. It's an issue that still hasn't been resolved yet.
So, NO, we aren't capable of creating artificial life yet and we aren't likely to be capable of creating it in the near future. That's the answer to your question.

I'm not denying the correctness of your answer but it would be nice to have some sources to help people put it into context. Thanks.

Strongly agree with @user438383 — this is correct (and better than the other answer), but doesn't meet the current site standards. Please consider reviewing the [tour] and [help] starting with [answer] and [ask]. I would also encourage you to focus on well asked questions rather than encouraging questions like this that show no evidence of the expected prior research.

Very perceptive answer.

While this answer contains some correct information, you may want to expand into viruses, where it is certainly sometimes possible to create viruses from the genome alone or using plasmid-based systems (done for a bunch of viruses, including adenovirus, influenza, coronavirus, plant viruses, bunyaviruses etc.)

This answer is incorrect, in addition to being poorly written.


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How does the surface of the eye remain moist during sleep?
When we are awake, blinking helps distribute the tears so the cornea and the entire conjunctiva are wet and moist. But how is this maintained during the night, when we are sleep and there is no blinking.
Doesn't the tear just pool down? Or is there some sort of tone in the palpebral muscle of the eyelids.

With the eyelid closed, what would cause the eye surface to dry out?

tears would be sucked by gravity into the nasolacrimal duct. So the tears aren't distributed throughout the eye surface, that's what I am saying.

Welcome to SE.Biology! You might find it helpful to look at this guide for asking a question that's more likely to get a good answer: https://biology.stackexchange.com/help/how-to-ask. Can you identify a specific source or a quote on eye wetting that is leading you to confusion? You might also consider posting this question on SE Medical Sciences where people are more familiar with human physiology.


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Basic Molecule Editor for use in journals / theses?
My background is Geosciences and Physics and I am going to study water and biomolecules in the Autumn.  I was reading a PhD thesis about peptides and peptoids by someone in my research group and I had a really basic question abouting the drawing program that they would have used to create molecular diagrams.  I found this link https://en.wikipedia.org/wiki/Molecule_editor and it looks like a good starting place but could someone recommend a default app for creating drawings like the ones below?

Thank you!

Might be better to ask on the Chemistry site.  Or the LaTeX site: I know there are some extensive LaTeX chemistry packages, though I've never used them.

With the exception of the protein, which may have been generated with Pymol or something similar, the illustration looks like an artist or designer job for a book or review.  Professionals would not be using diagrams in the style of the rest for presenting either chemistry or protein chemistry. If you search past questions on this list you will find some on protein graphics.

Thanks for the comments.  The references for the figures don't credit anyone so I assumed they had created them themselves.


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neural genes expressed in nasopharyngeal specimens
Is it possible in a nasopharyngeal specimen genes of neural system to be expressed? For example, genes about neural differentiation?

Can you please add some more details? Of course there can be some genes that are expressed in two different tissues. If you provide a background to your question then it would be a bit more clear.

I mean if it is possible to find genes that are specific for neural development and differientation in pharyngeal cells.

This paper mentions using a cytology brush (not the usual NP swab) to obtain cells from the olfactory epithelium. They obtained and cultured neural precursor cells. Have a look.
Trends in molecular medicine.
"The Olfactory Neural Epithelium as a Tool in Neuroscience"
Joëlle Lavoie, Patricia Gassó Astorga, [...], and Koko Ishizuka
from:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5399677/


text:
types of cells in a pharyngeal specimen
I would like to ask what type of cells should someone expect in a pharyngeal smear, in a person, who is infected with a viral infection. Thank you a lot!

I’m voting to close this question because it seems to be a medical question rather than one primarily about biology. This means it is not on-topic for this site. While this might be a better fit for [MedicalSciences.SE], please don't repost (instead request migration). Please consult the [tour], [ask], and other [help] pages for more information.  Thanks!

The tissue in the pharynx include:
Stratified squamous epithelium & mucus-producing glands.
However other cells that could be found would be other types of bacterial, is this what you're referencing?
Commonly scientists start with a gram stain to determine the classify the bacteria.
Gram+ bacteria have cell walls composed of thick layers of peptidoglycan. Gram+ cells stain purple when. Gram- bacteria have cell walls with a thin layer of peptidoglycan. Gram- bacteria stain pink.
The microbiome of a human consists of 100,000 billion bacteria. Therefore there are many types. E.g. Prevotella has been shown to be the most common type of bacteria in the human pharynx.
In a pharyngeal smear you would expect to find Stratified squamous epithelium, mucus-producing glands, bacteria and if a virus is present. Viral particles. This can be determined by RNA or DNA analysis.
E.g. COVID-19 is an RNA virus. If PCR analysis was completed on a sample obtained from a pharyngeal smear then we could confirm the presence of the aforementioned mammalian cells, bacteria and viral genetic material.

should someone expect lymphocytes?

@Marilu, lymphocytes continuously circulate between the lymph and blood until they encounter a foreign antigen. It would be possible, but it's usually not the aim of a pharyngeal smear. A blood test would provide better results to identify how 'hard' the immune system to working.

thank you so much!

Happy to help Marilu.


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blast search against UNIPROT
I would like to ask how i can search in blast against UNIPROT (TREMBL PLUS SWISSPROT) for a selected organism. In the BLAST site there is no option about UNIPROT(only Swissprot), and in the uniprot site i cannot limit the results only in one organism(E.COLI).
THANKS A LOT!!!

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. In particular, this question seems like it might be a better fit for [Bioinformatics.SE]. Thanks!

thank you and i am sorry!!

You can blast for E.coli proteins only using Uniprot. Firstly, you restrict the search to the "target database" UniprotKB...Bacteria. After performing the blast search, you can further restrict your search results to include only hits for one "Popular organism", e.g. "Escherichia".

thank you so much!!

@marilu Can you please mark my answer as correct?

is it ok?i think i did it

@marilu Yep, thank you!


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Is it possible to accelerate active transport in plant vascular system using some electronic method?
I am from electronics background and got an understanding that electrical current affect plant growth. Based on this phenomenon, I got an idea but before I formulate my hypothesis and start experimentation around it, I am looking for some expert opinion on this.
Can we accelerate mineral transport like water movement from root to leaf by some external influences?

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Including a summary of what you have learned with references (e.g. to electrical current affecting plant growth) will demonstrate that you have made this effort and provide context for your question. ——— Thank you for taking the [tour], but please also go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. Thanks!


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A poor man's COVID-19 vaccine?
If person A is infected (COVID-19) and person B is not, could the following work as a vaccination?  Person A exhales (coughs?) into a a transparent bag.  The bag is radiated for a long time with a strong ultraviolet (UV) light as is found in some residential well-water systems.  Person B inhales the contents of the bag.
I am curious mostly about how virus particles are damaged at the molecular level by UV light and how this relates to how vaccines are manufactured today.

SE Biology is a question and answer site — not a discussion site or a site for floating ideas. It is concerned with the mechanisms of biological processes, not medical aspects of biology. I therefore think  that your question on dealing with the coronavirus outbreak is off-topic here. You are advised to consult more appropriate reputable sources for such information, some of which are listed here.

@David Respectfully, my question is simply "Is this (a UV-light vaccine design) possible?"  "COVID-19" is just a modifier (it could be any pathogen).  I sat for minutes deciding whether to post this on Medical SE, but it's the DNA damage that's in question and how the body would respond to it, so I posted here.  And judging by your background, in relation to the last sentence of the question, I'm surprised you didn't offer an answer!

Short answer: probably not.
Long answer: for your body to build immunity against something, it needs to identify it as something harmful to you. Otherwise, how would it know if this is just some random particle in your environment that it should ignore? There are molecular clues that your body uses to recognize better whether something is likely a pathogen (that means it should try to build immunity against) and those are some of the additives (known as adjuvants) present in man-made vaccines.
Also, the route of administration is also important. Things that you eat or breath in are triaged by the waldeyer ring because maybe you just ate something that is alive, but not exactly a pathogen. Dysfunctions in this process (thinking a normal protein is part of a dangerous pathogen) is believed to be one of the possible causes of allergies. Injecting it into your blood-stream often makes it more effective (but there are exceptions: polio vaccine however can be orally administered).
A nice read about this topic is this: The dichotomy of pathogens and allergens in vaccination approaches.
This is perhaps a must read on this topic: What to expect of a good vaccine and how to achieve it.
I'm not really sure what else to tell you. The process you described is a part of the manufacturing of some vaccines, so you are on the right track. But vaccines are hard to make, you can't do it for every disease and involves a lot of experimenting.

As a layperson, I always thought vaccines were damaged, non-functional pieces of the original pathogen.  The body would then recognize these fragments as something to attack.  Perhaps that's incorrect thinking.  Thank you for the links, though.  It will take me a while to get through them.  Initially, I don't see much about the use of ultraviolet light in the design of vaccines in them, but they might point me in the right direction.


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Difference between rate of elimination and clearance?
I honesty don't get the difference. I need a simple explanation so that I can grasp it.
Rate of elimination is

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). For "homework" questions, you are required to show your attempt to answer the question and to use the "homework" tag. (Note that "homework" can apply to questions even if they were not assigned as homework.) ——— Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

Clearance is a measure of the volume of plasma from which something is removed, per unit time. For instance, it could be 2 mL/min, meaning that every minute, a two-milliliter of drug plasma is cleared. In other words, it is the rate of drug elimination divided by the plasma concentration.
Remember that the elimination rate is in units of inverse time, so dividing it by inverse volume gets you volume over time, which is the standard dimensionality of clearance.

Thank you! It finally clicked.


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what are the factors that can be used to compute the probability of getting the coronavirus?
Our team and I work on a project for the Lauzhack 2020 and to achieve this work, we need to determine some factors that can tell us what is the probability of contracting the coronavirus.  Is there any one who know what are the determining factor to compute the probability of catching the virus ? (for example some research paper about it). For example, we know that if we are old, and if we are in contact regularly with people, we are most likely to catch the disease. We would like to have some basic knowledge about the transmission of the virus. We would need data about the probability of being infected as a function of the time we had been in contact with someone who have the disease. Any help would be appreciated !

For example, we know that if we are old, and if we are in contact regularly with people, we are most likely to catch the disease. -- Yes, contact with other people is a risk factor for transmission, but is age?  Sure, older folks are more likely to succumb to the virus, but I think it's important that you parse the concepts of probability of viral transmission and likelihood of symptomatic viral infection.

I'd refer you to a couple of papers in Lancet, here and here. They, in fact, have a mathematical treatment of this very question, and in the supplementary material they list some parameters that might be useful to you. Good luck!

hello and thank you ! where can a find these lists  in the paper ?

In the supplementary information of the second reference (a PDF file you'll find at the end of the paper) you'll find a table with the parameters they used.


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What current evidence supports the use of hydroxycloroquine used as a prophylactic for (corona)-viral infections?
I've also read comments from doctors suggesting that hydroxychloroquine has been studied in the past as a potential prophylactic for viral infections.  A search through US clinical trials yields many results which mention this drug in connection to lupus, arthritis, and cancer.  But I have yet to find completed clinical trials which revolve around viral infections - does this exist somewhere or has this never been studied?

What has your research shown?

SE Biology is a question and answer site concerned with the mechanisms of biological processes, as you will see if you finish reading the Tour. Your question is about the results of clinical trials, which do not come into this category. There are ample reputable sources that provide expert and up-to-date information about efforts to combat the coronavirus, some of which are listed on our meta site. Please consult that.

The only double blind randomised clinical trial I am aware of is this one, examining the use of hydroxychloroquine for the treatment of HIV-1-infected patients.  It finds significant reductions in viral load, but not improvement of CD4+ counts.  How much change could be expected in 8 weeks I do not know.  There are in vitro studies, such as this one looking at dengue virus.
In combination with azithromycin it has been examined for the use in COVID-19 (pre-print, not peer reviewed), but without a control group I find it hard to call it a clinical trial, and there are other criticisms of the work.


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Why do E.coli form parallel clusters?
Discalimer: I am not a biologist. I am modelling E.Coli growth and in the Wikipedia gif one can see observe some groups where the bacteria are one next to each other, oriented at approximately the same angle. I did some simulations and obtained similar results. Is there any reason why this happens?

Cell division happens by division at the middle of the rod, so the result is two daughter cells that are at nearly the same angle. Over time in the absence of agitation moving cells around, this will lead to a groups of cells that have non-independent cell orientations.
For more information, including how people have induced it to do otherwise, see this paper.

Bacterial cells prefer to attach with each other in parallel orientation so that they have maximum surface of contact and could form biofilm clusters.
Both physical factors (like Brownian motion, electrostatic interactions, gravity, van der Waals forces and hydrodynamics)  and cellular function in bacterial cells (bacterial motility, production of polysaccharides, and functions of structures in outer membrane) are responsible for this orientation.
(Via: https://www.nature.com/articles/srep29516)


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Difference between infectivity and cell fusion abillity of Virus. (COVID 19)
I'm a computational chemist who have interest in COVID-19.
As a physical chemist, I'm lack of basic knowledge for biology.
What is the difference between 'infectivity' and 'membrane fusion activity'?
I thought that, for corona virus, infection is equal to membrane(cell) fusion, but it seems wrong idea.
Thank you for reading!

From what I read there are the concepts: there is the receptor binding, then either the S protein does active membrane fusion and genome releasing near the cell surface, or the receptor+virus is engulfed as endosome and the fusion+releasing is achieved later, closer to the ER & Golgi (where the ribosomes and the target membranes are located). You may think to the cell as a labyrinth of membranes and the virus needs to reach the correct one to do the translation and anchor its transmembrane proteins to achieve the replication and assembly. So infectivity = releasing many virions.


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Is there a reliable reproduction rate for adenoviruses?
I was trying to find a R0 for adenoviruses but the best I could find was a study done in a bootcamp in China that infected 375 people.
This states that the R0 was found to be 5.1:

The basic reproductive number was 5.1 (95% CI: 4.6 to 5.6)

Is there any other more reliable method that covers more data?

I expect it depends on the virus strain, social conditions etc. As such, this isn't a very good question.

@Fizz Well obviously, that is why the one example from the study isn't a very relevant answer - the R0 can vary, but all viruses generally have a mean R0 or range, that is what I am trying to find out.


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What is an "open system" when it comes to PCR machines?
I have heard the term "open systems", such as here when it comes to RT-PCR machines, but I'm not 100% sure what this means, does this mean machines you can purchase yourself? Such as this one? ... compared to one that would be in a lab?
Also, I have heard that they come with the statement that they are for research purposes only and should not be used as a diagnostic tool, is this because anyone can buy them?

Based on the this paper it seems that the majority (if not all) real-time PCR assays are a closed-system when compared to conventional PCR and the primary reason for closed-systems appears to be to reduce contamination - all of this is detailed below:
Real-time PCR versus conventional PCR:

Real-time PCR testing platforms provide equivalent sensitivity and specificity as conventional PCR combined with Southern blot analysis. Since the nucleic acid amplification and detection steps are performed in the same closed vessel, the risk for release of amplified nucleic acids into the environment, and contamination of subsequent analyses, is negligent compared with conventional PCR methods.

Reduced risk of contamination:

The closed system for amplification and detection used with real-time PCR virtually eliminates the amplicon contamination caused by the opening and closing of reaction vessels which is problematic with conventional PCR and detection methods. Even with the closed system of real-time PCR, the laboratory may still choose to add uracil-N-glycosylase to the PCR mix for another level of amplicon contamination control.

...and:

The risk of contamination is considerably less with real-time PCR compared to conventional PCR, but still can occur (341). Since real-time PCR amplification is performed in a closed system, there is no need for individual air-controlled rooms as is recommended for conventional PCR. In our experience with real-time PCR, specimen to specimen contamination has become a greater challenge than amplified product contamination. The most obvious situation where specimen-to-specimen contamination can occur is with the transfer of specimen to the PCR vessel or to the DNA extraction tube. Care must be taken to avoid contamination of the pipette device with specimen and to avoid the creation of an aerosol by blowing out the specimen from the tip.

As for my secondary question about the "Research Use Only" statements I have observed; it is not entirely clear, but along with my original assumption, I also found the below:
This CDC page references some Real-time RT-PCR Primers and Probes that are for NOT FOR VIRAL TESTING USE and then goes on to say that:

Only primers and probes labeled for EUA use and distributed by the International Reagent Resource may be used for viral testing with the CDC 2019-nCoV Real-Time RT-PCR Diagnostic Panel.

So one reason is it could be to do with approval / red tape issues?
This seems to also be a possibility with other products:
https://www.diagnostictechnology.com.au/products/altona-realstar-sars-cov-2-rt-pcr-kit
https://www.sigmaaldrich.com/catalog/product/roche/tosrtro
One other possibility is that it's simply because they may be without a partnership with a medical laboratory:
https://johner-institute.com/articles/regulatory-affairs/and-more/coronavirus/

b) Research-only approach
Some manufacturers are considering selling their devices for “research
use only” without a partnership with a medical laboratory. Medical
laboratories could then use these reagents to offer a lab developed
test.
However, this approach should be viewed with skepticism, as the
“research only use” statement could be seen as a self-serving claim
that does not reflect the actual intended purpose: the product is for
diagnostic purposes.

In an open system, "mRNAs are detected because of their property of being expressed in the tissue sample isolated for study. This approach is in contrast to what are called closed-system approaches, in which the mRNAs to be detected are selected as candidates in advance of analysis; a contemporary example of a closed system would be a gene “chip” hybridization experiment." [Sutcliffe, J.G. (2001) J. Neurosci. 21:8306-9. “Open-System Approaches to Gene Expression in the CNS”] https://doi.org/10.1523/JNEUROSCI.21-21-08306.2001

Thanks, but I was more looking for an explanation about open-system vs closed system RT-PCR machines; and a bit more in detail with an explanation rather than just a quote.

If the question were about analyzing gene expression in general, this would be a good answer, but as the question is about qPCR machines in particular, this doesn't answer the question.


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What unmanned monitoring techniques are available to measure coral reef health?
Most biological data for coral reef monitoring are collected by human observers. This could be resource-intensive for long-term studies and thus hard to maintain consistency on large spatial scale. While remote sensing can be applied on a macro scale, are there any automated observational platforms that are available to look at events on a smaller scale such as behavior of fish colonies around reefs?

There are several researchers I know, including myself and others in my former grad school lab that are collecting acoustic data, or video data, for monitoring coral reefs using deployed underwater microphones and/or cameras that run for days to months at a time.
There are some papers exploring how reef sounds can be measured to monitor health, e.g., some have found healthier reefs to be 'louder' and have more fish calls, and sometimes these correlate positively with metrics usually obtained from visual surveys, such as coral cover and fish abundance.
For some examples of different sensing platforms, I recommend looking at the following papers and others by these authors. Some are in habitats other than coral reefs, but utilize methods that could be applied to coral reefs:
Mooney et al. (2020) Listening forward: approaching marine biodiversity assessments using acoustic methods (a review of this topic)
Kaplan et al. (2015) Coral reef species assemblages are associated with ambient soundscapes. Marine Ecology Progress Series
Pagniello et al. (2021) An Optical Imaging System for Capturing Images in Low-Light Aquatic Habitats Using Only Ambient Light
Archer et al. (2018) First description of a glass sponge reef soundscape
reveals fish calls and elevated sound pressure levels
Some camera or acoustic systems were custom built for these studies. Others, like SoundTraps, are commercially available.


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What are the apomorphies of Streptophyta that delineate them from Chlorophyta in Viridiplantae?
I'm reading through Plant Systematics, 3rd Edition by Michael G. Simpson, and am having a hard time understanding the differences between the Chlorophytes and Streptophytes - discussed in Chapter 3: Evolution and Diversity of Green and Land Plants.

The cladogram (from the second edition) makes it seem like the development of oogamy and plasmodesmata delineate the Streptophytes from the Chlorophytes, yet, still we see a few lineages within Streptophytes without either of these apomorphies (even in the third edition's version of this cladogram).
Where do we really draw the line between these sister groups?

Welcome to Biology.SE. Don't know the answer, but a quick look at the relevant wikipedia pages suggests they may be helpful — the short version is it depends on how the groups have been defined ... Also note that from your diagram it seems clear that neither oogamy or plasmodesmata are relevant — they distinguish Charophytes from other Streptophytes.

@tyersome the figure in 3.1 of the third edition actually doesn't even indicate Charophytes, but does include a Charophyceae lineage diverging from the rest of the Stroptophytes directly after the development of oogamy and plasmodesmata. Confusingly, Simpson goes on to discuss apomorphies of the Charophytes and references that figure even though there are no Charophytes. This may be an error? I've gotten a hold of the article that this cladogram was roughly based on (https://bmcecolevol.biomedcentral.com/articles/10.1186/1471-2148-14-23), so I'll update this with whatever I find.

@tyersome looks like the evidence for the division between these two groups is primarily genetic data. I will answer my question below shortly.

In the article cited by Simpson in creating the rough cladogram of Figure 3.1, From algae to angiosperms-inferring the phylogeny of green plants (Viridiplantae) from 360 plastid genomes (Ruhfel et. al, 2014), the phylogeny of Viridplantae is inferred from a set of 78 genes.
Thus, the division of Viridiplantae into the two sister groups Chlorophyta and Streptophyta is inferred / supported by molecular evidence.


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What does "DS" stand for in some articles?
I'm super ashamed of asking such a question, but there is an abbreviation that often comes in some papers that I have to read, I have no idea what it stands for and I'm just too ashamed to ask my colleagues... so here I am on the internet to try to find an answer (obviously English is not my mother tongue so it doesn't help).
Here is a figure I found in a paper. What does the "DS" stand for?

I've been trying to find out for hours now (using google and everything) but I'm really desperate. So I'm really sorry for the dumb question... but please help me, I feel so stupid. I thought that maybe it could be "day start" but I'm not sure, so any confirmation would be very welcome... Thanks in advance and I'm really really sorry for the completely uninteresting question.

Can you add a link to the paper? Sometimes the context helps to explain it.

Sorry, here is the link: https://doi.org/10.1038/emboj.2009.170
It actually appears in many papers and it's always related to time in hours...

I never heard this abbreviation, so it may be connected to this field of research. The article mentions "dry siliques", basically dry seeds (if I understand this correctly) which can be abbreviated DS and would be the starting point of the experiment. Does this make sense?

Not really, because it also appears in articles where no siliques are involved... maybe "dry seeds", but why using such an abbreviation on an axis that is indicating time?
But thank you for your answer, I'm glad I'm not the only one not knowing what it could be... even if we're still not sure of what it means, at least it makes me feel a little bit better about myself :)

At least it helped a bit :-)

Can you link to some other papers where you see this?

It may be an uninteresting question, but the emperor — or the authors of the paper —  are the ones that should be ashamed of their nakedness. Not you.

@canadianer: This one is another example, but the topic is closely related so it probably won't help: https://www.pnas.org/doi/full/10.1073/pnas.1012896107 ... I guess Chris was right when suggesting "dry siliques" or "dry seeds"... And also thanks David for making me feel even better about myself :) My shame is gone!

This paper says it is “dry seeds”.

Thank you so much canadianer! :) I'm happy :)

It could also stand for "Dormant Seed". I agree with David; it's the responsibility of the authors to define their terms.


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Will lidocaine stimulate photoreceptors?
Lidocaine apparently blocks voltage-gated sodium channels in sensory neurons and thus prevents action potentials, but photoreceptors like rod cells require hyperpolarization (through blockage of its sodium channels) for the neurotransmitter to be released / generator potential set up, so would adding lidocaine to the retinal cells stimulate them? Would it hypothetically make us think there's light even when it's dark?

See Wikipedia for an overview of the signal transduction that occurs in photoreceptor cells.
Briefly, light results in increases in cGMP; cGMP binds a cGMP-gated sodium channel (not a voltage-gated sodium channel) causing the channel to close. Therefore, light -> less sodium entry.
Lidocaine blocks a different type of sodium channel: the fast voltage-gated sodium channels involved in neurotransmission. It's possible there is some cross-reactivity, but it would be entirely coincidental as it's from a completely different family of channels.
In any event, the retina has all sorts of other neuron types: bipolar cells, retinal ganglion cells, and various interneuron types, that all communicate with each other through action potentials mediated by voltage-gated sodium channels. If you were to apply lidocaine to the retina, you'd lose all this neurotransmission.

the last paragraph really hit the nail, I feel like I should've realized that before.

@Rayan Good, but paragraphs 2 and 3 are probably more important to the specific question asked here: it's important to recognize that there are different types of channels that conduct the same ions, this will come up in a lot more situations.