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About The Selfish Gene Book - How Replicators Molecules forms duplicates?
I was reading The Selfish Gene. In the 2nd chapter - "Replicators" I read:

Think of the replicator as a mold or template. Imagine it as a large molecule consisting of a complex chain of various sorts of building block molecules.
The small building blocks were abundantly available in the soup
  surrounding the replicator. Now suppose that each building block has
  an affinity for its own kind. Then whenever a building block from out
  in the soup lands up next to a part of the replicator for which it has
  an affinity, it will tend to stick there. The building blocks that
attach themselves in this way will be automatically arranged in a
sequence that mimics that of the replicator itself.  It is easy then to
think of them joining up to stable chain just as in the
formation of the original replicator. This process could continue as a
  progressive stacking up, layer upon layer.
This is how crystals are formed. On the other hand, the two chains
  might split apart, in which case we have two replicators, each of
  which can go on to make further copies.

I don't get the part in bold.

If these molecules joins the replicator then the replicator wouldn't change?
To what refers with "The building blocks that attach themselves in this way will be automatically arranged in a sequence mimics that of the replicator itself"? A new sequence? The same sequence?
In the part "It is easy then to think of them joining up to stable chain just as in the formation of the original replicator", what is it joined? replicator with this building block? these building blocks with other building blocks in the soup to form a copy of replicator?
Why you can infer that is how the crystals are formed?

Take into account that I don't have a solid biology background, so it would be great if you can answer it in detail. I really appreciate your help!.

If you have a crystal of table salt, sodium chloride (NaCl), and place it in a saturated solution of NaCl in water, the salt crystal will start grow as the individual Na+ and Cl- ions in solution, settle on the face of the crystal, and enter the solid phase.  In the example, the Cl- building blocks align to the Na+ ions in the crystal (so it is not “like with like”).

So, Ci- ions joins the Na+? And what about the others Na+?

Check out this page: https://en.m.wikipedia.org/wiki/Sodium_chloride. Na+ attracts Cl- AND that means Cl- attracts Na+.

This is how I think about it.  Here is the original large molecule, with each of its 'parts' represented by a letter.  There are a few different kinds of part:
C-A-A-C-T-A-T-A-C-G-A-C

As it drifts around in a 'soup' of parts, new parts stick to it one by one, like for like.  Here it is after two parts stick to it:
C-A-A-C-T-A-T-A-C-G-A-C
  A         T

Here it is after a few more:
C-A-A-C-T-A-T-A-C-G-A-C
C-A   C   A-T   C   A

Eventually, all the parts have got a similar part stuck to them:
C-A-A-C-T-A-T-A-C-G-A-C
C-A-A-C-T-A-T-A-C-G-A-C

Now, if the two halves split, the molecule has replicated itself.

So,

The replicator, in fact, changes, but it can only contains copy of itself?.
The string just mimics the original sequence of replicator?
These building blocks are joining with others to form a copy of the original string?
When the replicator repeats his string multiple times, it converts in a crystal?

Finally, just to confirm, duplicates of the replicator occurs when the replicator halves?

Yes to 1, 2, 3.  For 4 I don't think he meant exactly that the molecule forms a crystal, but it was an analogy - the idea of one layer being built from another layer by joining like to like is similar to a salt crystal being built up.  Finally, yes, when the replicator halves there are now two identical copies when there was only one before.


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Stained chestnut tree leaves
The leaves of the chestnut tree in our back yard have, for a while, developed these stains on them:

..which don't appear to be a normal feature of this tree's leaves, at least according to the pictures on Wikipedia (I'm no botanist).
Also, the grass at the bottom of & around the tree does not (no longer?) grows around its root:

Its fruit, on the other hand, appear to me to be healthy:

We've only moved here for a few months, so am not sure whether it has always been like this or whether the tree only got infested in the last period.
Does the leaves' degradation + non-fertile ground around its root, signal that the tree is sick? If so, is there some "medicine" I can get for it myself, or would I have to speak to the administrators of the garden? Thanks in advance for any thoughts!

This looks like Horse Chestnut Leaf Miner (https://www.rhs.org.uk/advice/profile?pid=533).  It is very common, and infects most of the horse chestnut trees around here.  Some years are worse than others. It has been spreading for the past few years.  It doesn't seem to seriously harm the tree, but there is no cure I have heard of.  The link I posted from the RHS offers some ideas about collecting the leaves and composting them in sealed bags, until the moth larvae have died. Occasionally, trees have been found that are genetically resistant to the disease.
Don't worry about the grass, the tree needs the light and water from that bit of soil, but you could try some bark mulch around the trunk to cover the soil, and keep the moisture in.

That's indeed what it appears to be - thanks so much!

source: Stack Exchange

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

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Is there a continuum between analogous and homologous traits?
How closely-related do two species need to be for a trait they share (say, bipedalism in mammals) to count as homologous (divergently-evolved) as opposed to analogous (convergently-evolved)?
In other words, is there a sharp dichotomy between analogous vs homologous traits (and if so, how is the cut-off criterion defined)? Or is there a continuum among them, and if so, again, on what bases is this defined?
Does said trait need to maybe "skip" a given number of intervening species on the tree of life for it to count as convergently evolved (in the example above: there being many mammals species in between humans and kangaroos, both bipedal)? Or is this somehow all about (continuously expressed) phylogenetic distance? Googling/chatGPTing didn’t really enlight me, hence this question.

The wings of bats and the wings of birds are analogous; their shared ancestor had no wings, their other close relatives have no wings, etc. They are quite different in form and structure despite each being used for flight. But, they also both evolved from homologous vertebrate forelimbs. Their common ancestor has forelimbs, all of their close relatives have forelimbs, etc. Is this the sort of thing you're asking about?

It is, but since it is a rather classical example of convergent evolution, I'm still not clear I understand what is the hard criterion that enables one to classify a trait as being homologous OR analogous between two species in more border-line cases where perhaps less is known about whether the LCA shared that trait or not.

I think the "close relatives" (as you note above) having or not having that trait gets us closer to the answer I was looking for, as it essentially invokes philogenetic distance, although, again, it's unclear just how many related species one has to count.

If nothing is known about the common ancestor I don't think anyone would bother claiming a trait as homologous or analogous, but you can often infer things about the common ancestor from just two species you are looking at plus a member of an outgroup. If, for example, some mutation conferring a different function of a protein is present in two species and absent in an outgroup species that doesn't have that trait or mutation, you'd infer it's more likely that the common ancestor of those two species also had the mutation rather than the identical mutation happening twice.

Do you have some specific example to consider?

One example I had in mind (though maybe not the best) was the one mentioned in the question: bipedalism. One can find this trait in animals closely related to humans (e.g. other great apes; and thus argue it to be homologous in the context of that comparison); but one can also encounter it in distantly related animals, and thus argue it to be analogous. Am I making sense? (I'm no evolutionary biologist - and it shows!)

In that example I think you'd say that bipedalism (to the extent that other great apes are bipedal; some would argue they are not even if they occasionally go up on two limbs) is homologous among apes and analogous with, say, theropods. There's no conflict in saying that. Just like wings in birds and bats are analogous, but wings are also homologous among birds. I wouldn't describe that as a "continuum".

I still can't seem to express what exactly my doubt was, but in any case I think I'm clearer now on the topic. Thanks again!

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


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Unknown Insect identification
Found this bugger crawling across my laptop.  Any help identifying would be appreciated.  After a bunch of googling it appears to be close to a lady beetle larva.  I am located in north east USA.

It looks most like a common Green Lacewing larva - Chrysoperla rufilabris. Lacewings are considered a benefit in the garden because they effectively feed on aphids and other soft bodied garden pests. Here are some links that may be of further help.
https://bugguide.net/node/view/16103
http://www.uky.edu/Ag/CritterFiles/casefile/insects/lacewings/lacewings.htm
https://greenmethods.com/chrysoperla/


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Spider of the American continent spotted Europe. Is it expected?
While hiking in a nature reserve in Bulgaria I saw a big yellow and black spider. I took some pictures and when I went back home I did some searches and identified it as an Argiope, common name is Yellow and Black garden spider.
The description matches, the body was almost as big as the upper phalanx of a thumb. But the Wikipedia page states that it is native of the American continent. Is it an invasive species? Is it common to find it in Europe?

Argiope is a cosmopolitan genus (the link is for the genus, not the individual species you linked).
Argiope species A. bruennchi, and A. lobata are found in Europe in particular. Based on your photos I think this is likely to be A. bruennchi rather than A. lobata, as it has strong yellow and black bands and lacks the lobed edge of the abdomen of A. lobata.

Yes, may be an A. bruennichi. One small doubt is that the body size was about the double of the average size of the female.


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Is there a vaccine against the plague (Yersinia pestis)?
There seems to be recurrent events of infections of the plage (Yersinia pestis), from the well known Justinian plague to the Black Death and to recent years. In fact, two cases were reported in China in November 2019. However, it seems there is not an effective vaccine yet. At least until 2013 there was no vaccine approved by the US FDA. There seems to be on-going research about vaccines for the plage.
Is then no effective vaccine against the plague? If yes, does it mean humanity is still at risk of yet another pandemic of the plague?

There is little motivation right now for vaccination against plague because:

Human infections with plague are fairly rare. A vaccine administered to the general populace would have to be very cheap and extremely safe to make it cost-effective and have a net benefit given the risks of plague are so low, and because
Antibiotics are effective against plague - this makes the likelihood of a widespread outbreak fairly low. Antibiotic resistance could be a concern, but plague would not be one of the most concerning pathogens from that perspective - there isn't much exposure to antibiotics in the reservoir species that the bacterium lives in, so there is less selective pressure towards resistance compared to other bacterial pathogens.

Additionally, plague lives in reservoir species, so extensive human vaccination is not a plausible way to eradicate the bacteria entirely, unlike pathogens that have humans as a primary host.
That said, vaccines are available and can be used for certain individuals at high risk. However, they take a long time to show immune protection (>1 month) making them not that useful during outbreaks. From the same WHO report linked above:

Worldwide, live attenuated and formalin-killed Y. pestis vaccines are
  variously available for human use. The vaccines are variably immunogenic
  and moderately to highly reactogenic. They do not protect against primary
  pneumonic plague. In general, vaccinating communities against epizootic
  and enzootic exposures is not feasible; further, vaccination is of little use
  during human plague outbreaks, since a month or more is required to
  develop a protective immune response. The vaccine is indicated for
  persons whose work routinely brings them into close contact with Y. pestis,
  such as laboratory technicians in plague reference and research laboratories
  and persons studying infected rodent colonies (23).

WHO plague manual:
https://www.who.int/csr/resources/publications/plague/WHO_CDS_CSR_EDC_99_2_EN/en/

So basically, a cheap, widespread and effective antibiotic based treatment exist? I guess that is the benefit of the plague being a bacterial and not a viral disease like Covid-19.

@luchonacho Yes, exactly. Plague is still dangerous because the antibiotics need to be given quickly, but antibiotic resistance is relatively rare for plague.

It might be worth pointing out that the main reason why antibiotic resistance is of limited concern with Y. pestis is that the natural reservoir from which it sometimes jumps to humans consists of wild rodents, which (unlike humans and domesticated livestock) aren't normally treated with antibiotics. Thus, there's little to no selection pressure for Y. pestis to evolve antibiotic resistance in its natural hosts.

@IlmariKaronen Indeed, I thought I implied that but I guess I never did! I'll edit.

There is already plague vaccine in use, which is only administered to lab workers working on Y. Pestis or people residing in areas affected with plague.  (Via: https://www.cdc.gov/mmwr/preview/mmwrhtml/00041848.htm)
Plague can also be treated with antibiotics if detected at earlier stage (such as streptomycin, ciprofloxacin, gentamicin or doxycycline). Very few antibiotic resistant strains of  Yersinia  pestis have been reported till now. So, this may not become the reason for  pandemic.
As it is known, Y. pestis exhibits intrinsic genetic plasticity to transform into antibiotic resistant strain, which makes it  potent agent of bioweapon. So, Centers for Disease Control has listed Y. pestis under the category A select agent. And researchers are working for development of next generation vaccine which is more reliable by exhibiting strong cellular immune response. (Via: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5155008/)


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What happens when pure chlorophyll A absorbs blue light?
When pure chlorophyll A is put in the presence of only blue light, what happens? My guess is that the extra energy is released as heat/kinetic energy, and then the electron has dropped to the lowest energy state above the state that would normally release red light when UV light is shone. Then, it would drop to ground state and release red light as normal. Is this correct? The reasoning behind this is that UV is even higher energy than violet/blue light, so the same phenomenon should happen, except with less kinetic energy added. On a side note, what is the next electron state after the one that sends out red light?

chlorophyll a or chlorophyll b?

chlorophyll A. 15char


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How long does each of the stages in meiosis take?
For each stages of meiosis (i.e. Interphase, Prophase I, ...), I wanted to know the time between each stages either in percentages or minutes. However, while I could find the cell cycle for mitosis like the image (original link), I couldn't find such thing for meiosis. Does anybody know anything about this?

If you take a look at the figure directly above the image you posted in the link you posted, you'll see a very different set of figures.

It turns out, time spent in different phases of the cell cycle depends on species, cell type, and conditions, specifically, the presence of cell cycle regulating signals like cyclins. You can also read about that in the link you posted.
Meiosis is similarly varied. For example, in a female human, oogonia start meiosis while the female is still a fetus. Meiosis is then arrested in prophase 1. Further progression in meiosis doesn't occur until puberty at the earliest. Spermatogenesis in a human male, on the other hand occurs over a 64 day period. Since oocytes sit in prophase 1 for ~ 13-50 years, they will have a very different proportion of time spent in each phase. You can read about this in Costanza Physiology, chapter 10.


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How to design a permanent vaccine to cholera using CRISPR?
I know that Vibrio Cholerae infects the body through the GM1 ganglioside. So, would it be possible to engineer a CRISPR gene editing tool to prevent Vibrio Cholerae from getting into our cells?
Specifically, would it be possible to insert a piece of DNA into our genes that allow the synthesis of cholera toxin-suspressing protein shown  here (Pubmed link).
The reason I ask this question is that there are obvious benefits to being immune to cholera from birth. While I'm definitely not planning on being the next He Jiankui, I find the prospect of such a vaccine highly intriguing.
Edit: changed link because I posted the wrong link.

So, would it be possible to engineer a CRISPR gene editing tool to
  prevent Vibrio Cholerae from getting into our cells?

Vibrio Cholerae doesn't get into our cells.
Did you observe that your paper has no in vitro experiments?
It's going to be tough to get a cell to transcribe and translate something so small, and will the peptide work if it needs a leader sequence to be exported out of the cell?
Its much much easier to break a gene in every cell than to add a new gene and have just a small subset of cell types make large quantities of that gene product.


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Can low melatonin levels and/or LED lights cause or exacerbate macular degeneration?
I have two questions that may or may not be interconnected. My first question is:
Does melatonin prevent macular degeneration? Could low melatonin levels (caused by blue-rich light exposure in the evening and night and/or by insuffient sleep) heighten the risk for macular degeneration due to shorter amount of time that melatonin scavenges free radicals in the retina?

Evidence is conflicting as to whether exposure to sunlight contributes to the development of macular degeneration. A recent study on 446 subjects found it does not [1]. Other research, however, has shown high-energy visible light ("blue wavelengths") may contribute to age-related macular degeneration [2 and 3].
Data indicates that melatonin, being an efficient antioxidant with antinitridergic properties, has a promising role in the treatment and management of glaucoma. Melatonin could protect the ocular tissues against disorders like glaucoma, age-related macular degeneration, retinopathy of prematurity, photo-keratitis and cataracts [4].
However, melatonin secretion is inhibited by short or low quality sleep and by the ubiquitous blue-rich light exposure in the evening and night, hence for many people melatonin secretion starts as late as 90 minutes after falling asleep (i.e. 90 minutes after the last exposure to shorter visible spectrum wavelengths). As a consequence, melatonin has less time to function as an antioxidant in the body in general (which has been proved to result in higher cancer incidence) and also in the eye. When people are not exposed to blue wavelengths in the evening (e.g. by using firelight or dimmed incandescent bulbs or wearing red glasses) melatonin secretion starts roughly 90 minutes before sleep so melatonin has more time to do its antioxidant work.

My second question is about the relationship between macular degeneration and LED lights.
Could LED lights also increase the risk for macular degeneration?

Typically, LED lights (CCT = 4000 K) have a maximum peak at around 451 nm and a minimum in the 460-500 nm range (as is shown in their spectral power distribution of such LED lights below).

Melanopsin that controls pupilary reflex (pupil constriction), however, has maximum sensitivity around 479 nm - right in the LED spectral power distribution's (SPD) minimum. Could it be that due to this gap in SPD the pupil does not constrict enough and hence allows more of this blue rich light into the eye that as a result generates more free radicals and contributes to macular degeneration? Could this in combination with low sleep quality contribute to the onset of macular degeneration as LED (and lack of sleep) are widespread?
PS: I vaguely understood that at the moment it might be hard to answer some questions regarding melanopsin, but I am not sure how much it is related to my question. "It would be desirable to be able to quantify light as experienced by non-visual systems (melanopsin) using a single, one-dimensional unit (the equivalent of photopic lux). Achieving this for lights of divergent spectral content, however, awaits elucidation of a suitable spectral weighting function" [5]

Thanks for all of the prior research you have done. Can you maybe clarify what the actual question you are asking is, edit that question into your title, and make your question more prominent in the body? As-is, I think your background information, while appreciated, is masking what you are getting at, and many people won't take the time to read your whole question.

Thank you, I agree with you, will clarify it immediately!

@BryanKrause is it better now? I am sorry it was unclear.


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Is chromatic aberration related to the spectral sensitivity of the human eye and can it cause "relative myopia" and "relative farsightedness"?
in the text below, the authors equate chromatic aberration and the spectral sensitivity of the human eye. Aren't these two very different phenomena though? They also propose a so-called "relative myopia" and "relative farsightedness". Are these claims valid? Does chromatic aberration even pertain to the human eye? I can only find sources that discuss this phenomenon within the field of photography.
I would very much appreciate any citations that debunk this text.
Here are my summed-up points that I, as an amateur without any formal education or training in ophthalmology, find problematic. I think that the text:

equates chromatic aberration and the spectral sensitivity of the human eye – which are two very different phenomena
proposes that chromatic aberration (which is a property of a lens) happens in all human eyes and it causes a so-called "relative myopia" and "relative farsightedness" – terms I cannot seem to find online. Would not this result in all of us seeing blurred colourful fringes and haloes around objects, just like you can see in a photograph taken by a camera that strongly exhibits chromatic aberration? I can't find a study to support my point though.
states that the human eye is most sensitive to the yellow-green wavelength range because this range is most predominant in the Sun's spectrum – but isn't it so because the weighted function of the spectral sensitivity of our cones simply lies around 555 nm? Maybe these studies might help, I am not sure [1,2]. They also vaguely state that this yellow-green range has "the most favourable effect on humans" which is confusing, what does that mean? For example, "favourable" during the night certainly is light devoid of blue and green wavelengths that suppress melatonin secretion [3,4,5] – so "favourable" is debatable without being specific.

The text:

When designing lighting, the chromaticity of the light used must be carefully considered. Due to the predominant yellow-green component in sunlight, the human eye is most sensitive to the yellow-green wavelength range and this light also has the most favourable effect on humans. On the contrary, red or blue light of the same intensity is much more difficult to perceive. In the eye, light with a high proportion of blue wavelengths falls in front of the retina, causing so-called relative myopia; on the contrary, light with a high ratio of red wavelengths falls behind the retina and causes relative farsightedness. This phenomenon is also called chromatic aberration (also a chromatic defect or colour defect) and it is necessary to keep in mind when designing the lighting systems or electronic displays.

The text is not published anywhere, it is an excerpt I got sent which I translated into English.
References
[1] Stockman, A., & Sharpe, L. T. (2000). The spectral sensitivities of the middle- and long-wavelength-sensitive cones derived from measurements in observers of known genotype. Vision Research, 40(13), 1711–1737. https://doi.org/10.1016/S0042-6989(00)00021-3
[2] Hofer, H., Carroll, J., Neitz, J., Neitz, M., & Williams, D. R. (2005). Organization of the human trichromatic cone mosaic. Journal of Neuroscience, 25(42), 9669–9679. https://doi.org/10.1523/JNEUROSCI.2414-05.2005
[3] Brainard, G. C., Hanifin, J. R., Greeson, J. M., Byrne, B., Glickman, G., Gerner, E., & Rollag, M. D. (2001). Action spectrum for melatonin regulation in humans: Evidence for a novel circadian photoreceptor. Journal of Neuroscience, 21(16), 6405–6412. https://doi.org/10.1523/jneurosci.21-16-06405.2001
[4] Al-Naggar, R. A., & Anil, S. (2016). Artificial light at night and cancer: Global study. Asian Pacific Journal of Cancer Prevention, 17(10), 4661–4664. https://doi.org/10.7314/APJCP.2016.17.10.4661
[5] Bonmati-Carrion, M. A., Arguelles-Prieto, R., Martinez-Madrid, M. J., Reiter, R., Hardeland, R., Rol, M. A., & Madrid, J. A. (2014, December 17). Protecting the melatonin rhythm through circadian healthy light exposure. International Journal of Molecular Sciences. MDPI AG. https://doi.org/10.3390/ijms151223448

Which of the references actually contains the text you quote - 1?

@MattDMo it is not an English text and it does not come a from a published work – it is just something I got sent.

OK, then you need to [edit] your question clarify it. All quotes need to have attributions.

There are two phenomena described in the quoted text, and while there is some relationship between them, they are indeed distinct:  spectral sensitivity of the human eye, and longitudinal/axial chromatic aberration of the eye resulting from variation of refractive index of the lens by wavelength.  I found the following on Physics.SE:
https://physics.stackexchange.com/questions/12602/do-eyeballs-exhibit-chromatic-aberration
which links to this interesting page:
https://www.telescope-optics.net/eye_chromatism.htm
Note that the existence of such aberration is a purely optical phenomenon, but biologically, the structure of the eye (in particular, the distribution of retinal cone cells, and neural processing) compensates for the resulting perception to a significant extent.
That said, I think the way the information is explained in the quoted text is not particularly clear, as it sort of jumbles the concepts together.  If you want to learn more, do a web search for key phrases such as "human spectral sensitivity" and "human lens dispersion."


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What do these novel splicing sites mean?
I'm sure that the anwser is obvious for some of you but I just endend my internship where we found novel splice junctions (junctionseq; RNAseq data) (see the attached file) and I have some difficulties with splice junctions.
I understand that reads can map in the junction of 2 exons (which can be linked to quality assesment) and that comparing 2 conditions, we can find groups of exons more "associated" but I dont understand :

How a novel junction can be discovered in a previous junction (sub1), or behind the last exon of a gene (sub2) and thus, what can be the consequence(s)

I think you should explain the graphs a bit more. junctionseq is not a standard method (I have never heard of it before) and showing the read counts of junctions and exons side by side like this (not even indicating the size or type of each elements) is - at least to me - almost confusing. So I can't properly interpret this data for now (without reading up on the details of the methods used, but that's too much work right now)

Can you please explain the diagrams as @Nicolai said?

A splice junction is formed from a pre-mRNA (or primary transcript) whenever an intron is removed, or spliced out.  Two segments of RNA that used to be separated in the pre-mRNA are now ligated to each other, forming a junction of two exons.
RNA-Seq reads that span such a splice junction site would not align very well to the genomic sequence, however if you create a file of all the potential simulated splice junctions there may be some RNA-Seq reads that now align perfectly.
The distinction between what constitutes an intron, and what constitutes an exon is purely empirical.  While it is true that the spliceosomal complex preferentially recognizes and binds to properly juxtaposed splice donor and splice acceptor sites, a variety of different processed, mature, transcripts can result from a single primary transcript.  This differential parsing of the cis-acting sequences at the boundaries of potential introns and exons is called alternative splicing.


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Do animals lie?
Have there been any studies that show or suggest that species known to be able to communicate information between individuals ever intentionally communicate false information i.e. lie?
(Apart from Homo of course).

Koko the gorilla once tore a sink from her living quarters, and when asked about it, blamed it on her pet kitten, signing, "Cat did it." If that's not a lie, then nothing is.

This question has been well studied by cognitive scientists who are interested in which aspects of complex human behavior are also exhibited by animals.
The only real problem here is that the word "lie" has a very complex bundle of meaning when we use it to speak about humans, and one can debate just how far various aspects of "lie" apply regarding other species. Cognitive scientists avoid this issue with more neutral terminology of "tactical deception."
At this point, it has been very clearly established that many species will engage in tactical deception. The most obvious and human-like manifestations (unsurprisingly) typically occur in more intelligent species with complex social interactions, such as primates and corvids.  Likewise, the subjects of deception also often occur in similar places as with humans, such as food, mating, and status/conflict.


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Regulation of LBD33 genes Arabidopsis. If LBD 33 gene is up-regulated by auxin then why does expression decrease when increasing auxin concentration?
I have a question regarding the regulation of lateral boundary domain genes in Arabidopsis (specifically LBD33). I am an undergraduate student trying to understand the results of a lab where I measure the regulation of gene activity by using GUS staining technique. I have included a photo of images taken of Arabidopsis under different treatments:

A) Wild type no auxin, the wild type has no GUS gene inserted thus no transcription of genes that code for GUS. This was our negative control.
B) Positive control CyclinB1 where the promoter has been fused upstream of the coding sequence for GUS. GUS staining always present.
C) LBD 16 mutant no auxin GUS promoter is fused downstream, without auxin genes GUS is not transcribed.
D) LBD 16 mutant exposed to 1um IBA, GUS staining on lateral roots.
E) LBD 16 mutant exposed to 10um IBA, even more GUS staining on lateral roots compared to D) treatment.
....So far I think I understand, below is where I am having problems interpreting my results.
F) LBD 33 mutant no auxin. staining in leaf and roots (all the literature I have found says LBD genes are only active in lateral roots but the stain is present in leaves)
In images G) LBD 33 mutant exposed to 1um IBA, and H) LBD 33 mutant exposed to 10um IBA, the expression of LBD 33 genes seems to decrease by adding more auxin, but when I read journal articles they all say that auxin up-regulates the transcription of LBD33 gene. I thought that if these genes are auxin induced shouldn't expression increase when more auxin is added?


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Can non-carbonated energy drinks boost alcohol intoxication?
I just read news article about

banning caffeine in alcohol drinks and
about that energy drinks increase the urge to drink alcohol.

Energy drinks cause sugar intoxication - answer about it here in the thread Decreasing the alcohol proof and faster in hangover, why?.
Sugar dehydrates faster as well as causes a cascade of hormonal changes that are more immediately troubling than the alcohol.
I want to understand why energy drinks boosts you to drink more alcohol.
This suggests me that

malaise (caused by energy drinks) can be improved shortly by alcohol drinks

by some unknown mechanisms to me; and this can be the reason why people like to drink more alcohol after energy drinks.
I think that the mechanisms are related to some cascade which I do not know.
This mechanism can lead to improvement in the dehydration very shortly

by acting on the membranes of the cells
or by stabilising the architecture of the endothelium i.e. stabilising the hormonal changes.

My conjecture is that the alcohol can affect on the secretion of the substances from endothelium (EDRF, EDCF).
There are three types of substances secreted by the endothelium

NO
Endothelium hyperpolarising factors
Endothelins

So sugar intoxication causes changes in the endothelium architecture which alcohol intoxication reverts shortly back which boosts people to drink more alcohol to recover from the malaise caused by the energy drinks.
How can non-carbonated energy drinks boost alcohol intoxication?

This is not very broad. If I am not wrong this phenomenon is attributed to caffeine.

A very well-written question, so I'm sorry if my answer is a bit too simple. Perhaps it will attract attention of somebody with a better answer.
I think the effect could be mainly caused by the fact that sugary drinks slow down alcohol absorption. So while those who drink just alcohol already know they've had enough, those who have had a couple of energy drinks still feel fine and continue drinking, not knowing that they are about to become even more inebriated.
Also, the stimulants in energy drinks can somewhat reverse the sedative effect of alcohol, leading to higher overall activity of the person and thus faster drinking.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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How did Smith et al 2004 deal with missing HI [Hemagglutination Inhibition assay] values and HI values <10?
In the scientific paper "Mapping the Antigenic and Genetic Evolution of Influenza Virus's" Supporting Material, Smith et al write about determining antigenic distance Dij. However, I don't understand how one could calculate Dij from HI values of <10. Is it better to remove these data values or to change it to 9?
Also, regarding the missing data, how does one make a comprehensive antigenic map using shape space distance dij? I see that an error function must be minimized, but how does that give dij for all the missing data? Should missing data be ignored for the error function?

I don't know how Derek's group handles it (don't have time to look now) but conventionally HI assays less than 10 are called "9" for statistical purposes, and I assume that's how they did it. Have you looked at Henry Wan's antigenic distance web site (http://sysbio.cvm.msstate.edu/software/AntigenMap/about)? I think he talks more about his approach

You're clearly serious about this project, but asking on se.biology isn't the best problem-solving approach for this kind of in-depth question. Can you find a mentor in the field who can work with you specifically?

Thank you @iayork. I am a high school student and I am working on this project for a research competition. I appreciate your answering my questions for the past few months.

I'd like to help more, but this isn't my speciality, not to mention that I have my own group to run. Since you have good, specific and focused questions, you could just try writing to Derek Smith, who is a very friendly guy. Trever Bedford is enthusiastic and committed to open-source software and has a strong Twitter presence, and you might get answers from him too. Jesse Bloom is very knowledgeable and has open-source projects.

Alright, thank you @iayork. I will contact the people whose names you mentioned.


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Where can I find hemagglutination inhibition (HI) assay data?
I am looking for hemagglutination inhibition assay data for type A influenza virus. I've checked in databases such as fludb.com, however it seems to only have genetic data. A lot of the time, scientific papers don't include the HI assay data they used, so I was wondering if anyone knows where to find such data. I specifically need influenza type A HI assays, not influenza type B.
HI data comes in the form of titers (the reciprocal of the last well plate concentration of antibody that was able to inhibit the virus from binding to the blood sample and forming a shield on the well plate.)
Could someone please give me a link to a database with this information?
Thanks.

You can search in the NIAID Data Discovery Portal: https://data.niaid.nih.gov/

I don't think there's any universal database containing ongoing, widely representative HI assay output. The Antigenic Cartography group has made available some historical datasets that were used in published articles, such as

Influenza A/H3N2 data published in Smith et al. 2004. Science 305:371-376
Data from H1N1pdm09 assays in 2009/2010 (click on the links for html/Excel/OpenDocument tables)
Data published in Koel et al. 2013. Science 342:976-979

Trevor Bedford et al. make their large set of historical HI data described in Integrating influenza antigenic dynamics with molecular evolution available in DataDryad.


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How does one predict how large of an effect on antigenic drift a substitution in the amino acid sequence of a surface protein of influenza has?
I know that some amino acid substitutions are more effective in causing antigenic drift than other substitutions based on their location in the 3d structure of the HA protein (proximity to the receptor binding site).
I would like to be able to determine using a program whether a virus will be dominant based on multiple factors including genetic difference from the previously dominant virus. How can one know how much bigger of an effect one AA substitution will have on the antigenicity of a virus compared to another?
Any help is much appreciated.

Your understanding of influenza antigenic drift is, unfortunately, hypersimplified and mostly wrong. In particular, your notion that some mutations are more important for antigenic drift because of their effects on structure is at best oversimplified.
Rather than spend many paragraphs reviewing the complex patterns involved, I'd suggest you start by carefully reading papers from people who have correlated antigenic drift with sequence change, such as

Sequence-Based Antigenic Change Prediction by a Sparse Learning Method Incorporating Co-Evolutionary Information
Using Sequence Data To Infer the Antigenicity of Influenza Virus
Mapping the Antigenic and Genetic Evolution of Influenza Virus
The genomic and epidemiological dynamics of human influenza A virus
Selection of antigenically advanced variants of seasonal influenza viruses
Antibody landscapes after influenza virus infection or vaccination
Substitutions Near the Receptor Binding Site Determine Major Antigenic Change During Influenza Virus Evolution

This is a field that a lot of extremely smart people have been looking at extremely closely for many years; all the simple approaches have been tried already.


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Could the inability of adult mammals to digest lactose be partially explained by the loss of lactose-metabolizing bacteria from the microbiome?
BACKGROUND:
1. Lactase persistence
Lactase persistence is the continued activity of the lactase enzyme in adulthood, allowing the digestion of lactose in milk.
According to Wikipedia, only a small proportion of human mammals keep the ability to digest lactose when reaching adulthood:

In most mammals, the activity of the enzyme is dramatically reduced after weaning. In some human populations though, lactase persistence has recently evolved as an adaptation to the consumption of nonhuman milk and dairy products beyond infancy. (...) Worldwide, most people are lactase non-persistent, and are affected by varying degrees of lactose intolerance as adults.

The scientific consensus is that the enzyme lactase is encoded by the mammalian lactase gene (LCT), and that Hypolactasia is known to be recessively and autosomally inherited. Most mammals lose the ability to digest lactose once they are old enough to find their own source of nourishment away from their mothers, and there is still debate about the selection mechanism which yield  the   human excepcion:
Lactose malabsorption is typical for adult mammals, and lactase persistence is a phenomenon likely linked to human interactions in the form of dairying.
2. Gut Flora inheritance
Our understanding of the gut microbiota has recently evolved
(the study of gut flora began in 1995): the digestive tracts hosts a whole population of microbiotes, each with their own DNA, playing active (positive and negative) roles in the digestion process and co-evolving with their host. The composition of human gut microbiota changes over time, when the diet changes, and as overall health changes.
The gut flora are believed to be inherited, in particular from the mother and from people living around the infant:

During birth and rapidly thereafter, bacteria from the mother and the surrounding environment colonize the infant's gut. The exact sources of bacteria are not fully understood, but may include the birth canal, other people (parents, siblings, hospital workers), breastmilk, food, and the general environment with which the infant interacts. (Wikipedia)

QUESTION
Could an environment selecting for lactase persistence phenotypes select both human and gut flora genotypes in paralel, so that the survival or disappearance of gut flora able to hydrolyse lactose to glucose and galactose play as important a role in the ability of selected humans to digest or not fresh milk as the various genes previously identified?
PERSONAL REMARKS
I wonder if  these hypothesis have been previously ignored because the gut was considered "neutral" rather than "active" in the digestive process (the alternative being that theses hypothesis have been already proven wrong beyond questioning, which I am curious to learn about).
I understand that this is not the scientific consensus, and I am not claiming that the scientific consensus is wrong. But the scientific consensus was once that the earth was flat, or that the sun was rotating around the earth, and it evolved. I am wondering if there is place for doubt in the current scientific consensus about the genetic causes of the ability or inability to digest lactose in human adults (from a scientific point of view).

What brings you to the conclusion that this is not (as it is the fact) caused by our genetics?

Just a thought, but try looking up the LCT gene. It's a human one, producing lactase. I'm not sure how your experiment tests the hypothesis - wouldn't that work equally well if the enzyme continued to be produced by the growing organism because of continued milk intake due to something in the milk interacting with the organism directly? Do you mean to suggest that the LCT gene expression is regulated in some way that's mediated by gut flora?

@Chris: The intestinal flora has genetics (distinct of our own), is transmitted from parents to children (as our genetics) and evolve under the same selection mechanism as our genetics. I am aware that the current state of scientific knowledge is that the ability to digest lactose is based on genetic, but I wonder if an alternative or complementary theory based on the genetics of the microbiome could also explain the ability and inability to digest lactose in adult mammals. (Sun and stars rotating around the earth used to be a scientific fact too!)

Scientifically spoken, tt was not a fact - it was a hypothesis. Which was proven wrong. Besides this the mutation which leads to persistent expression of lactase nicely explains the mechanism.

I suggest reading this paper: "Human adaptation, demography and cattle domestication: an overview of the complexity of lactase persistence in Africa".

@mgkrebbs I will, thanks!

Preamble
The original version of this question has been edited, so the first part of my answer, which addressed certain arguments and proposed experiments has now been removed. The question now incorporates material accepting the role of the enzyme lactase in determining whether humans can continue to digest milk after weaning, but I retain the section I wrote on that point, as it presents some precise genetic evidence and points to a useful review. In my update in response to the changes in the question I have extended my consideration of the role of gut bacteria.
The mechanism of lactase persistence has been established to be genetic
A recent (2017) review in Annual Review of Genomics and Human Genetics covers the topic in detail. There are five separate genetic variants and details of one of these are:

In 2002, a study of Finnish families by Enattah et al. (30) identified the first mutation associated with the LP [lactase persistence] phenotype: −13.910:C>T (rs4988235).

A further study showed that the −13.910:T variant creates a new binding site for octamer-binding protein 1 (Oct-1), a transcription factor that interacts with human hepatocyte nuclear factor 1α (HNF1α) to bind to the LCT [lactase] promoter (77). This allele therefore leads to an alternative path for LCT expression that is not downregulated, as the original path is.

There are questions about lactase persistence that still have not been answered — primarily why it arose in some human populations, but not others. However experimental evidence and scientific logic lead to the conclusion that cessation of expression of the gene for lactase ([lactase non-persistence) results in loss of ability to metabolize lactose. Any “scientific consensus” rests on this experimental and logical basis and the absence of any experimental evidence for a different or additional explanation.
Intestinal flora and lactose tolerance
The poster now accepts the role of genetics, but posits that the microbiome might be an additional factor in lactose tolerance. I shall now consider studies in this area.
CORRELATION OF LACTASE PERSISTENCE WITH PARTICULAR MICROBIOTA
The review already quoted does provide some information on Bifidobacterium, a bacterial constituent of human microbiota able to metabolize lactose:

Interestingly, although most of the focus has been on the cost of drinking milk for LNP [lactase non-persistent] individuals, arguments can also be made that consuming milk or dairy also has advantages for these individuals. Indeed, recent studies have shown that the gut microbiota of LNP individuals differ from those of LP individuals from the same population in that they have a higher prevalence of Bifidobacterium (11, 15, 47), which is explained by the larger amounts of lactose available for bacterial fermentation. In fact, this represents one of the strongest associations to date between genetic variants and variation in gut microbiome composition (11, 15, 47).

Thus, humans who for genetic reasons do not expresses lactase (a trait that correlates with the inability to digest lactose) have a larger intestinal population of lactose-metabolizing bacteria. This is consistent with their having unabsorbed lactose in the gut. However it provides no evidence in support of an additional role of such bacteria in lactase persistent individuals, even assuming that there was a mechanism by which these bacteria could contribute to lactose tolerance. (This latter point will be considered next.)
LACTOSE-METABOLISM IN BIFIDOBACTERIA
The implicit assumption — now made explicit in the title of the question — is that bacteria possessing a lactase (generally known as β-galactosidase in bacteria) could or would supply the products of lactose hydrolysis (glucose and galactose) to the human host. This is by analogy with ruminant bacteria, and perhaps the supply of vitamins by human bacteria. Unfortunately there is no evidence to support this idea. It has been demonstrated that bifidobacteria take up and utilize lactose for their own growth, employing the (anaerobic) fermentation pathway known as the bifid shunt, which also involves glucose. The products of this are lactate, acetate and ethanol.
THE MICROBIOTA & THE PATHOLOGY OF LACTOSE INTOLERANCE
It is worth recalling that lactose intolerance can be a pathological condition if the subject consumes dairy products. This is not my area of expertise, but it would appear that this results from the fermentation of lactose by bacteria other than bifodobacteria, with the formation of different products — fatty acids, hydrogen, methane and carbon dioxide. The gas produced causes various problems (flatulence, bloating etc.), and the acidification of the intestinal contents can cause diarrhoea — a major problem in this condition.
It should be noted that bifidobacteria are regarded as beneficial (‘probiotic’) in lactose intolerant individuals, although the basis of this is not known. (Perhaps they compete for the lactose with the bacteria whose metabolism produces more harmful products.)

I am confused: you seem to equal "Lactase non persistent" humans and  "humans who cannot digest lactose", when my understanding (from your own quotes) is that humans with a higher prevalence of Bifidobacterium do indeed digest lactose without producing lactase?

Thanks a lot for the pointer to the survey! I am sorry if my question seemed unscientific to you: if no biologist, I am nevertheless a scientist, and a "believer" that science progresses by asking the right questions (and that stack exchange is a good engine to make science progress). I am not sure than mine are the right ones to progress, but at least they are the right ones for me (and others) to learn!

@J..y B..y — I have now modified my answer. I did not read your original point properly. "when my understanding (from your own quotes) is that humans with a higher prevalence of Bifidobacterium do indeed digest lactose without producing lactase". The quote says nothing about digesting lactose only "beneficial effects" which may be due to the protein or fat content of the milk. All this implies is that they tolerate some milk — i.e. don't show the lactose intolerant pathology. As I mentioned in my wild speculation, the bifidobacteria may outcompete those responsible for the pathology


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How to measure the ability to discriminate between two colors experimentally
CONTEXT
Species differ greatly in their vision ability in general, and in their ability to discriminate between colors in particular.
Humans' color vision is usually (some rare human individuals have less or, even more rarely, more types of cones than the norm)  based on three types of vision sensors, called ``cone cells'' (red, green and blue, making it trichromatic). Those three types of cone cells allow them to distinguish various colors depending on how much each cone is stimulated. The three pigments responsible for detecting light have been shown to vary in their exact chemical composition due to genetic mutation; different individuals will have cones with different color sensitivity.  Digital devices produced by and for humans are calibrated on such vision abilities: the reader is probably familiar with interfaces defining a color by its red, green and blue components.
Cats' and dogs' color vision is based on only two types of cone cells (green and blue, making it dichromatic, reacting to what humans perceive as blue and green, but mostly ignoring variations in the light frequencies perceived by humans as red: various shades of red will appear as different shades of gray. A red, pink, or orange toy lying in a green patch of grass may be difficult to see for a dog or cat. Similarly, a digital life enrichment application requiring to distinguish between two colors differing only in their shade of red (e.g. black and red, white and cyan, or blue and magenta) would be completely unusable by a cat or a dog, and most probably frustrating.
Many types of birds and fish have a fourth type of cone receptor to absorb ultraviolet light, making their vision tetrachromatic. Birds see in four classes of color -- blue, red, green and shorter wavelengths -- violet or ultraviolet (UV) – depending on the species.
A RIGOROUS PROTOCOL
Given a task and an interface previously known to be visible to the subjects,
an intuitive protocol to explore the limits of the visual abilities of OATH subjects consists in requesting them to perform the same task, but using an interface such that being unable to discriminate between colors makes it impossible to perform such task.
Such a protocol is rigorous but seems unnecessarily frustrating for the subjects.
A PLAYFUL PROTOCOL
Barbay et al. proposed in 2022 an alternate protocol to decide which pairs of colors can be discriminated by a given subject, displaying colorful balloons with colored marks mixed with plain balloons, rewarding the selection of marked balloons, and noting the pairs of colors of marked balloons which are less often selected, assuming that they are perceived as plain balloons.
Such protocol is less rigorous than the previous one (some balloons can be clicked by mistake, independently of whether they are marked or not) but seems potentially less frustrating for the subjects.
QUESTION
Which experimental protocols do biologists (and eventually ethologists) use in order to measure the ability to discriminate between two colors  of other animals than humans?

A good place to look would be the "Methods" sections of papers that use these sorts of experiments, such as this one on cichlids.

It also seems that researchers often look at the anatomy of the retina in addition to behavioral studies to study color vision in animals.

The methodology is going to depend on the specific research question; what are the visual abilities is not a sufficiently specific question.


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Are evolutionary algorithms calculated in polynomial time?
How complex are evolutionary algorithms? Also, what is the relationship between variational principles (Lagrangians, minima and maxima,) and evolutionary algorithms? Basically, how hard is it right now to construct an algorithm that reproduces what we see in the evolutionary history of life? Could you, in theory, use variational principles to reduce the complexity of evolutionary algorithms, and gain novel understanding of how evolution works in the process?

I think you need to clarify just what you're asking.  Evolutionary algorithms themselves tend to be quite simple, and run in pretty close to linear time.  The problem is that evaluating the fitness function can be very time-consuming.  One application I worked on involved solving a set of fairly complicated differential equations on a 3D volume, so O(n^3) - several seconds for each evaluation, microseconds to test the evaluation in the GA. I would guess that evaluating fitness functions for evolutionary biology would be more complicated still.

Yeah it is rather vague now that I look at it. Essentially, the question is about the possibility of using variational principles to feasibly create an algorithm which reconstructs exactly what we see in the evolutionary history of life, and, if we did that, how would it enrich our understanding of the intricacies of evolution. The philosophy behind it is that you can use variational principles to make everything so much easier in understanding evolution, so why aren't people doing it? Are they doing it? If you took the intrinsic variational principels of ecology, wow! Insight!

For instance, this article applies dynamic equations of motion derived from the principle of stationary action to ecology. We know there's an intimate relationship between ecological conditions and evolution now. If we can apply Hamilton's principle to ecology, and ecology directly impacts evolution, how can we use this approach to further understand evolution? Article link: https://www.sciencedirect.com/science/article/pii/030438009400046K

Your question is very broad a quite unclear. You ask four different questions (a post should always be restricted to a single question). How complex are evolutionary algorithms? 1) This question is broad and unclear 2) Evolutionary algorithms are a concept in computer science, not so much in biology, hence this specific question should not be asked on biology.SE. Basically, how hard is it right now to construct an algorithm that reproduces what we see in the evolutionary history of life? ...

... Evolutionary algorithm, in general, don't aim at answering questions in evolutionary biology. Evolutionary algorithms are a type of optimization algorithms, used to solve a number of optimization problems, many of them are completely unrelated to biology. That being said, we do perform a lot of simulations of evolutionary processes. Aside obvious issues of ressources, simulating "evolutionary history of life" in general is quite of an impossible task as the process is quite chaotic....

... It is like asking "can we simulate this specific wave?" without giving the starting conditions of the wave rather than asking "can we simulate wave-like processes?"

For all the reasons mentioned above, I'm voting to close this question as off-topic.

Well, to be fair its basically 2 questions, but sure. I don't see a conclusive or logical reason to believe evolution is random or "chaotic" though. There seems to be good evidence for it being a product of specific initial conditions in the environment, which can be modeled by an optimization function. Secondly, it is like asking if we can simulate this specific wave! That's the point! I'm asking if you can generate the "initial conditions" of that wave from the already known initial conditions of ecology.

@Liam Wasserman: Even if one accepts for the sake of argument that evolution is not random, the initial/ongoing conditions certainly are.  For example, suppose that the Chixulub asteroid happens to miss the Earth: then from that point on evolution takes an entirely different path.

The conservation of information implies that we can reconstruct an image of those types of events, so the randomness is purely epistemic/technological in nature. Nonetheless, I’ll admit a gentleman’s defeat: my question is just too broad.

@LiamWasserman You might underestimate the fantastic complexity of evolutionnary processes, with the feedback loops between evolution and ecology, geology, the details of how genotype affect phenotypes and the resulting fitness of an individual. Numerical simulations are very common (typically, in the form of of individual-based simulations) but only to investigate specific, clearly defined, questions and not to reproduce the entirety of the evolution of life on earth. (I am doing my PhD in computational evolutionary genetics and performs loads of individual-based simulations)

You're partially right. I am an ultra novice, if even that. But! If you found the equations of motion for ecological change, and had a dope evolutionary algorithm, you could in theory gain incredibly novel understanding of evolution. The arguments are sound. This is where variational principles would come in handy. Anyways, it was an interesting convo, thank you all.

This article is fascinating: https://arxiv.org/pdf/0911.4032.pdf

This question is off topic in Biology.SE because it is mostly about the computational algorithm. [scicomp.se] may be be better site for this question if other issues regarding general SE rules are addressed.


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Acid splashing beetle | Germany | Middle Europe
I found a beetle trapped in the bottom of a staircase. When I tried to put it on a paper, it turned and splashed something like acid in my face. I saw drops on my glasses and it begun to burn on my forhead. It escaped then through the drain grate.
It was about 4 cm long and probably brown (not sure about the colour). All I found were the Brachinus beetles but they seem to be smaller and I heard no explosion.
Does anybody know what kind of beetle this could have been?

@SonicSplasher where I live? Germany, Middle Europe (as written in the title)

oops , didn't really read the location in the title


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On the genetics behind caste marriages
I am in India where it is typically a custom to marry within one's caste. The caste system originated with roots in people's professions - Each of priests, carpenters, troupers, etc had a caste of their own. My question is based on the genetic basis of marriages performed within one's caste.

I know the concept of alleles where there is a dominant allele and a recessive one, like the A and O resp. in blood groups and Rh+ and Rh- in Rhesus factors. Is there similar genetic information based on our ancestral profession in our chromosomes? Is the son of a couple engaged in farming better suited to the same profession unless he receives a couple of recessive alleles from both parents?
Generally, there is a lot of unscientific information floating around about these matters. One of the grapevines is that it is genetically better for one to marry outside their caste to create diversity(?). Is such a thing true?

If genetics or biology have any role to play in these fields, I will be happy to know and learn.

I think a fresh answer is needed based on the current research results.

Is the son of a couple engaged in farming better suited to the same profession unless he receives a couple of recessive alleles from both parents?

Not everything is coded in the genome, environmental cues play a very important role in shaping who you are. Profession is just one of those things that is not encoded in genes.
Many people do not continue doing the job of their parents, but they do very well in life.
Also note that, aside from the fact that there is no "agriculture" gene, having a recessive allele does not mean you will miss a certain phenotype.
What is true is that someone who has higher education will probably be more keen to have their kids studying. On the contrary, the kids of someone who is a poor farmer and is barely able to provide for his family will probably not have the opportunity of going to school (let alone university) and therefore will continue to work the land. It has nothing to do with genetics.

Generally there is a lot of unscientific information floating around about these matters. One of the grapevines is that it is genetically better for one to marry outside their caste to create diversity(?). Is such a thing true?

Continuing to reproduce in the same group of people will limit diversity in the genome, and create an accumulation of mutations, which is generally a bad thing. That is why it is very common to have particular illnesses in closed communities.
For instance Amish people have an higher incidence of genetic disorders such as Ellis-van Creveld syndrome (a form of dwarfism)
From The Gene for the Ellis–van Creveld Syndrome Is Located on Chromosome 4p16 - Ruiz-Perez et al., Nat. Genetics 2000

Autosomal recessive transmission of the disorder is supported by
  multiple affected siblings with unaffected parents in families with
  known parental consanguinity. The largest known pedigree segregating
  with EVC is that reported by McKusick and his colleagues in the Old
  Order Amish (McKusick et al., 1964). The prevalence of living persons
  affected with EVC among the Lancaster County Amish was estimated to be
  2 in 1000, whereas the frequency of occurrence among live births was 5
  in 1000. McKusick et al. estimated that the frequency of heterozygous
  carriers in the Old Order Amish is as high as 13% (McKusick et al.,
  1964). All cases of EVC in the Amish at that time were traced to a
  common founding couple, Samuel King and his wife, who immigrated to
  Pennsylvania in 1744.

This is a well known effect, called the founder effect.
As for India, a study on the genetic behind casts has been done a couple of years ago.
Reconstructing Indian Population History - Reich et al., Nature 2010
From the paper:

Haldane wrote 45 years ago that “if inter-caste marriages in India become common, various… recessive characters will become rarer”. However, it has not been generally appreciated that this applies to groups throughout India, and not only to groups in the south where consanguinity is common. We hypothesize that founder effects are responsible for an even higher burden of recessive diseases in India than consanguinity.
  To test this hypothesis, we used our data to estimate the probability that two alleles from a group share a common ancestor more recently than that group’s divergence from other Indians, and compared this to the probability that an individual’s two alleles share an ancestor in the last few generations due to consanguinity. Nine of the 15 Indian groups for which we could make this assessment had a higher probability of recessive disease due to founder events than to consanguinity, including all the Indo-European speaking groups.
  An additional reason why some diseases are expected to occur at elevated frequencies in India is shared descent from a common Indian ancestral population. An example is a 25 base pair deletion in MYBPC3 that increases heart failure risk by about 7-fold, and occurs at around 4% throughout India but is nearly absent elsewhere.

They conclude that:

We have documented a high level of population substructure in India, and have shown that the model of mixture between two ancestral populations ASI and ANI provides an excellent description of genetic variation in many Indian groups.
  [...]
  By showing that a large proportion of Indian groups descend from strong founder events, these results highlight the importance of identifying recessive diseases in these groups and mapping causal genes.

It is very important to understand that this results in no way show a genetic basis for the existence of casts, which remain purely social entities. They rather show that an environmental constraint can influence the distribution of genetic traits, due to a restriction in the possibility of mixing genes in the population.

Indian Castes aren't the only place where this is observed - any relatively small group that does not have children outside will. Ashkenazi jews also exhibit several well studied genetic diseases because they tend not to intermarry.

@shigeta: surely, there are many examples of this. The point is: you can have a geographical founder effect, such as that shown by cases like the populations of Iceland, Easter Island, Scilly Isles, Pitcairn Island (see a pattern there?) and Martha's Vineyard. You can have a social/religious founder effect such as Indian casts, Amish people or Askenazi people (and there's surely more). In the first case people are physically isolated, in the second case they are not and the only constraint to marry an outsider is social.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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What does differential consumption mean?
I have not been able to find any definition of differential consumption online. What does it mean in this quotation?

Vertebrates can influence natural fire regimes in several ways. First, herbivores limit fuel quantity by consuming and recy- cling plant matter that would otherwise accumulate as litter, and by reducing the density of vegetation [3]. Second, differential consumption of plant growth forms can enforce changes in the composition of vegetation and thereby alter the type and arrangement of fuel. Third, herbivory can gen- erate large-scale habitat heterogeneity, as a result of variation in herbivore activity in response to factors such as terrain and water availability [3,11], and this can mean that zones of low and high flammability are interspersed in arrangements that could impede the spread of landscape fires. Finally, herbivores and other animals may alter the abiotic environment in ways that affect flammability: by forming trails, dust-baths or leks, large animals create lines or patches of bare ground that can act as fire breaks, while some species forage by turning over or digging through the litter layer and surface soils, and in the process bury fine fuels and thus reduce fuel loads. In the sections below, we explore the evidence supporting these effects of herbivores on fuel and fire regimes, in the past and present.

Johnson, Christopher N., et al. “Can Trophic Rewilding Reduce the Impact of Fire in a More Flammable World?” Philosophical Transactions of the Royal Society B: Biological Sciences, vol. 373, no. 1761, Dec. 2018, doi:10.1098/rstb.2017.0443

Welcome to SE Biology. I am afraid we cannot answer this question unless you provide us with the context in which you met this term, which might relate to anything from shoppers to livestock. We need a full quotation and source. See the section of our Help entitled Be Specific.

A differential consumption is a difference between two consumption levels. This is all one can tell without a direct quote and a context. I am VTC as unclear.

Thanks for editing your question. It’s allowed @BryanKrause to give you an answer.

Second, differential consumption of plant growth forms can enforce changes in the composition of vegetation and thereby alter the type and arrangement of fuel.

This sentence means that herbivores eat more of certain plant growth forms than others. "Differential consumption" just means "different consumption." This can be important in the context of fire risk because herbivores will tend to not eat certain types of plant biomass, such as full-grown trees, but will eat new growth, grasses, etc (therefore the total amount of fuel by type is different).


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Why is the capirally electrophoresis rarely carried out?
I'm a student at the university in Japan.
I search details and advantages with each electrophoresis.
I think the capirally electrophoresis has much nice method at the points of resolution, rapidity and so on. However, just my thought, there are not very many of papers using it.
I have asked at a Japanese site (not professional one), and the answer is on cost. But no sites explain so.
Please give me a help for this confusing.
Thank you for your reading.

Are you asking why capillary electrophoresis is rare compared to normal agarose gel electrophoresis?

Can you also clarify what kind of analytes you are interested in?

For WYSIWYG; It is protein. Our laboratory studies it. Except of me, however, none knows capirally's in detail. So the more you teach me, the happier I am.

For user137; I was going to search in terms of PAGE, but agarose is also OK because I could get few data about the capirally electrophoresis.


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What are the (statistically) normal pH levels in the most-outer part of human sexual organs?
What are the (statistically) normal pH values of the outer skin/epidermis of human sex organs (groin/crotch) in the male and female? e.g male testes, female vulva, male glans, the enveloping epiderm, etc. I was trying to find information to no avail.
Edit:
I googled different terms, like anatomical ph index map of the body, and couldn’t find any ph data about specific anatomical structures.
When I googled, I read through reiterations that the body has neutral ph mostly. Again, nothing anatomically specific.
Due to the ‘unique’ per structure microbiome, it does make sense to foresee a different ph, more to the acidic scale.

Hi and welcome to Bio.SE! Could you provide a clearer indication of where you've already searched and what information you did learn along the way? We as that question askers not only do background research of their own, but that they also demonstrate it. Please update your question using the edit button and add additional detail about your research process thus far.

Can you explain why you would expect the values to differ from those in the skin at other parts of the body? This would provide context for your question. Otherwise it appears rather strange and is likely to be ignored.

@David I don't know if this is related or not, but recently a rumor began circulating on the Internet saying that women's vaginal areas are more acidic than the stomach. I wonder if that is why this question is being asked. Ironically, I was just thinking about asking this question... Beat me to it lol

@L.B. — "A rumour began circulating on the internet". I vote to close.

@David still would be interesting to know if there's any merit

@L.B. — I would imagine that three days' silence tells its own story.

@David, the question makes no attempt to ask about a personal medical question, so voting to close as such doesn't seem appropriate. It also doesn't seem strange for someone to ask this fairly straightforward question given the different environments, bacteria, etc. that these sex organs are associated with compared to the rest of the body. I vote to keep open, and I ask that you more patiently judge people's posts.

Hi, @theforestecologist I used google with difference keywords, for instance, I just can’t seem to find a ‘map’ of some sort of the human ph index presuming such a map even exists in biology books. I just can’t find any ph data about specific anatomical structures.

@Ryan, for the sake of making your question more robust and assuaging other users' concerns, I recommend editing your question by including a rationale for why you think the pH is different. I would think a slightly more drawn out form of your last comment (perhaps with an additional explanation of why you think the groin would have different pH) would suffice. Thanks.

@theforestecologist — In relation to your request, may I say that I read your original personally offensive comment before either the moderators or you removed it. You should therefore know what is required before I respond to that request or any future comments you might make on my posts.

I might suggest googling "normal vaginal pH", "normal urethral pH", and "normal skin pH". This will get you better google results than your prior search strategy.


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What may these eggs belong to?
Today I've found these eggs on the outside of my house.
This is located on the north of Spain.

Do anyone knows what it belongs to?
I'm leaning towards something related to the Reduviidae family?
google image search for Reduviidae

Oddly enough - English being the weird language that it is, the phrase is "leaning towards" for something you are thinking might be the right answer. Leaning against would mean not the right answer.

Just did a snap Google search for "assassin bug eggs" and the images that came up were very reminiscent of yours; here's a link to a good article with an image: https://www.canr.msu.edu/news/michigan-insects-in-the-garden-week-3-assassin-bugs. So yeah, most likely possibility is assassin bug eggs.


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Do you know which is this small flower in Asturias?

Was located in the Turón valley on Mieres, Asturias, Spain (https://goo.gl/maps/BMwyfWtiSdw). Found it at 900 meters of altitude. The plant is just about 8 cm high maybe. All the ones I've found were alone. Just one flower from a couple of leaves.
Kind of reminds me of a Cyclamen?

It is an Erythronium lily commonly called a "dog's-tooth-violet" or "trout lily". I see that one of the species Erythronium dens-canis is found in Spain, being native to Europe. Most of the Erythronium species are native to North America. The foliage is very attractive and they are commonly grown as ornimentals. The flower in your photo is just opening. I have included a few links that better describe these lilies.
https://en.wikipedia.org/wiki/Erythronium
https://en.wikipedia.org/wiki/Erythronium_dens-canis
http://www.srgc.org.uk/bulblog/log2008/160108/log.html


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Insect ID, Ecuador
Picture was taken in the Ecuadorian Amazon in January 2019, during the day, elevation about 300 meters. The size was not recorded but might be no bigger than a housefly judging from the photo. It appears to be a leafhopper of subfamily Gyponinae. Any additional info on the genus or species would be appreciated.

I am no entomologist, but that looks like it may be a type of cicada. Is it one of these perhaps?

Hi, terdon. Thanks for the comment. The bug was quite small, and does look like a cicada, but a very small one. From some info I received, I think this might be a leafhopper. Leafhoppers are relatives of cicadas.

Please [edit] your question and add the size since that will likely help identify it. Also tell us what kind of environment you found it in (jungle, yes, but was it in the canopy? On a tree bark? On the forest floor? Did it have a nest you could see?) The more details you give, the likelier it is someone will be able to identify it.

Well, it was taken about a month ago, along with about 600 other subjects, so what I know about it is pretty well in the photo. It was on a leaf. It was small compared to the leaf, although I don't have a record of the size of the leaf. I'm satisfied that it is a kind of leafhopper, subfamily Gyponinae. That is a varied group, but that is fine for now.

Please [edit] your question and include these details. Comments are easy to miss, hard to read and can be deleted without warning. You want the next person to read your question (who might actually know what they're talking about and not just be stabbing in the dark like I am) to have all the details easily accessible.


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10 inch spider near Mexico City
Four years ago I found a spider so big that I'll never forget. Unfortunately I don't have a picture but I guess there isn't a lot of big spiders in Mexico. So here are some things I remember:

It wasn't a brown spider, I think it had red legs with some parts black and others white.
Its legs were skinny and very long
The main body was tiny compered with the spam of its legs.
I found it at noon, after I moved to my new house. Unfortunately it wasn't moving when I found it
The spider didn't have any visibly hair.

That's all I can remember. I know that this may be impossible but I don't know what else to do.

It almost definitely wasn't 10 inches, but there are some pretty big spiders in Mexico. There is a species of spitting spider with a 9 inch legspan but it lives in South America not Mexico.
Scytodes globula

The cellar spider has a legspan of up to 3.6 inches and a comparatively small body with long skinny legs and no visible hair, but I can't see how that would be confused for 10 inches.
Pholcus phalangioides

The giant crab spider fits that description to some degree. It has a legspan of up to 4 inches.
Heteropoda venatoria

The golden silk spider is very large with long skinny orange and red legs.
Trichonephila clavipes

Sounds like a Mexican Red Knee Tarantula. they are kept as pets. not dangerous except for irritant hairs which they can project and which can get into eyes.
https://www.google.com/search?q=mexican+red+knee&source=lnms&tbm=isch&sa=X&ved=0ahUKEwiJlvWuyvLgAhULlhQKHbfrD3IQ_AUIDigB&biw=1431&bih=734&dpr=1.65

It isn't the spider that I saw, but you made me remember something else.


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Why do BRAF mutations appear more in skin cutaneous melanoma?
When looking at the tissue expression of the BRAF protein it seems that BRAF is regularly expressed in almost all of the tissues. There is elevated expression in tissues like the Testis and the Parathyroid gland, but the expression in the Skin is about average. So how does it make sense that for example in tumor samples of skin cutaneous melanoma (TCGA-SKCM) the BRAF mutations are so dominant (about 50% of the cases contain a BRAF mutation)? And on the other hand, it occurs less frequently in other cancer types?

This is a good question - I will try to answer it later.

Chris, if you know why, I will like to hear it please. Even if you only have an assumption about it.


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Multiple numbers in the Ishihara test?
When I was in high school (30 years ago), I took a biology class, and the instructor showed us an Ishihara color test for color-blindness. (This is the "hidden numbers" test.)
What I thought I saw once or twice was two different numbers* that had been embedded in the same slide. Were there slides in the test that had two or more numbers, or was I hallucinating?
[EDIT:] * "Two different numbers" means "different numbers in different colors."

I got a chance to look through the actual images, and it appears I hallucinated the third number.

The Ishihara Color Test consists of plates containing one number. But that number may consist of two digits (Fig. 1). After scouring the internet I have also found variants of the test where the each of the two digit had a different coloring (Fig. 2), but these tests may not all be validated/standardized or used by health care professionals. The plates may also contain one or two wiggly lines that have to be traced (Fig.1). In all, my conclusion is that there are many variants of this specific test around, at least on the web. I am not aware whether there are certain standardized versions being used by health care professionals. In all, my answer to your question...

Were there slides in the test that had two or more numbers, or was I hallucinating?

...is that there might have been two digits of different coloring in the plate, dependent on the specific make of your teacher's plates. You might, or might not have been hallucinating. To give a more affirmative answer, the specific test with the specific make would have been dug up by your teacher.

Fig. 1. Ishihara test with a plate containing one number of two digits (left) and one or more wiggly lines (right). source: Colour Blindness

Fig. 2. Ishihara variants, showing two digits with different shades in the middle panel. source: allinesnowmop, a personal web page, credibility questionable

@user237650: Once again, I consider that one number. Maybe I need to add: "the second digit wasn't lined up with the first one"?


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Is UV radiation more likely to cause mutations during mitosis?
According to Life: The Science of Biology (10th edition), UV radiation might cause the formation of pyrimidine dimers, which are the primary cause of skin cancer in humans.
Are mutations more likely in case a cell is exposed to UV during mitosis?
My TA (who is a stem cell researcher) implied that the answer is yes, as she explicitly said that the risk of getting cancer from gel manicure is non-trivial, due to the following reasoning:

During the treatment, small cuts are made (not on purpose) to the skin around the nails.
The exposure to UV occurs just after that, while the tissue is healing.
This significantly increases the risk of cancer.

However, I didn't find information about that by googling. On the contrary, I encountered studies about using UV to enhance healing of wounds, e.g., Is UV radiation beneficial in postburn wound healing?.

In addition, Wikipedia's scar page says (though I didn't find a reference for that claim in the Wikipedia page):

scars in the skin are less resistant to ultraviolet radiation

Also, people are instructed to avoid exposure to UV after laser hair removal.
Is these two related to mitosis? Or are they instead related to some property of scar tissue?

references:
Rennekampff, H-O., et al. "Is UV radiation beneficial in postburn wound healing?." Medical hypotheses 75.5 (2010): 436-438.

This question does not make sense. Human fingernails are inert, acellular, structures made primarily of keratin.  There are no living cells in them and therefore cutting or trimming the nails is not a wound.  Without a wound the term healing does not have a clear sense.  Fingernails “grow” at a constant rate, regardless of trimming.  Wound healing does require mitosis, manicures do not.  Ask your TA about the incidence of fingernail cancer.

@mdperry Thank you. I wasn't aware of keratinization. Quite fascinating. I might have misinterpreted her explanation (though she definitely said that the risk of getting cancer from gel manicure is non-trivial). Anyway, I sent her an email.

@mdperry She answered that during the treatment small cuts are made (not on purpose) to the skin around the nails. I edited my question accordingly.


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Explain to a layperson how cigarettes smoke might cause cancer
I have a very intelligent friend who is a light smoker, and also a Biology layperson.
I wondered whether understanding exactly how cigarettes smoke can cause cancer, might encourage him to smoke less (or quit entirely).
So how would you explain to a Biology layperson how cigarettes smoke might cause cancer?
To clarify, I am looking for a detailed explanation for a layperson, that makes the cause-and-effect much more vivid for them, and thus makes it much more likely that the intelligent layperson would internalize the risks of smoking.
Online resources that I found either gave a too simple answer or concentrated on statistics (which are usually hard for humans to internalize, if I understand correctly).
(Nothing wrong with such explanations, they are just not what I am looking for.)

I'm voting to close this question as off-topic because it is a request for proof-reading a document, rather than for an answer to a biological problem, which is what is appropriate to SE Biology. It might possibly be re-phrased as "How does smoking cause cancer?" with the bulk of the question being moved to an answer from the poster (which is allowed).

@David Is a solution for a biological problem in layman terms appropriate for biology.SE? anyway, I edited according to your suggestion (hopefully). Thanks :)

@David By the way, I wrote the question after I had already sent my friend my explanation (which wasn't even in English). I just thought that surely many biology.SE users could explain it better than me, and so I posted the question (which included my attempt at explaining it, as I thought that biology.SE requires showing your efforts in the question).

There are tons of resources on this, especially for laymen. Did you even try looking at them? Simple answer to your question is that cigarette smoke contains many harmful substances and some of them are carcinogens. Regarding your original question: you start with DNA replication and how a particular carcinogen can cause mutations in DNA. That is a very broad background and is actually counter-productive. In your current form, I might say that your question is broad and also not useful as there are loads of resources on this topic from reputed organizations, for laypersons.

@WYSIWYG I did some googling, but I admit probably not enough. I turned to biology.SE as I assumed that like this resource, most of the resources for laypersons don't get into detail, and aim at simple answers like yours. I probably didn't explain myself well: I am looking for a detailed explanation for a layperson, that makes the cause-and-effect much more vivid and thus makes it much more likely that the intelligent layperson would internalize the risks in smoking.

@OrenMilman If they go into details then laypersons won't understand. If one wants to understand how mutations happen in DNA then they have to look at other sources. Stackexchange format is definitely not suitable for answers like these: starting from DNA composition to the effect of carcinogens. There are too many processes involved and one can learn a lot about any of those processes. If you want to educate people then you can try writing a blog.

@WYSIWYG I posted at first because I thought my explanation isn't optimal, so if you think explaining DNA composition isn't relevant, I don't disagree :)  Anyway, I guess different SE sites are different, as I first got the idea to ask this from a stats.SE post.

In reply to your query whether an answer in layman's terms is appropriate for SE Biology, that is a matter of opinion. My opinion is only one of five needed to vote a question off-topic, and others may not agree with my reading of the rules. That said, it depends. On looking at your answer, I'd say that it probably isn't very useful here.

I encountered the following paragraph in the textbook Life: The Science of Biology:

Some chemicals add groups to the bases. For instance, benzopyrene, a component of cigarette smoke, adds a
  large chemical group to guanine, making it unavailable for base
  pairing. When DNA polymerase reaches such a modified guanine, it
  inserts any one of the four bases at random. Three-fourths of the time
  the inserted base is not cytosine, and a mutation results.

After finding the following quote in Wikipedia's Benzo(a)pyrene page, I decided to explain specifically how BaP can cause cancer:

BaP has since been identified as a prime carcinogen in cigarette
  smoke.

My explanation:

A protein molecule is a chain of amino acids. Proteins are hugely important, as they are responsible for most of the cellular functions.
A DNA molecule is a chain of nucleic acids. There are 4 types of nucleic acids in DNA: A,G,C,T.
Having intact DNA molecules is crucial, because they include the encoding of proteins, according to which cells synthesize proteins.
A mutation is an alteration of a DNA molecule.
A mutation might lead to our cells synthesizing a malfunctioning protein. If a protein that should regulate cell division is malfunctioning, then the result might be uncontrolled cell division - cancer.
When you smoke, the chemical BaP (which is found in cigarettes smoke) might alter a G nucleic acid in a DNA molecule in some cell in your body. Later, when this cell tries to divide, it makes a copy of each of its DNA molecules, but it won't be able to identify that G nucleic acid (that BaP altered), so it would put a random nucleic acid in the copied DNA molecule. Thus, there is a 3/4 chance for a mutation.


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Is there a term for the opposite of intergenic?
I am looking for a term that describes DNA regions that overlap genes, i.e., non-intergenic DNA regions.
For example, say I am writing a paper about DNA-binding sites (i.e., DNA sequences that proteins bind to), but my paper focuses exclusively on DNA-binding sites that happen to overlap genes. What would my title be? "Non-intergenic DNA-binding sites are [...]" is one option, but I wonder whether a more appropriate term exists.
If I understand correctly, "Gene-overlapping" seems to be used for referring to genes that overlap other genes (https://en.wikipedia.org/wiki/Overlapping_gene).
Also, Google says that "genic" means "relating to genes".
Is any of my ideas appropriate? Or maybe another term?

To clarify what I mean by intergenic and non-intergenic, here is the figure from https://en.wikipedia.org/wiki/Intergenic_region. I added an example for a non-intergenic DNA region.

Explicitly, an intergenic DNA region is a DNA region that doesn't share any base with any gene. A non-intergenic DNA region is a DNA region that shares at least one base with a gene.

What do you mean by "regions that overlap genes" and how is that different from genes themselves?

inter means between, intra means within, think inter-state highway.

@BagiM and John, I tried to clarify. Please point out if it still isn't clear.

Your "non-intergenic DNA region" overlaps the purple gene and possibly some of the red, too, so I don't understand what's non-intergenic about it.

@MattDMo If I understand correctly, "intergenic" means between genes, i.e., doesn't overlap genes. Thus, "non-intergenic" means not between genes, i.e., does overlap genes. If this is not accurate, please let me know

@MattDMo I apologize. I made a horrible mistake in the definition I gave at the end. I fixed it now.

I wouldn't use non-intergenic to refer to sequences that contain at least one base of a gene, because, at least according to your graphic, a large portion of it still could be intergenic material. Maybe just call them gene-overlapping regions? I'm really not sure.

@BagiM There are sequences/regions in a genome that are not genes, e.g.: https://en.wikipedia.org/wiki/DNA_binding_site, https://en.wikipedia.org/wiki/Enhancer_(genetics)

I understand the terms genic and intergenic to be dichotomous, so non-intergenic to me just means genic and I doubt you will find a term of art applicable to your scenario. Some kind of descriptive phrase may be more useful: ”DNA binding sites at the boundaries between genic and intergenic regions are…” or perhaps ”DNA binding sites at intergenic boundaries are…”

It seems to me that "genic" is a perfectly good word.
This paper uses "genic" directly as a contrast to "intergenic", so that seems like a reasonable precedent:

‘Noncoding DNA’ can be found both surrounding genes, and within genes (see schematic Figure 1). We will call the first type ‘intergenic’, and the second type ‘genic’, a ‘gene’ referring here to a transcribed DNA sequence.


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What is the origin of plasmids?
As I understand it, plasmids, like mitochondria, have their own genetic material and are capable of self-replication.
According to Wikipedia: Plasmids are considered replicons, units of DNA capable of replicating autonomously within a suitable host. However, like viruses, they are not classified as life. Plasmids are transmitted from one bacterium to another through conjugation. Unlike viruses, plasmids are "naked" DNA. However, some classes of plasmids encode the conjugative "sex" pilus necessary for their own transfer.
My understanding of that is that a bacteria gets their plasmids not because of the replication of their circular chromosome, nor because that chromosome have genes to code for the plasmid (I don't really know if that's possible), but because of the self-replication of their own plasmids.
So, my question is how the first plasmid got into the first bacteria, if they are not in their chromosomes? Were they a virus other prokaryotic cell that had circular DNA, and got phagocytosed by that bacteria ?

Do you mean plastids? Becaue otherwise I get a feeling you don't seem to understand what a plasmid actually is: a piece of (circular) DNA. Also note that the human genome does contain a majority of the genes that are needed for / originate from mitochondria.

@Nicolai, I really meant Plasmids, see if the explanation is better now.


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Why can AB people receive blood from A, B or O?
AB people don't have agglutinins anti A or anti B so it might seem they can receive any type of blood. But if the donator is A for example, it's own blood will have agglutinins anti B that will agglutinate the AB blood. So why can AB people receive blood from non AB people?


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Finding total concentration of enzymes
Sorry if my question is very basic for biology majors because I am not. I am trying to build a mathematical model of a particular pathway using systems of differential equations and in order to reduce the number of parameters, I need to know the total concentration of multiple enzymes. How are enzyme concentrations usually reported in the literature so I can google it? Also, this does not seem to me to be a straightforward measurement for professional biologists, so how are enzyme concentrations actually measured or approximated? Thanks in advance!
I am interested in the following pathway:

I wonder whether you could clarify whether your equations deal with concentration in term of physical amount of enzyme (mg/ml) or (functional) activity (enzyme units per ml). The reason I ask is the latter is what I would think determines the operation of the pathway. But perhaps I misunderstand what your mathematics is modelling. Presumably you are trying to quantify the effect following some stimulus — can you elaborate. Oh, and in what tissue in what organism do you wish the concentrations?

@David: I am interested in the physical amount of enzyme, because I intend to use an oversimplified relational equation: $E_T=E_f + ES$ where $E_T$, $E_f$, and $ES$ stands for total enzyme (physical) concentration, "free"-enzyme, and enzyme-substrate complex, respectively. I think this would be a way to approximate a model of inhibition where $S$ is an inhibitor of the enzyme $E$, since the inhibitor would "eat up" the amount of free-enzymes. Ideally, I am interested in human fibroblast or endothelial cells. However, if data is too scarce for human cells, then mice would be fine.

@David: Also, by functional enzyme, did you mean an active enzyme?

Yes. I was trying to use layman's terms (not very helpful). I'll think about your approach and see if I have anything useful to contribute.

Hi again TheLast Cipher,
Enzymes in a cell are usually semi-quantified by the: Western Blot technique.
But there are lesser known techniques.
E.g. For a Western Blot the unit of measurement is the color intensity of the enzyme band on the blot membrane.
If I were you I would look for journal articles covering your pathway of interest.
E.g. https://iubmb.onlinelibrary.wiley.com/doi/abs/10.1002/biof.5520320129
Covers the electron transport chain (Co-enzyme Q10)
If you can get through the pay-wall & read their results and you will find:

"Western blot analysis of membrane protein isolated from keratinocytes derived from one young and old donor. A representative picture out of five experiments is displayed."

Also they used and I quote:

"Arbitrary Units"

Maybe you could comment on which pathway and I can find some assisting material.

Thank you very much, Andrew! I've uploaded an oversimplified version of the pathway as a rough sketch of what I am working on. So there are kinases in between the interactions and I'm interested in their concentrations (e.g. PIP2, PRAS40, TSC2, Rheb-GDP, Rheb-GTP, as found on figure 3 of https://pubmed.ncbi.nlm.nih.gov/28069808/).

Your attachment is unfortunately RNA concentrations. I'll see what I can find.

The BioNumbers site (https://bionumbers.hms.harvard.edu/search.aspx) is often useful for these types of questions, if you're interested in an order of magnitude. However, if you want precise concentration ratios (i.e. something like "is there twice as much Ras as ERK, or more like half as much"), you are unlikely to get a definitive answer.
These may be cell type-dependent and even vary from cell to cell due to noise. You probably want to simulate your network with a variety of absolute concentration, and then the most interesting behaviors are those that are reasonably robust to the exact numbers used (results that depend on, e.g., having almost exactly the same number of molecules of Ras as ERK are likely irrelevant as they would be too "brittle" inside a living cell). Once you find out what the necessary limits are for a given behavior that you find interesting, you could think about checking whether values reported by the literature indeed tend to fall within those bounds.

Hey, thank you very much for this. This looks like a great resource!