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Is there any way bicondylar/bigonial, bizygomatic or bitemporal breadth can change in adults?
Without cosmetic surgery or etc., are there any cases/example wherein a human adult has had a change in significance regarding these regions of the face? I have seen many anecdotes where people have asserted that certain things (not surgery) like diets, drugs, or etc. has affected these regions.
Is this possible and what are any such means in which these regions of the face can change?
This isn't a personal medical question as this is widely applicable and generic to any human adult.

Possibly many things can affect the morphology but the question is whether they are controllable in any manner like a surgery. Can you please elaborate your question and try to keep it to the point such that it can be answered in a few paragraphs?

There's no way I can think of to better word/organize the question -- it's as simple and straight as I can get it.

Acromegaly (pituitary gigantism) is a disease that causes enlargement of the bones of the face.  There is interest in computerizing facial measurements to catch subtle enlargements and prompt testing for the disease.
https://www.researchgate.net/publication/261409008_Three-dimensional_facial_analysis_in_acromegaly_a_novel_tool_to_quantify_craniofacial_characteristics_after_long-term_remission

Sixteen patients in remission of acromegaly for over 24 months (50 %
  male, mean age 56.0 ± 10.7 years, mean body mass index 29.3 ± 5.5
  kg/m(2)) were compared to 16 matched control subjects. A 3D cone beam
  computed tomography scan and 3D stereophotograph of each individual
  were acquired and analyzed using 3D cephalometry. In addition to an
  accurate quantification of the classical craniofacial characteristics,
  3D cephalometry, shows that many typical soft tissue deformities
  persist, even after long-term remission. Furthermore, we found that,
  compared to controls, the patients in remission of acromegaly have a
  wider face at the level of the zygoma and longer maxilla (p < 0.05)

Apocryphally, enlarging hat size goes along with acromegaly.

Pagets disease of bone causes enlargement of the skull and also an increase in hat size (so bitemporal dimension); the hat size increase was one of the chara eristics first described in the disease.

Thalassemia is a group of blood diseases characterized by ineffective red blood cell production.  The body compensates by making more marrow anywhere it can.  Some people wind up with expanded bones in the skull or maxilla as a result.

https://www.slideshare.net/ismahharon/thalassemia-is

These are all systemic diseases that affect the bone.  Of course one can have a tumor of bone (primary or metastatic) that expands it and changes the shape of the face or the head.


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Characteristics of a giant squid’s skin
Is the skin of a giant squid/colossal squid similar to the common squid? Does it possess chromatophores to change color? Or did it lose that ability because of the depth at which it resides or due to the comparative lack of predators?

source: Stack Exchange

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

sort: votes


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Are all genetic disorders inherited?
I know that genetic diseases such as cystic fibrosis are often passed down through generations and are therefore classified as genetic disorders, but if a mutation occurs spontaneously, which for example leads to cancer, is this then classified as a genetic disorder?

Are all genetic disorders inherited?

Not all individuals with a genetic disorder inherited that disorder. Some genetic disorders are caused by spontaneous mutations.

Is cancer a genetic disorder?

Yes. The seminal paper by Hanahan and Weinberg, the Hallmarks of Cancer, is a good place to go to get a sense of what we understand cancer to be. This paper is quite influential and has its own wikipedia page. These authors wrote an updated review in 2011. Re: your question as it relates to cancer, yes, genetic changes result in tumorigenesis. Cancer is a genetic disorder of cell populations. One can view cancer diagnosis and treatment from the framework of cancer as a metabolic disease, but this adds to, rather than subtracts from the framework of cancer as a genetic disease.

Are other diseases caused by spontaneous mutations genetic disorders?

Yes. Achondrodysplasia is one illuminating example. It is a form of dwarfism caused by a mutation in the FGFR3 gene. It does follow mendelian autosomal dominant inheritance patterns, but in 80% of cases, the mutation is, in fact, acquired spontaneously (that is, not present in either parent). As noted by @Eff in the comments, Down syndrome, Trisomy 21 (and other chromosomal abnormalities, e.g., Turner, Kleinfelter, Patau, Edwards) are other common examples.

Down syndrome is a similar genetic disorder that isn't inherited right?

Yes, there are many examples

Down syndrome can be heritable, but most cases are spontaneous.

@swbarnes2 yes, cancer, down syndrome, and achondrodysplasia are three examples of genetic disease that can be heritable but are spontaneous in most cases.

Great answer, though I'd personally recommend expanding the "yes" you start off the answer with, since the question in the title and the question in the body lead to different conclusions from a simple "yes."  Just a bit confusing.

@rotaredom good note. Done.

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


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What's the name of this green fruit with little pikes fallen from a city tree on the pavement?
What's the name of this green fruit with little pikes fallen from a tree on Paris (France) pavement ?

Seems horse chestnut.

It would be very  helpful to know the location of the photo (city, country).

Also something idea of the size.

Its 100% a euro or an indian conker tree species.

Welcome to Biology.SE! Identifications questions should include: 1) one or more clear closeup photos of the organism (photos from multiple angles if possible) — in this case clear pictures of the leaves and bark of the tree; and 2) an estimate of the size of the tree and the fruit. Please [edit] your post to include this essential information. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site, which differs from the SE sites that you are more familiar with. Thanks!

It is horse chestnut it is very common to plant chestnut trees in public parks and a lot of people do have them around their property and by the side of many roads.
What you have in your picture is the fruit and the leaves on the ground confirms that this is horse chestnut.
Source https://en.wikipedia.org/wiki/Aesculus_hippocastanum
The nut is poisonus and the toxin can cause loss of coordination and tremors in horses if they eat the nuts.
Touching or handling the nuts do not cause any adverse effect to humans they are only dangerous to humans if they are eaten.
Horse chestnut contains alcaloid saponins and glucosides that have a toxic effect on mamals.


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skin colouration in thalassemia
Now when i was studying about thalassemia, I read that anaemia is its major characterstic. I can understand that fact. But it was also written that the skin gets pale.

Wikipedia says that the skin turns yellowish.

I want to ask firstly is it that the skin gets darker when the affected person is exposed to sun and is otherwise pale?
And also why does the skin turn yellow/pale in the first place? Does that have to do something with Iron?

Thalassemia is a genetic disease, in which either the alpha- or the beta-globins are missing or mutated. The hemoglobin of the blood is a protein complex which in adults consists of 2 alpha- and 2 beta-globin subunits. The ratio of these proteins needs to be exactly right, if one of them isn't produced enough or even missing, this leads to non-functional hemoglobin and subsequently abnormal erythrocytes.
These are then removed and broken down in the spleen (which is often abnormally enlarged), which also leads to the breakdown of the non-functional hemoglobin. The main product of the hemoglobin breakdown is Bilirubin, which is yellow. The yellow skin is a sign of jaundice, which is caused by high levels of Bilirubin in the blood.
The cause for the high Bilirubin levels in the blood of Thalassemia patients is the abnormal high rate of Hemoglobin breakdown.

But how is it even related to thalassemia? @Chris

@Ishi It is. I will expand the answer.

@Ishi Is this clearer now?

This is such a great answer, thankyou so much, I understand it now ! @Chris


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Where can I find and download HMMTOP training set?
I would like to perform redundancy reduction for my test set for membrane topology prediction. I checked the 1998 paper and website of the HMMTOP server but haven't found any download links for the dataset that they have used for training.
Links:

paper
server

In the Appendix Section of the paper, there is a table of entries and topologies.  Below, there is a note:

*Entries which are included in the initial parameter and
  pseudocount settings from the 83TMP set.

Please correct me if I'm wrong, I suppose these those 63 protein entry names with an asterisk are the data used for training?

From materials and methods: The first data set was originally collected by Jones et al. (1994), and was also used by Rost et al. (1996) (83TMP set). The second one is an extension of it by Rost et al. (1996) (48TMP set). The third data set contains prokariotic transmembrane proteins collected by Cserző et al. (1997) (prokTMP set).

You might have to look at these papers individually or mail and ask the authors for a properly formatted dataset that they used for training. The last update was 18 years ago; so I'm not sure if the author is still active (alive)!! Perhaps you should try more recent tools based on HMMTOP. Check for citations.


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Laurasia and Gondwana
The Cambrian explosion was 540 mya. Laurasia and Gondwana didnt collide until 330 mya. So for 210 million years the land was divided into two large continents. Plants and insects had already colonized the land long before Pangaea formed. It should therefore be possible to divide land plants and insects into two broad groups. One group that inhabited Laurasia and one group that inhabited Gondwana. I have googled around but I cant find any good info on this.

I think phrasing it as a question would help!

Is there an actual question here?


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Is this headlice or bed bug

This is very small. About the size of a grain of rice. I Felt it crawling in my hair.  When I brushed my hair off this fell out in the sink. I was wondering if it's lice. I'm in Mojave county Az

Please add your location and the approximate size of the specimen. Both are needed for an accurate ID. I also advise that you upload any additional pictures you may have of the specimen. Currently, your post is lacking adequate detail and will be closed and unanswered. Please [edit] accordingly. thanks.

That is a Thrips, order Thysanoptera. Not harmful. Not a bedbug or a louse. You can read about them here.
https://en.wikipedia.org/wiki/Thrips
(by the way the singular form of "Thrips" is "Thrips": there is no such thing as a "Thrip")


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Chargaff Rules (confusion)
A professor of mine wrote that: $\frac{A+T}{G+C}$ is constant in double stranded DNA of different origin. However
The Chargaff rules state that due to base pairing in the DNA it holds that :
$A=T$ and $G=C$ and from that follows that $A+G=T+C$ in all DNA molecules
and thus: $\frac{A+G}{C+T}$ should be constant, no?
Who is in the wrong?

Was your professor talking about Chargaff rules or about GC content? Why didn't you ask the professor to clarify?

Constant in what sense? For all organisms? Please edit your question and make sure you recall correctly and completely what your professor said. And please, no ‘rules’ in any argument — just invoke what is known about the structure of DNA.

It states verbatim: for double stranded DNA of different origins it holds that : $\frac{A+T}{G+C}$ , the ratio is wrong, and the one I gave in my answer is correct, right?

Context is important.
A/T ==  1 and G/C == 1 (approximately, to within a measurement error) are Chargaff's rules for double-stranded DNA, occurring because A pairs with T and G pairs with C.
(A+T)/(G+C), or (G+C)/(A+T+G+C), are completely different ratios unrelated to Chargaff's rules. These are roughly constant across individuals for a given species and can be used to distinguish different species' genomes in an approximate manner.
I am not your professor, but it is possible in writing what they wrote, the professor was referring to whole-genome GC content within members of a species, in which case the professor is correct. If the professor was discussing Chargaff's rules, then the professor was wrong, but probably just made a mistake in writing: these things happen.

He states (verbatim): with double stranded DNA of different origin , the ratio $\frac{A+T}{G+C}$ is constant. Your answer doesn't really answer or help with anything , and just creates more confusion.

@schokakola I prefer to not just assume your professor is an idiot: in my experience, assuming people are idiots is counterproductive when other explanations exist. Thinking through multiple possible meanings is a good way to test your knowledge, so that was the intent of my answer. I've clarified my answer to make clear that if your professor wrote that ratio referring to Chargaff's rules, it is a mistake.

Read your "answer". It doesn't answer anything that I stated in my question. Do yourself and me a favour and stop replying to me please and let somebody who understands what I am asking answer instead!

@schokakola Can you clarify what exactly is still unclear to you compared to what you already know? "Your professor is right" or "your professor is wrong" is not an appropriate answer for Biology.SE, answers need to explain the concept and underlying biology.

I am asking whether the ratio I stated is correct or not. It's a very simple matter if you understand what I am asking. The answer is either yes or no. What you are doing is posting mindlessly anything that could peripherally have anything to do with the question in order to sound smart without answering the question itself. Stop.

Let me remind you of the Code of Conduct - I am being very patient with you because you are addressing me, but if you were addressing anyone else I would not have such patience. See also https://biology.meta.stackexchange.com/questions/3377/homework-questions

As I've said before. You not only didn't answer (or read and understand) my question, you intentionally added more confusion to make things MORE unclear just to sound smart. I don't want to have to deal with "you". I'm looking for somebody who is knowledgable in this area and can give a clear answer for which I'm very thankful.

@schokakola The answer to your question depends on the context. I don't want you to go to your professor and tell them they are wrong if they are actually correct but you misunderstood. Therefore, my answer gives two explanations: a case where they could be wrong (if they were in fact talking about Chargaff's rules), and a case where they could be right (if they were talking about something else). Now you'd have to go to your notes and find what the context was so that you know which one is the case. The only one here who is knowledgeable about what was said in your class is you.

If you don't understand the question, or it is unclear to you, then don't answer! Judging from your answers, you have no clue what I'm asking (you didn't even consider the ratio I gave because you are only interested in posting whatever you want to sound smart). After 100 comments, I still don't know whether the ratio I wrote is the correct one or not, instead you started a discussion about why I did or didn't ask the professor etc. etc. everything that has nothing to do with the question itself. Just save yourself the time and don't answer/reply if you don't understand the question.


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Does the frequency discrimination of the outer hair cells of the ear increase with sound pressure?
I'm wondering whether the frequency resolution of the inner ear increases/decreases with the volume level (caused by sound pressure $(N/m^2)$.
My assumption would be that as long as the pressure level is high enough to cause a pressure wave in the scala media/corti-organ, the frequency discrimination has nothing to do with the volume level.
There doesn't seem to be any information regarding this question!
Let me give an example to illustrate better what my question is:
If I have a sound with $20 \ dB$ and a certain frequency $1000\ Hz$ will the ability to judge the note (frequency) increase or decrease with the pressure?

Do you mean the inner hair cells?

lol no, i think they are called outer hair cells; also there are inner hair cells and outer hair cells, the outer ones are responsible for frequency discrimnation, so i want to know whether or not that depends on the pressure/volume or not or if there is a optimal pressure level where frequency discrimination is the ighest

The outer hair cells are "motor" cells, mechanical amplifiers. Inner hair cells are the ones behind perception (aka frequency discrimination). You still could really mean the outer hair cells, because they also respond to sound, but their function is to modulate the response of inner hair cells. Also, why are you differentiating between volume and pressure (do you mean to?) A 20 dB 1 kHz sound is a sound of a specific volume; if you change the pressure it is no longer 20 dB.

Well I found an answer: the optimal range (highest possible frequency discrimination) is supposedly at $1 dB$ so it does not increase with soundpressure/volume


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Microscope Recommendations
I am a Engineering University student, in my last year of completion of my degree. I had interests in biochemistry and biology since I was a kid, and been learning about that side by side in my spare time.
I want to get into biomedical research and buy a suitable microscope for that purpose.
After following various guides and info I could find, I have decided to go for a well manufactured compound microscope of high quality. But these fishy companies majorly Chinese are troubling me, with top companies like Leica, Nikon, Zeiss etc having quite same reviews.
I haven't yet decided the Manufacturer I want to buy from. I am willing to go for around $1000 for a well reputed manufacturer. There are numerous choices even within the top companies.
What are some best suggestions and recommendations for Compound Microscope according to my needs?

all suggestions are welcomed.
edit 1: Many Indian manufacturers called me, but I want some reliable global manufacturer, well known by its quality. I also need some expandable scope for future upgradations. Am I going the right way or should I buy from Indian manufacturers? and which manufacturer if well known one?
edit 2: The price I am going into is $1000.

What do you actually want to accomplish? A compound microscope isn't going to get you very far in biomedical research.

I am currently going for entry level one. Probably I will invest more later but for now, I want to get the basics clear.

Buy a microscope if you want to pursue a fascination with observing microscopic things as a hobby. But it will be of no use in biochemistry or molecular biology, where your hard skills are most likely to be applicable. The biochemistry labs in my university do not sport a single microscope, and I personally have only ever used one to check cell growth or virus infection (when I have to ask someone else how to use it).

Then I guess, currently I wish to do the basic things(not complex though). Thanks for clearing that out. But where should I start for getting one.

@David: And for a hobby-level microscope, $1500 is way overkill.  (I think I paid under $300 for mine, a few years ago.)  I think you would be better served by spending the extra money on things like a USB camera, polarizing filters, stains, &c.  Plus if you get a job in microbiology or some other field that requires microscope use, your employer will buy your equipment.

I used microscopes my whole adult life: provided by school or employers . I would look for a different job if  microscopes were not provided. Also , considerable support infrastructure is required for microscope  work.

@David Thanks for suggesting that. Maybe I should see the big picture instead of directly going for a high end one.

Can you suggest which manufacturer would be the best for that price range and quality?


text:
What kind of plant is this? (looks like periwinkle)
Found this flowering plant near my house in Pennsylvania, USA. What kind of plant is it?
I really like it because it is keeping out the weeds. I think the previous owners had planted it.
It looks like there might be some mint to the left but I am interested in the flowering plant.
If I had to take a guess I think it is periwinkle.
I was hoping to plant more of it to keep weeds out.

You're correct, it's periwinkle.

Common periwinkle is a low-growing mat-forming, vine-like perennial nonwoody plant with green, shiny, smooth stems that are woody at the base. It spreads by underground runners or by its vine-like stems that take root at the nodes. It is not native to North America and has proven to be invasive in several states. Planting it is not recommended.

The leaves are opposite, simple, evergreen, ½–1½ inches long, ½–¾ inch wide, egg-shaped to equally rounded toward the ends, the tip blunt to pointed, the base rounded or heart-shaped, the margin lacking teeth; upper surface dark green, shiny, smooth, the central vein light green; the lower surface paler, smooth; leaves at the end of twigs often in clusters of 3 or 4, the leaf stalk ½–1¼ inches long, exuding a milky sap when broken.

That little plant with serrated leaf edges is what we called "Indian Strawberries" years ago, now better called mock or false strawberry.

I've left a message in The Biosphere but I don't think you will receive a notification because the room has been inactive for so long.


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What species of worm is this? Found in underwear on Ecuador coast

My wife found this worm in her underwear this morning when she woke up.  It wasnt attached to her or anything. About 4-5 inches long. Redish in color and slightly see through, meaning you could sort of see its organs.
We are in Puerto Lopez Ecuador.

Do you think it's possible to be a parasitic worm? if yes it could be an ascaris lumbricoides and in that case I would recommend your wife to go to a doctor because those worms can lead to bad symptoms.

Anyway whatever is the type of worm, I would consult a doctor in any case a parasit goes out of my body.

Oh for sure. We all got on parasite meds immediately.  Definitely a parasite. Was just curious what type :)

See my first comment, the worm seems to be an ascaris lumbricoides but  I am not specialist. It would be better if a specialist in parasitology can confirm or infirm this.


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How does increased resistance to flow decrease blood pressure?
I have recently encountered this question:

Waldenström's macroglobulinemia is a condition which causes increased blood viscosity due to high protein content in the blood. How would Waldenström's macroglobulinemia influence blood flow and pressure?

(A) Blood flow would be increased, blood pressure would increase
(B) Blood flow would be increased, blood pressure would decrease
(C) Blood flow would decrease, blood pressure would decrease
(D) Blood flow would decrease, blood pressure would increase

My immediate thought was to consider the relationship between viscosity and resistance. If the viscosity of the blood increases, the resistance (to flow) should also increase. According to the equation for vascular resistance:
$$R=\frac{\Delta P}{Q}$$
Resistance is directly proportional to blood pressure. This lead me to believe that the increased resistance should lead to an increase in blood pressure. But even without the use of equations, intuitively, I suspect that the heart should work harder (thus raise blood pressure) if there is resistance to blood flow.
However, the answer key indicates that choice (C) is correct, and that the pressure decreases. How is this possible? The explanation given in the key is:

Viscosity is directly proportional to resistance.
Blood flow is inversely proportional to resistance.
Blood pressure is directly proportional to flow.
If you have increase viscosity, you'd have increased resistance, resulting in less flow, and consequently lower pressure.

There is not enough information in the question to solve it.
The answer key from the original question makes a logical error:

Viscosity is directly proportional to resistance.

This is true. An increase in viscosity increases resistance. Flow and pressure do not matter for this statement to be true. You are correct to assume an increase in resistance.

Blood flow is inversely proportional to resistance.

This is true, but it's missing a qualifying statement: blood flow is inversely proportional to resistance for a given pressure drop. You can only assume blood flow decreases when resistance increases if you also assume pressure stays the same. Maybe this is a reasonable assumption, though I'll note it is not one that you seem expected to make since all the answers involve changes in pressure.

Blood pressure is directly proportional to flow

Again, this is true, but is missing an even more important qualifying statement than the previous one. Blood pressure is directly proportional to flow for a given resistance. Importantly, you know this does not apply because you know resistance changed. If resistance is different between Situation A and Situation B, like in your problem, you cannot assume that flow and pressure change in the same direction from A to B.
What you do know is that
$$R=\frac{\Delta P}{Q}$$
holds. You know that R increases. So you know that the flow decreases if the pressure drop is constant, and you know that the pressure drop must increase if the flow is to remain the same. More generally, you can say "there will be a greater ratio of pressure to flow rate". You cannot solve the problem prompted by the question, which asks you to know the direction of flow and pressure change, without additional information about one or the other. The only way you would get a decrease in both flow and pressure is if the drop in flow is proportionately greater than the drop in pressure differential; nothing in the question suggests this is an assumption you should make.
I would rewrite the solution as:

If you have increase viscosity, you'd have increased resistance, resulting in a greater ratio of pressure to flow rate.

You can only make statements about the ratio with the information given.

Perfect explanation!


text:
Are there any barriers to telomere sequencing other than length?
In the comments to an answer on this question, it was noted that long read sequencing methods (e.g., from PacBio or Oxford Nanopore) have largely eliminated repeat-based assembly problems for bacteria. This paper on centromeres suggests that this is nearly the case for those sequences as well.
Telomeres, however, can be much longer, up to 50kb for humans. Read length is thus obviously still a barrier for telomere sequencing, even with the best current technologies.
My question, however, is this: are there any other barriers besides read length? Telomeres also have other modifications, such as their loop structure, and are famously subject to degradation. Do these or other issues also pose barriers to sequencing, or are they readily dealt with in normal protocols?


text:
Are there known genome sequencing issues in E. coli?
Despite the fact that the human genome project was declared "complete" in 2001, there are even now still gaps due to difficult-to-sequence regions of the genome such as telomeres and centromeres. Only last year was the first entirely complete chromosome sequence produced.
Telomeres and centromeres, however, are specific to eukaryotes.  Are there similar challenges with prokaryotes? A recent publication on a gapless E. coli sequence implies that there are indeed typically gaps, but I can't tell whether this indicates any systematic challenges, as with the human genome.
Thus, my question: are there known genome sequencing issues that currently make it difficult to acquire complete genome sequences from common lab strains such as E. coli?

Generally, gaps in genomes occur due to failure of de novo assembly -- the DNA can be sequenced accurately, but cannot subsequently be placed into a contiguous assembly due to alignment ambiguity with adjacent sequences.  In eukaryotes, telomeres and centromeres are difficult to assemble from short reads because they are highly repetitive. In bacteria, repetitive regions of the genome can cause similar problems when assembling from short reads.  Such regions include CRISPR arrays, integrated mobile elements (e.g. transposons), and gene duplications.1,2
So, what made a short-read no-gap assembly of E. coli strain C difficult, specifically? Alignment of the original short-read assembly 3 to the long-read reference 4 with Mauve 5 gives positions and length of gaps.

The first gap in the ordered short-read assembly (left-most red line in the figure) occurs at position 15,085 in the first contig and is 320 bp long. Looking at the same region in the long-read assembly, this closely corresponds to a 236 bp tandem repeat (CTGG × 59) at position 14,848. The authors of the short-read paper used 150 bp paired-end MiSeq reads to create their assembly, which, after adapter trimming, would likely not give enough sequence context flanking the repeat region to span it with a single read, thus creating a gap. This is just one example, and the rest of the gaps could also be repeats or other aforementioned mobile elements.

Treangen TJ, Abraham AL, Touchon M, Rocha EP. Genesis, effects and fates of repeats in prokaryotic genomes. FEMS Microbiol Rev. 2009 May;33(3):539-71.
Ricker N, Qian H, Fulthorpe RR. The limitations of draft assemblies for understanding prokaryotic adaptation and evolution. Genomics. 2012 Sep;100(3):167-75.
https://www.ncbi.nlm.nih.gov/nuccore/MNKV00000000
https://www.ncbi.nlm.nih.gov/nuccore/CP029371
Darling AC, Mau B, Blattner FR, Perna NT. Mauve: multiple alignment of conserved genomic sequence with rearrangements. Genome Res. 2004 Jul;14(7):1394-403.

Does this mean then that long-read sequencing, like with PacBio or Oxford Nanopore, shouldn't expect to run into any gap issues in E. coli and similar?

The key point is that many regions that cause short-read assemblers to fail (causing gaps) can be spanned by long reads. Repeated regions and tandem repeats in bacteria tend to be on the order of hundreds or thousands of bp long, and can therefore be captured by single long reads, which can be >10k bp for Nanopore and >100k bp for PacBio.

Thank you, this is very clear @acvill. Out of curiosity, are the eukaryotic repeats much longer and thus harder to deal with, or are those readily addressed by recent sequencing technology as well?

I know less about eukaryotic repeats, but the background of this paper seems to be a good resource: https://genomebiology.biomedcentral.com/articles/10.1186/gb-2013-14-1-r10.  If you have more questions, I'd encourage you to make a new post.

Summary
The publication of the first complete DNA sequence of Escherichia coli was for strain K-12 substr. MG1655 in 1997. Because of historical limitations in the technology used (rather than problems with repeat sequences or instability in the genome) this contained mistakes, which were subsequently corrected as the sequencing technology improved. An international consortium reported on this (and revisions in gene annotation) in a paper in 2006. Because of the extensive use of E. coli in biological research in the 20th century, many different strains have been used for different purposes and many sequences have been reported. The strain referred to in the question is strain C, which has only just been completely sequenced (or its sequence only just reported), presumably because nobody had the need to do so previously.
Technological context
The Wikipedia entry on DNA Sequencing contains the graphic reproduced below, showing the decline in the cost of sequencing between 2001 and 2019.

[Based on data from the National Human Genome Research Institute]
This decline in cost was the result of both improvement in methodology and automation, and also reflects the speed with which sequences can be obtained and hence the ease of repeating them. The E. coli DNA sequence published in 1997, and was only the seventh complete genome to be reported. The following extracts from the section of the paper on sequencing strategy gives an idea of the the various methodologies employed and problems encountered:

Sequencing was carried out in sections, with steadily improving technical approaches. The M13 Janus shotgun strategy proved to be the most efficient strategy for data collection and closure… The first 1.92 Mb… was sequenced from our overlapping set of 15- to 20-kb MG1655 lambda clones by means of radioactive chemistry and was deposited in GenBank between 1992 and 1995. Subsequently, we switched to dye-terminator fluorescence sequencing (Applied Biosystems). In addition to greater speed and lower cost, this new technology avoided electrophoretic compression artifacts, which, owing to its 50.8% GC content, occur in practically every gene of E. coli…The final stages entailed special attention to problem areas. The region between positions 0 and 22,551 did not yield a suitable I–Sce I fragment, so three lambda clones were selected to finally complete the genome. One of them was found to contain a deletion and had to be finished by shotgun sequencing of a long-range polymerase chain reaction (PCR) fragment.

Note in particular that newer, more accurate, sequences were combined with individual genes previously sequenced, and the reference to compression artefacts — the bugbear of separation of fragments by polyacrylamide gel electrophoresis. Not mentioned is the mistakes that can be made using the Maxam–Gilbert (chemical) method if one is not aware of the effect of methylation.
It is not surprising that there were mistakes in this sequence (and, indeed, in many much shorter sequences, often published in a hurry to obtain priority.)
Tracing the history of the K12 sequence
I think it worth explaining how I found out about the subsequent changes in the sequence, as the general approach may be useful to those that are not aware of it.
I started by locating the original paper by a simple Internet search. From this I obtained the accession number (an ID) of its deposition at GenBank — AE000137 — and searched for this on the NCBI website and found that it had been replaced by another entry, U00096. In the header of the entry, after the summary information regarding the organism and sequence, there is a reference section of the type:
REFERENCE   1  (bases 1 to 4641652)
  AUTHORS   Blattner,F.R., Plunkett,G. III, Bloch,C.A., Perna,N.T., Burland,V.,
            Riley,M., Collado-Vides,J., Glasner,J.D., Rode,C.K., Mayhew,G.F.,
            Gregor,J., Davis,N.W., Kirkpatrick,H.A., Goeden,M.A., Rose,D.J.,
            Mau,B. and Shao,Y.
  TITLE     The complete genome sequence of Escherichia coli K-12
  JOURNAL   Science 277 (5331), 1453-1462 (1997)
   PUBMED   9278503
REFERENCE   2  (bases 1 to 4641652)
  AUTHORS   Hayashi,K., Morooka,N., Yamamoto,Y., Fujita,K., Isono,K., Choi,S.,
            Ohtsubo,E., Baba,T., Wanner,B.L., Mori,H. and Horiuchi,T.
  TITLE     Highly accurate genome sequences of Escherichia coli K-12 strains
            MG1655 and W3110
  JOURNAL   Mol. Syst. Biol. 2, 2006 (2006)
   PUBMED   16738553
REFERENCE   3  (bases 1 to 4641652)
  AUTHORS   Riley,M., Abe,T., Arnaud,M.B., Berlyn,M.K., Blattner,F.R.,
            Chaudhuri,R.R., Glasner,J.D., Horiuchi,T., Keseler,I.M., Kosuge,T.,
            Mori,H., Perna,N.T., Plunkett,G. III, Rudd,K.E., Serres,M.H.,
            Thomas,G.H., Thomson,N.R., Wishart,D. and Wanner,B.L.
  TITLE     Escherichia coli K-12: a cooperatively developed annotation
            snapshot--2005
  JOURNAL   Nucleic Acids Res. 34 (1), 1-9 (2006)
   PUBMED   16397293
  REMARK    Publication Status: Online-Only

These three are journal references: there are 15 others which are just direct submissions to GenBank, most by Blattner’s group. Some of the earlier ones are marked as corrections. The later ones I assume are mainly concerned with the annotation of genes rather than the sequence itself. The latest date is 2014.
The authors of the 2006 Nucleic Acid Research paper write:

“Corrections to the original MG1655 genome are at 243 sites (totaling 358 nt), a correction rate 8 years later of ~7 in 105.”

They also make clear the problems of differences in what purport to be the same strains, which have mutated over the years through passaging and transfer to different labs (despite, no doubt, the best efforts to control this).
Reporting bacterial sequences today
Even in 2006 it required some effort to collaborate and correct a bacterial sequence, whereas today (2021) it would appear trivial to resequence any strain of interest. Thousands of E. coli sequences must have been determined. It may be of practical importance to workers using different bacterial strains to know when they have been sequenced, but it is now impossible to publish such in a standard scientific journal. It appears that the American Society for Microbiology has addressed that problem in a section of their journal (Microbiology) entitled “Resource Announcements”, which are little more than announcements of the deposition of a particular sequence. This would be the case for E. coli, strain C, which provoked this question.

I'm afraid that, while this is a nice summary of historical challenges, it doesn't really address the current state of play.

With all due respect, your question was about whether there were general problems sequencing E. coli and why a recent report made a point of the fact that the sequence was ungapped. I don't see anything about the current "state of play" in the question. It seemed necessary to explain why that the gaps in E. coli sequences were due to deficiencies in the technology when they performed, rather than structural problems, as in telomeres. And rather than just telling you this, I explained how to find this out for yourself, as your question seemed to indicate an ignorance of sequencing history.

Apologies; I thought that was clear from my discussion of systematic challenges and the nature of the organism, as opposed to technological challenges. I've added the word "current" to make it explicit.

@jakebeal Whatever. I try to make answers generally useful, rather than merely to the poster. I think this one is, as ignorance of the development of science and how to use GenBank entries is widespread.


text:
Confusion about how to compute probabilities for linked genes
I am confused about how to compute probabilities for linked genes.
The problem that I am solving is this:

P generation: AAbbddEEff X aaBBDDeeFF. If A and B are 40 centimorgan apart, what is the probabilty to get aabbddeeff in F2?

Here is what I have:

F1 is: AaBbDdEeFf.
The next cross it goes through is this: AaBbDdEeFf X AaBbDdEeFf.
To compute this cross, I drew the 2 chromosomes for AaBb (in coupling), and then the probability for a is 0.5 (A or a) and the possibility for no recombination is 0.6. So 0.5 x 0.6 = 0.3. The same goes for b, so aabb is: 0.3 x 0.3 = 0.09.
For ddeeff: 0.25x0.25x0.25 = 0.015625.
Multiplying these gives 0.09 x 0.015625 = 0.00140625.
Extending that and for 2 gametes gives this: (0.00140625)^2 = 0.00197x10^-3.

But the correct answer is not what I have computed, but instead is 0.000625.
I'm really confused with this question. If we know that only 2 of the 5 genes are linked, is it still correct to multiply: 0.09 x 0.015625 = 0.00140625?  Maybe I should use a Punnett square somehow? Because in that case, the probability for a recessive homozygous is 0.0625 but I'm not sure it fits to this question.

0.000625 looks right to me.  On one chromosome, you have a 50% chance of a.  Then you have a 40% chance of b (if and only if a crossover occurs).  These multiply out to 20%.  You multiply that by 50% for three unlinked genes to get 2.5% abdef.
Your approach was correct overall, but you used a 60% chance of b, so your final answer was too high by (60%/40%)^2.  Don't let capital and small letters trick you - ab comes from a recombined chromosome.

Thank you. Just to clarify, when you say: "ab comes from a recombined chromosome", it's only in the case that the alleles are in 'repulsion'?
And for the unlinked genes I used 25% because I thought I need to use Punnett square (for example, if we want dd from Dd x Dd the chance is 25%). But the correct way is to say "50% chance of d/e/f", because I need to consider the chromosomes? @Mike Serfas

Repulsion is a sort of old-fashioned way to put it.  Just think that A and b are physically linked by a strand of DNA inherited from one parent, as are a and B.  The odds that these strands will be cut and spliced to make ab and AB is 40%.  For the unlinked genes your math was accurate - I multiplied by 50% chance of d, e, and f, then multiplied the 2.5% chance of abdef by itself, while you multiplied by 25% chance of dd, ee, and ff one at a time, but it works out the same.


text:
How can monkeys be ancestors to people when they are herbivores?
How monkeys can be ancestors to people when monkeys are herbivores but humans are omnivorous?
Maybe it is monkeys that evolved to become omnivorous gradually?
How does the generally accepted theory of human origins explain it?

Do you have a reference for monkeys being herbivores?

The first hit on Google's "similar questions" seems to refute that claim pretty solidly.  Also, humans and apes share the most recent common ancestors, the closest being chimps

The following information the first thing to face on websites about human evolution. For examples, with similar quotes:

"These and other anatomical features suggest that the early monkeys were becoming mostly diurnal fruit and seed eating forest tree-dwellers." (refer to link)
"Herbivores include gorillas, cows, horses, elephants, rhinos and giraffes". (refer to link)

Welcome to Biology.SE! You would probably get a more positive response to this question if you: 1) focused on a single clear question (e.g.s: the grammar of your title is so scrambled that it isn't even clear if it is intended as question, you have at least two questions in the body which need to be separated), and 2) state clearly in the body of the question (comments are ephemeral) what sources you are using and summarize what you think you have learned from them. ——— Please consult the [tour] and [help] pages starting with [Ask] questions effectively on this site for details. Thanks!

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

I also encourage you to check out some of the online resources available for learning more about evolution. For example, this a useful introduction to evolutionary theory from UC Berkeley.
——— Finally, many "herbivores" will eat other animals if given a chance — for example deer will eat eggs and chicks from birds nests — this illustrates that the premise of your first question is faulty.

Ok, so there are several erroneous assumptions here:

Monkeys are not the ancestors of humans. Both humans AND monkeys share a common ancestor: an animal species that was neither monkey nor human.
The evolution of diet specialization is one of the most common phenomena in evolutionary biology. It is totally plausible for a species to evolve an omnivorous diet from a vegetarian one, and vice-versa. So you cannot use diet-specialization as a way of inferring the ancestry of a group of species (there may be some inferences done with diet-specialization and phylogenetic evolution but it is usually to re-confirm other types of data).

So, to sum-up, monkeys ARE NOT the ancestors of humans. Both monkeys and humans have a common ancestor, an animal that could have been herbivore or omnivore.

Also we do have our own veggies.


text:
Enzyme inhibitor leads to higher turnover rate?
I'm currently working on a project where I have to deal with enzyme inhibition.
The purified enzyme shows a good substrate turnover. When I try to inhibit it with different inhibitors described in literature, however, I receive quite awkward results.
I have now tested 3 different inhibitor compounds. One showed good results (it reduced the substrate turnover), while the other two compounds instead led to increased substrate turnover?!
I know it sounds ridiculous, but has someone experienced something like this before? The measurements of the "working" and "not working" compounds take place on the same plate.
How can it be that widely described inhibitors lead to such results?

This is very vague (purity of the enzyme, etc.) You might be messing wit the rate limiting step somehow. But my question is, why aren't you asking someone senior in the lab? Is this a homework question?

Adding on to anongoodnurse, you say the rates change but...by how much? What's the variance in your measurements? How many replications? How are replications performed? In what order did you do the experiments and how were the reagents handled during the process? What other conditions are you maintaining constant?

What do you mean by a “Signal increase”? This is not a term I have ever encountered in enzymology. Please reword your question using standard enzymological terms. Running your question through an English language spelling checker is also recommended. Modern software and operating systems make this easy. I routinely do checks in French, German and Italian.

@David The language was a bit rough, but I found the meaning pretty clear, as well as the starting points for debugging. I have now cleaned it up and hope others will retract their close votes.

@jakebeal I am afraid this question is still completely unclear, and until the poster uses the precise scientific terminology to describe what he observes — together with detail on the so-called "inhibitor compounds" the question cannot be answered. Nor does it deserve to be as the poster has not responded to this basic request to use enzymological terms, leaving one to wonder whether he understands the basics of enzyme measurement and quantitation. The term "substrate turnover" typifies this problem. I spell this out in my next comment.

One measures "the rate of enzyme reactions", which when expressed in standard terms (e.g. nmol substrate converted per min) is referred to as activity. To convert this to meaningful information for enzyme or effector (inhibitor or activator) one determines activity over a range of substrate concentrations to calculate the Km and Vmax (from which the  turnover number can be determined for pure enzymes). The type of inhibition can be deduced from the effect on these parameters and the kinetics (MM, allosteric etc.). You need this information to make sense of your results.

@user338907 — If your remark was directed at me, my point was that there are standard methods of studying and assaying enzymes and the effects of inhibitors and the poster should describe which if any he has used. I imagine he has done none of these, so nit picking my comment is unhelpful. I would make an observation about the terminology remaining in the edited question — "substrate turnover". In general turnover implies that something is used and then replenished, as in protein turnover. Turnover number relates to the active site cycling between occupancies. Substrate does not turn over.

While it's difficult to know just what is going wrong in somebody else's laboratory, apparently paradoxical effects like these are unfortunately common in laboratory work.  Assuming that these are indeed well-established inhibitors that really should be working, let's consider why they might not be in your hands.
The mechanisms of molecular interaction are complex enough that there are many cases where a substance that acts as an activator in one condition can act as an inhibitor in another condition. Another way that you could see such an effect is if your purified system is not actually as good as you think and the problem is being partially relieved by one of the inhibitors, e.g., imperfectly purified and addition of the inhibitor neutralizes some of the imperfections.
Not knowing the details of the compounds you are working with, it is not possible to guess which of the possibilities might be at work. I would suggest, however, that you begin by:

Comparing your quantitative turnover rate with the purified enzyme to the predicted rate from the literature to see if your baseline system is actually working correctly.
Make sure your system is also (not) processing substrate at the appropriate low rate when the enzyme is absent.
Checking for potential differences between your method and the method that you are trying to adapt from the literature, which might give clues to the condition differences that may be impacting your results.

@user338907 Indeed: so many assays go wrong because there isn't sufficient use of process controls or because somebody only checked controls for the qualitative and not quantitative behavior. Your comment reminded me that the OP also didn't mention a negative process control, so I've added that as well, which would detect something like the case you mention.

There's also the factor of error - OP didn't mention the statistics they did on the data they generated, but it is highly likely that the curves are within "no significant difference" of each-other.


text:
Why do predatory mites have to be introduced multiple times?
I'm combating spider mite infestation using either Phytoseiulus persimilis or Amblyseius californicus. After extensive study of the literature, I'm still unsure why the producers of these predatory mites suggest that they have to be introduced several times (2-3 times depending on manufacturer). I know that adult predatory mites are very agile and scout for new prey. Phytoseiulus is also known to wipe out spider mite populations. So as long as spider mites are present, why should one introduce them at intervals rather than just introduce a large number of predatory mites at the beginning?

You are right that ideally it should be enough to apply them once, but predatory mites seem to be quite sensitive: If it gets too cold or too hot or the moisture is too low, they might die.
I applied several rounds of predatory mites in non-optimal conditions without any success. They just kept disappearing without any effect whatsoever. Funnily, some small type of Heteroptera came to save my plants. (from nature without my doing)
Next time I would try some Chryson instead.

Thanks for the input. This paper (https://www.eje.cz/pdfs/eje/1993/01/02.pdf)  suggests that P. persimilis can even survive temperatures below zero for brief periods of time. I think the problem is that it takes to long for the beneficials to arrive, because they are produced in the Netherlands and shipped to the distributor so it can take up two 2 weeks for the benefials to reach the target destination. Also a big producer (entocare) lists the shelf-life of 1 day.

OK, I see. From a non-biological and rather economical standpoint, it's always advantageous for companies to recommend triple use: They make more profit, there is a higher chance of success due to the duration of time alone, and it shuts down customer complaints, if it doesn't work the first attempt.


text:
Has autogamy been observed in any animals?
By my understanding, autogamy, i.e., reproduction that is sexual, but with both gametes contributed by the same individual, is not at all uncommon in the plant kingdom.
Does this also occur anywhere in the animal kingdom?

@kmm I appreciate the help! But your revision greatly changed the meaning of my question, including cases I wanted to exclude and vice versa.

Then I suppose I don't really understand your question. What do you mean "animals that have sex with themselves?"

@kmm is it not adequately elaborated on, explained, in the text body? If not I think the text is what may need further sharpening up!

Yes, there are some animals which are known to self-fertilize (although generally not exclusively).  For instance, among invertebrates some nematodes are known to use self fertilization, as discussed in this paper about its evolution.  Among vertebrates, it seems to be very rare, apparently known only only in a single genus of fish.

It sounds like you're referring to self-pollination. This is a specific subset of the larger category autogamy, in which two gametes from the same individual fuse.
It looks like this has been documented most completely in starving Paramecium, although Britannica seems to think it is common in invertebrates as well (without a source).
One source thinks that plants are the most successful example of autogamy because the development of several pollen tubes simultaneously allows the plant to carefully choose the fertilizing source, enabling it to select for genetic material that can mask the deleterious recessive alleles.

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


text:
What is the difference between non-coding and intergenic regions?
The initial question was about understanding what is in the downstream of a gene in a eukaryotic organism. I understand that this region is located 3' of a gene, and therefore I would expect to find non-coding regions, but is there a difference between non-coding regions and an intergenic region?
A small background of what I am doing: I am studying the effect of retrotransposons in S. cerevisiae populations, and I already identified the potential impacts of these retrotransposons and these were the consequences:
Upstream gene variant   49
Downstream gene variant 42
Intergenic variant  4
Transcript ablation 3
Coding sequence variant 1
Feature elongation  1
3' UTR variant  1

So is it clever to say that downstream of a gene there are non-coding genes?

There may be non-coding regions (introns) within a single gene.

But up/downstream of a gene should not consider the introns as these are happening within the gene.

"Intergenic" is, well, an embarrassment, though it can be hard to avoid.  Intergenic means, literally, between genes.  Genes are, as you'd expect, genetically defined as regions of the chromosome with some genetic role.  Between genes, we have, well, junk, spam, without meaning or significance, since otherwise, it would be a gene.  In the 1990s everybody knew most of the genome was "junk DNA" and it was pretty straightforward.  And the central dogma was DNA makes mRNA makes protein and if there was no mRNA making protein, or even no long protein, then they assumed there was no gene.
Well, the problem with using these terms nowadays is, first, it is very hard to show any given piece of DNA never has a role.  After all, you can often remove a whole gene without visible effect on an organism, so how can some noncoding sequence 'between genes' be proved conclusively to be meaningless and of no relevance to either of its neighbors?  And second, DNA definitely does have a role even if all it does is produce non-coding RNA, or act as a regulatory sequence that does.  So for example, on OMIM you can look up many records for "intergenic", with results like H19, for which one term is "LONG INTERGENIC NONCODING RNA H19".  Note also H19 is listed as the HGNC approved gene symbol, so it is an intergenic gene.  Tricky, eh?  (I have great respect for OMIM - this isn't their fault)  Also, enhancers can be quite a long way from a gene, even past the end of another gene or affecting multiple genes, so even though a mutation in the enhancer might genetically act as an allele of a specific gene, it might be described in sequence terms as located in an intergenic region.
Bottom line: the intergenic regions you're reading about are going to be between things that are recognized as genes, and may or may not be known to have some effect on one or the other (or both...).  They won't contain CDS, which is always considered to be a gene, nor 5'UTR or 3'UTR because those are transcribed before or after a CDS.  Past that, how they are being distinguished from "upstream sequence" and "downstream sequence", that could be completely arbitrary.  They might have gone to WormBase and pulled out curated gene records, and added some number of base pairs before the start site as promoter - but I don't know that.  You'll just have to try to find the particular reference for whatever tool you are using.

An intergenic region is just one of many types of non-coding sequence.
Others include:

promoters
regulatory binding sites
terminators
introns
aptamers
ribosome entry sites

There's a lot of stuff that's part of genes besides the protein coding sequence.
A good way to get a picture of the sorts of things there are besides coding regions is to browse the Sequence Ontology.  If you browse to coding sequence and start browsing parent and cousin terms, you'll find a vast number including all of the things that I mentioned above, as well as intergenic region, with definitions associated with ear.

correct me if I'm wrong but poly-A sequences are not coded into the DNA, they are the result of RNA processing

You're right; the poly-A attachment site gets marked, but it's a junction and not a region; I've dropped it from the list.


text:
How do microbes spread from a small place to a very large place?
Bacteria are very small, so they cannot move very far on their own. Viruses cannot move themselves at all. So how does a specific type of bacteria or virus spread from a small place to a very large area (such as the whole Earth)?

Studies of the human microbiome suggest that gut and skin bacteria strains are localized to regions not larger than 1000 km so transport in general is limited. Look at works about ocean microbiology and aerobiology for transport through water and air. If you travel around the world and defecate, then your gut bacteria are extremely lucky.

The answer by @SMcGrew is essentially correct, but let me add a technical term (at least in the context of infectious diseases): the bacteria and viruses a carried by vectors. Since word vector is a kind of overused, even if we limit ourselves to biology, it is also common to be more specific and call the disease vectors.
Vectors are classified into biological vectors and mechanical vectors, depending on whether they biologically interact with the microbe (i.e., they get infected) or whether they are simply carried from one place to another.

Birds migrate for thousands of miles, carrying diseases on a time scale of months or less.  With climate shifts, insects and animals shift their ranges on a time scale of hundreds of years or more.  Bacterial spores like anthrax can be in a form that is easily blown around the whole Earth, ready to thrive wherever they touch down. Plant diseases travel with their plant hosts, and over time scales of thousands of years the plants - e.g., dandelions and conifers - can spread thousands of miles of latitude and longitude.

Or for a more topical example, the COVID-19 virus travels mostly by airplane and cruise ship.

@jamessqf technically the vast majority of its "trips" are over distances of <2m, but yes - most long-distance introductions occur via rapid international travel. :)


text:
Is human skull size related to brain size?
Me and my dad have a disagreement about this. He thinks that if a person had a larger skull they would naturally have a larger brain. I think that he is assuming the evolutionary trend holds on an individual scale and that it is odd to assume that they would be correlated.
We are having a hard time finding information on the topic as everything is about skull or brain size when related to intelligence. Sorry if this is not the right place to ask this, please direct me to the right place if I have misjudged.
Who is right?

It is worth adding that larger brain does not necessarily makes one smarter.

It seems that there is a correlation between the two: https://pubmed.ncbi.nlm.nih.gov/20229240/

Are you asking about human skulls?

yes I am. Is there a separate human related biology stack exchange to ask?

This paper doesn't directly answer your question, but does say that skull size is related to brain volume

Have a look: https://en.wikipedia.org/wiki/Brain_size

Probably yes. There are reasons why this is not always the case. For example, a mutation can lead a person to have a thicker skull; a genetic disease causing a large skull unnecessarily, etc.

As a disclaimer, first please remember that brain size is only partially related to intelligence, and that whenever this comes up with regards to humans you should remember the long and ongoing history of badly-justified racism on the topic. So let's ignore intelligence, and just focus on brains and skulls.
If a person has a bigger skull, then they have a bigger volume inside that skull (neglecting the question of thickness). There's not really much inside the skull besides the brain (average volume ~1350 $cm^3$) and the cerebrospinal fluid (average volume ~125 $cm^3$). There's quite a bit of difference in size between skulls (men's brains are on average ~200 $cm^3$ bigger than women's brains, and individual variation large as well). Folks with big heads don't have their brains sloshing around in massive amounts of cerebrospinal fluid (and it would be quite dangerous if they did!): that space is filled with brain.
Bottom line: in humans, a bigger skull generally means a bigger brain.


text:
Is there a scale suitable for continuous tracking and recording of plant weight?
I want to measure water transpiration and evaporation in a bonsai tree, and measuring the weight of the tree in its pot is my proxy for water usage.  This has worked well with manual measurements, but I want to go to the next level.
I would like to monitor the weight of something continuously (e.g. once a minute) and access the data easily via a phone app.  Is there something like that?
There are numerous options for similar devices if you want to measure ambient temperature and humidity (e.g. https://www.amazon.com/SensorPush-Wireless-Thermometer-Hygrometer-Android/dp/B01AEQ9X9I).
But all my searching for balances with similar functionality have failed.  I've found many lab balances and kitchen scales, and body weight scales.  Only the body weight scales interact with apps on your phone, but they do not record continuously.
If you know of one, or just have better google-fu than me and can suggest a more precise search term, any pointers would be appreciated.

I'm afraid this has absoultely nothing to do with biology... please take the [tour] and check out the [help] for details on what is on-topic here.  Thanks!

I’m also voting to close this question as it isn't about a biological mechanism or process.

Fair enough.  Moderators, feel free to delete, too.  I didn't because there is a penalty for deleting an answered question.

In my defense, I thought the application, trying to measure plant water use, was biology related, and this seems like a community that might use similar equipment to what I am looking for.  But if you think it is off-topic, I don't object.

maybe this company  https://www.industrial-needs.com/scales-and-balances/recording-scales.htm

Our scale software allows a real-time measurement on a computer and
depending on the weighing data, they can also be saved with a date
stamp as a TXT file on the computer


text:
Why are people not given every possible vaccine?
Vaccines for some diseases, like cholera, are not given in Australia because of how rare they are. Nonetheless, I don't see the harm in giving a cholera vaccine to every child like we do got Hepatitis B. If there's no harm, why not just give children vaccination against every single disease we can? Just for safety's sake. What if a child happened to get cholera whilst playing in a bin and caused an outbreak?
Is the reason why this is not done just because of cost?

Vaccines cost money, and can have side effects.

Lots of in depth info here, starting from the third result down: https://www.google.com/search?q=pros+and+cons+of+vaccine+programs&oq=pros+and+cons+of+vaccine+programs&aqs=chrome..69i57j33i10i160.5147j1j4&sourceid=chrome&ie=UTF-8

Every public health decision is a cost-benefit decision involving at least two considerations:

Will the positive benefits of this intervention outweigh the potential harms?
Will the money spent on this intervention produce more benefit if spent on a different intervention?

Some vaccines, like the measles vaccine, are extremely safe and long-lasting, so it makes sense to give them universally. Others are less effective, less safe, or last for a shorter time, and so it just isn't worth it to give it to people who aren't likely to be exposed to the disease.
In the particular case of the cholera vaccine, it appears that it rapidly decreases in efficacy, even over the course of a single year. Mass inoculation of a population unlikely to encounter cholera before the vaccine becomes ineffective thus is not a particularly good use of resources.


text:
Designing primers with restriction sites
I want to design a forward and reverse primer that include overhangs with restriction sites, with the dna used for restriction enzyme cloning.
If I want to send my dna to a synthesis company should I include the attached overhang with the restriction sites to the dna? Does it matter if the primers have the overhang of the dna within their sequence ?
From the sequence right at the end what bp sequence would be recommended I use for my primers if I want approx. 20-25bp for the primer?
See below for cDNA sequence:
Nde1 cut site: 5' ... CA|TATG ... '3'
Xho1 cut site: 3'...GAGCT|C...5'
cDNA with overhangs that have restriction sites, Ndel1 (5'->3') and Xho1 (3'->5')
5' catatg - ATGGGTTCAAACACTTCCAAAGTGGGTGCTGGTGCAGAAAAACAACAAGTCTATACTCCG
CTAACACAGATCGATTTTTCACAGTCTTTGGTTTCTCAATTGGATTCATCGAAGGAATCA
GACTATGTCACCAAGCAAAATGCAGAAAAGTTCATTGAGAAGAAGGTTTCACAAAGGCTA
TCTAACCTAGAAGTTGAAACGTTAAAGAAGTTTGAAGATACTTTGAACAATTCACTATTA
TCAGACGACGACAAGGATGCCGTTGATGGAATATCATCAAGTTCATTGAATAATCAAATC
GAGTCGTTGAACAAGAAACTAACATTATTTGATCAATTAGAGTTACAAAAGTTGGAGAAA
TATGGGGGTGCCAAAGGTAAATCTGATAAAAAAACCGACAACGGCAGCATTTCTATAAAG
GCAAAATTGACTGAGTGTCTTTTGGCCAATAAGGGCAAGCCATTGAATTGTTACGAAGAG
ATGGAAGAATTCAAGAAGCTCGTTATGGGTTGA - gagctc 3'

I've added an answer, but I don't fully understand what you mean when you say: >"From the sequence right at the end what bp sequence would be recommended I use for my primers if I want approx. 20-25bp for the primer?"
Are you asking us what sequence you should use for the reverse primer?

Yes I was just wanting to get an idea for the primer sequence, or essentially if I could just start (i.e including entire overhang) the primer right at the start of the overhang

Your priming sequence should be the reverse complement of the last ~20bp of the coding sequence. Add the restriction site at the 5' end of this, then your overhang after that. All in all your primer will be 20+6+3= 29 bp

Yes.
If you intend to subclone the fragment via classical restriction enzyme cloning you need the overhang.
Different restriction enzymes require different lengths of overhang to allow them to sit fully on the strand and then cleave the sequence.
NEB has a great page detailing how many bases are needed for the enzymes they sell:
https://www.neb.com/tools-and-resources/usage-guidelines/cleavage-close-to-the-end-of-dna-fragments

No, it doesnt matter if the overhang appears elsewhere in the DNA, just so long as your restriction sites don't (obviously).
Here are some considerations I use when designing primers for PCR (though not wholly applicable if you're just having it synthesised):

Use the 3+ basepairs present the given number of nucleotides in your restriction site away in the sequence you're PCRing from as your overhang sequence to allow a few more bases to bind. I.e
With the following primer:
Overhang - Restriction Site - Priming sequence
AAA-GGATCC-ATGACATGCAGTAGC     PRIMER
|||        |||||||||||||||
TTT--------TACTGTACGTCATCG     TARGET SEQUENCE
Alternatively, I use those 3 or so basepairs to add or remove GC content and manipulate the Tm if the annealing temperatures of the 2 primers aren't ideally matches

Thanks that makes sense, but if the restriction enzymes I am using cut the overhangs they are also going to leave a few base pairs upstream and downstream of the actual gene, will this cause framing issues or doesn't it matter where the GOI is inserted in a plasmid MCS?

To fix framing you should / could add bases in between the restriction site and the fragment of interest. But as your NdeI ATG is in frame with the start-ATG I don't expect any problems. You could even remove one of those ATGs if you want.

Ok so should I delete TATG from 5' ... CA|TATG ... '3' (Nde1) and C from 3'...GAGCT|C...5' (Xho1)? If I add bases wont that just create blunt ends?

The only concern I have is the space the leftover base pairs creates upstream, not really sure if this will affect translation

The overhang will disappear when you digest with the restriction enzymes. the only sequence that will persist is the restriction sites that allow seamless incorporation in to your vector.
The extra bases of the restriction sites can't be translated as they will be before your start codon, and after the stop codon.
If this doesn't make sense to you I'd suggest reading up on the basics of cloning in Sambrook et al or another good textbook.

The bases will make a difference if you want to clone something in-frame with a tag / fusion protein or something like that. Also changing the space between the RBS and the start codon might alter expression a bit.

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


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'Terminal' and 'lateral' apical buds. Monopodial and sympodial branching
Macroscopically, it seems to me that the difference between 'lateral' apical buds and 'terminal' apical buds and monopodial and sympodial branching is often rather superficial, if not random. Therefore I'm suprised that such things are sometimes used in identification keys (since in some shrubs and trees, there are no apical buds at all). Does anyone know if in Biology, there is an objective definition of those phenomena, e.g. based on inner workings of a plant or microscopy?


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How did our bodies decide on the right enzymes and where did we get them?
I have read that enzymes act as catalysts to reactions in our bodies and that they are extremely target-specific.
My question is how did our body know that a particular enzyme could act as a catalyst for a particular reaction? How did de we get the perfect combination of reactants and their catalysts?
Note:- I am not a person who is studying biology so I might not know that which is pretty obvious to you people.
Anyways, the least expected answer is that ancient aliens carried out some sort of Worldwide Enzyme Injection Programme ;-)
Edit:- By the knowledge gained after asking this question I've figured out that it might be something like this -
There were species which had a different set of enzymes than us but as these weren't the right match the species perished. Those who had the right enzymes survived. Am I right ?

The problem here is that you've reversed cause and effect.  The body doesn't "decide" to create a new enzyme for some purpose.  Instead, various slightly (or sometimes, but not very often, drastically) modified enzymes happen to be produced by genetic rearrangements.  If those new enzymes happen to do something useful, they're probably conserved in following generations.  Remember that "our body" is the product of a billion or so years of evolution, and that variations on those enzymes are shared by all life.

@jamesqf Do you mean all the catalysts were tried one by one ,by nature, and then the right ones were fixed by evolution ? I had thought of this answer before asking, but the sheer time it would take made me ignore this one. Anyways, I think with references and all you should make this into an answer.

Raghav: Not one by one, but in a very massively parallel process, with each living creature potentially getting to try out slightly different versions, and only the survivors getting to reproduce.

Please check this site out. You seem to have some misconceptions about evolution.

I can understand why your asked this sort of question so I will clear your doubts one by one.
First of all Enzymes are not scattered inside our body, every enzyme is localised in a particular orgenelle or compartment of protoplasm in the cell, where they play their specific role.
Such as the enzymes of glycolysis ( the process by which you create ATP and breakdown glucose to pyruvate) are present in cytoplasm where as the enzymes for TCA ( Oxidative-decarboxylation of AcetylCoA) are present in mitochondria.
Enzymes are very specific.(1) If you have heard of lock and key hypothesis which states that an enzyme binds to the substrate that is complementary to its active site. Enzymes have very high specificity for their substrates the active site where reactions happen are somewhat complementary to the Enzyme substrate complex and thereby it provides the binding energy that lower downs the activation energy of that particular reactions that enzyme is going to catalyse.
I hope that helps!
References: (1) please refer to lehninger principles of biochemistry for further information!

Hi welcome to Biology.StackExchange! Please provide citations to support your claims. We expect and encourage citations or other references to ensure accuracy of responses. "Answers" without citations/references are better off as comments. Thanks!

Hi I am somewhat new to this forum so I just posted an answer without giving any references but thanks will keep in mind for next time!


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Book recommendation to know and understand the brain and the phenomena and processes related to it
I need a book recommendation or, more properly, any source recommendation to know and understand more about the phenomena related to the brain, as far as we know how the brain works. I'm interested in the very structure the brain has and how it leads to what we experience. Due to the way biological processes happen, how the things we define for ourselves are related to each other. It would be cool if it adds more to the biophysics of those processes and the possible picture of their evolution, as well as the physical characteristics of those biological structures.

I have been away from stackexchange for long if the question is not according to the site's guidelines please edit it or if you can make the question better please do it (I know I wasn't that good at it). I didn't find any other question or answer helping so I asked it, if there's any question or answer already that can help please add it into comments.

Your question would be a better fit on CognitiveSciences.SE. In fact your question is possibly a duplicate of this post.

I'd agree with @Remi.b to check CogSci - the recommendations in the linked question will probably get most of what you want, but your question touches on a lot of areas that probably won't all be found in detail in the same book; you will probably find more on biophysics in a more basic neuroscience textbook like this question; I'd expect more coverage of evolution of behavior in an Animal Behavior textbook.

My other advice is that I'd recommend staying away from "evolutionary psychology" because that field is tainted with a lot of pseudoscience and disguised speculation, and it will be difficult to evaluate the claims critically without a lot of background knowledge.

@Remi.b the books suggested into the answers to that question possibly aren't answering the questions i do have, neither there's much of discussion about the books in the answer. I checked on CogSci.SE few simillar questions were there but the recommended books weren't really getting around what i want as I have mentioned in the question, and few were bit perspective based.

@BryanKrause Yeah what I want I might not get in the single book , It's not necessary for it to be a single book but the ones which are really good getting around the questions. Ok I will remember your advice. And the question you mentioned helped. I found recommendation of those same books before coming to SE,they seem to be bit expensive purchase but yeah they seem going with the subject. It will be helpful if somebody can recommend some similar books not that long and expensive but as cool as them. If you think I will get better answers to the question on CogSci can my question be migrated?

Probably the best options for general knowledge are going to be textbooks, which unfortunately are going to be expensive. However, there are also lots of used textbooks, so you might be able to find a used, older edition of the books that people recommend that is much more affordable. There are some more affordable books in the pop-science category, but those can be problematic; Steven Pinker for example is an entertaining writer, but his books are meant to be persuasive: he won't give you an unbiased perspective of the literature (and one of the reasons I warned about evolutionary psychology)


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why is LPL (lipoprotein-lipase) down-regulated during fasting?
During fasting our body needs additional sources of energy and that's why triglycerides are broken down into fatty acids and glycerol. where fatty acids can be used to generate acetyl-coA and contribute to the citric acid cycle or build ketone bodies.
So if we are wishing to get more fatty acids why is LPL down-regulated although it's the enzyme needed to break down Triglycerides in lipoproteins?

Please provide a reference or link to your assertion that LPL is down-regulated. See "how do I ask a good question" in the Help. In particular it is imperative to state what tissue(s) you are referring to.

An edit was requested, and I have updated the answer below. Let me know if there is any confusion.

LPL is largely expressed on tissues that metabolize or store a lot of fat, including muscle and adipose tissue, and it's regulated by a number of factors (1). This includes diet, hormones and other protein regulators. The current literature on LPL has shown that regulation of LPL is tissue-specific. The activity of LPL, like other proteins, may be controlled at the transcriptional or the post-transcriptional level. A review by Goldberg et al (2009) notes that the activity of LPL in adipose tissue during fasting is low, but high in skeletal and cardiac muscle. They also note that insulin increases transcription of LPL in adipose. So why the down-regulation? One of the proposed mechanisms for LPL down-regulation in adipose tissue is rapid inactivation by a protein inhibitor known as ANGPTL-4 (2)
ANGPTL-4 (also known as a fasting-induced adipose factor), is up-regulated in adipose tissue two to four-fold in response to glucocorticoid stimulation (3). It's commonly known that you have a cortisol spike within a few hours of fasting, which is intended to try and increase glucose availability, for example.
The idea is that ANGPTL-4 attempts to control the distribution of fatty acids (4). In a mouse study, Cushing et al. demonstrated that ANGPTL-4 in fact diverts uptake of fatty acids and triglycerides away from adipose tissues (5). And this study was published in August 2017, so the phenomenon is still under investigation. It makes sense though, right? Why does the adipose tissue need to continue to receive fats during fasting? They can be better served elsewhere like muscle, the brain or the liver. Not only so, but Catoire et al. also demonstrated in 2014 how the interplay between ANGPTL-4 and LPL between non-exercising and active skeletal muscle during exercise allows for fine-tuning of fatty acid delivery to sites that need it most (6). So the regulation extends to both inter- and intra-tissue needs.
In closing, LPL is regulated during fasting in a targeted manner, but it is not generally down-regulated. Regulation is controlled in a manner that allows the demands of tissues to be reactive to their environment.

I'm sorry but I do not understand your answer. I can understand why the skeletal muscle is regulated differently than adipose tissue, but Is LPL down-regulated in adipose tissue during fasting and if so why? If not, please say so. And you may know a lot about it but do you really have to bring ANGPTL-4 into this?

@David LPL is not generally down-regulated during fasting. One of the take-home points that I may not have communicated properly is that LPL is regulated at the tissue level. Adipose LPL activity is low during fasting, but high in muscle. The proposed mechanism for rapid adipose LPL inactivation is the up-regulation of ANGPTL-4 in that tissue. I will edit the answer.

Furthermore, I wanted to make note using ANGPTL-4 as an example that it wasn't a fat vs. muscle dichotomy, and that LPL may be regulated within a single type of tissue, as well.


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Mechanism of redirected blood
I've read several fitness articles mentioning redirected blood flow to muscles that are in use. However, they never mention how it works. Is it local and specific to the muscles in use? Or, for example, I guess more blood has to flow through the entire arm if I am training my forearms..? So, won't the entire arm benefit to a certain extent?
I did some research and discovered the vascular shunt mechanism through the opening and closing of capillary sphincters. However, I cannot find any resources discussing how local this effect is. So, as an example, how much does blood flow to the arm improve if someone is training their forearm for six months?

I'm voting to close this question as off-topic because this is a biology site not a sports training site.

@David Well  I originally posted this at the physical fitness SE. They apparently felt it belonged here, and it got migrated. So, apparently it's too technical for them and too sports related for you. I clearly need to edit this question to make it belong in one of the SEs.

I think could be on topic, though it should be changed to keep it on-topic here: 1) Your question contains aspects of both acute (immediate) changes during exercise and also chronic (long-term) changes. It would be better if your question focused on one or the other to focus on a specific biological question. We like questions that have some prior research here, too. 2) The background on conditioning/training is a bit problematic, because some people might interpret the question as asking for personal advice.

@BryanKrause Alright, thanks for the feedback! I have now tried editing it to make it on-topic for the biology SE.

A major determiner of blood flow redirection among muscles is increased oxygen demand in the working muscles.
When a muscle works, it uses oxygen, so the partial pressure of oxygen (PO2) in the muscle falls, which signals small arteries (arterioles) to dilate, which results in increased blood flow and hence oxygen and nutrients delivery to the muscle (Skeletal Muscle Circulation, NCBI Bookshelf).

When you exercise your forearm muscles without exercising upper arm muscles, the arterioles in the forearm muscles will dilate but in the upper arm muscles will not. The blood will just flow through the large arteries of the upper arm toward the forearm, but it won't be delivered to the upper arm muscles.
A long-term effect of exercise is the formation of new capillaries in the exercised, but not in other muscles (PubMed, 2008). So, six months of exercising forearm muscles without exercising upper arm muscles will result in better circulation only in the forearm muscles.


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Reading list to understand the theory of mycelium based materials for beginners
I have read tons of articles and seen presentations about people making materials with mycelium. From mycelium bricks to mycelium fabrics. I want to understand the processes that allow this. That is, I want to learn the theory about how mycelium can be used to create materials and what properties those materials will have. What should I read?
I guess it should be possible to start by reading the patents I have seen, but they probably assume some knowledge. My background is mostly computational, so I have read up on systems biology, computational biology and mathematical biology. However, I don't know how much of that is relevant, so for the sake of this question, lets assume I am a complete beginner.
What is required to understand the patents in this field?

Unfortunately this question is a bit too open-ended for a Stack Exchange format. I can see tons of tutorials on how to make the mycelium products - what exactly is it that you want to know? Systems and comp bio will be more or less useless here, mathematical slightly - growth curves etc. But all that is moot because you will need to actually grow the fungus and the best way to do that is to have a go...

@bob1 I am not looking for tutorials. I am looking for theory. That is, I want to understand what is going on and how it can potentially be modelled. That is, which variables can be tweaked to change material properties.

But there's nothing in your question that indicates what you want - all you say is "From mycelium bricks to mycelium fabrics. I want to get into this." Which to me means you are interested  in making them, not the theory. If you had said "I want to understand the theory" that might make it a suitable question .

@bob1 Fair enough, I agree that it is poorly worded; I assumed that the remainder of the question would be enough to clarify what I was looking for. I'll edit it.

@Avatrin The first thing that comes to mind when it comes to “mycelium modeling” is finite element analysis. I think that you can find a lot of deeper theoretical materials there (for example): https://www.sciencedirect.com/science/article/pii/S0264127518307482

As one of the early investors in the field of mycelium based materials, I can give a brief answer.
Mycelia are the underground cellular network of some fungi and bacteria.  Under some conditions they can form dense enough networks to produce various materials.

The main effort in mycelial materials I believe is in private companies right now.  Mycelial materials are being used to make leather, packing materials, and scaffolds for plantbased meat.  New applications are coming on line regularly these days as fungi are deeply interesting, so this list should be longer.
The details on how to create these materials is rarely made public but starting by growing your own fungal mats is available and a great place to start. The founder of Mycoworks, Phil Ross is an artist who made furniture and some building material from mycelia as well. He has done workshops and kits to grow his favorite fungi, the medicinal mushroom reishi are available.
Image uploading doesn't appear to be working at this moment but if you follow the links you can see
that the texture, flexibility, hardness and toughness of mycelia represent a broad range of material properties.  It should be expected that the field will continue to broaden.
In addition to these topics, a good place to start is reading the renown mycologist Paul Stamets.  His book, "Mycelium running" talks about the uses of fungi in sustainability exhaustively, touching on this topic and quite a few others.


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What are the effects of buffer on genomic DNA shearing by sonication?
Expt: I have isolated genomic DNA from LNCaP cells and would like to crosslink a small molecule (Chem-seq) to the DNA.  The small molecule is an alkylator so it will crosslink DNA on its own.  The buffer I am using for the crosslinking is TKMC (10 mM Tris-HCl [pH 7], 10 mM KCl, 10 mM MgCl2, 5 mM CaCl2).  After crosslinking I want to fragment the genome to 100 - 600 bp (300-400 bp average).  I am using a Bioruptor 300.
Question:  Should the TKMC buffer be sufficient for sonication?  Most references I have found use TE buffer (pH 7.5 - 8), and I can't find a reference using TKMC.
More info:  I tried a direct comparison between the two buffers (TKMC v TE pH8) and the TE buffer seems to fragment to smaller sizes compared to the TKMC buffer.
For example: Biorupter 300, Low setting, 1 cycle = 30/30 ON/OFF @ 3 C, 5 ng/uL DNA in 300 uL
average frag size @ 30 cycles: TE = 350bp, TKMC = 500bp
Any suggestions?  Using TE buffer for my alkylation crosslinking would not work due to presence of EDTA.  Should I play around with the cycle ON/OFF times?
Any help would be awesome!  Thanks.
UPDATE:
After running a comparison between TKMC, TKMC + 1mM EDTA, TKMC + 10 mM EDTA there was a slight tightening up of the fragment range as I added EDTA.  In addition, the fragment range (sizes) was smaller when EDTA was added (compared to TKMC w/o EDTA, after the same number of cycles).  The results were not drastic but there was indeed a noticeable effect on fragment size and range.  I will proceed with adding EDTA before sonication.  Thank you for your suggestions!

As long as kept cold I would increase the on/off until you achieved the average size you are looking for.  I'd start the next one with 40 cycles and examine.  This manual page 17 seems to indicate this would be very appropriate https://www.diagenode.com/files/products/shearing_technology/bioruptor/Bioruptor_manual.pdf

I know nothing about this, but if divalent cations somehow affect fragmentation, you could try adding EDTA in excess after cross-linking.

@canadianer Yes, of course, better than my suggestion of buffer exchange!

@AlanBoyd I'm kind of curious if it works. It's surprising to me that Mg would have such a drastic effect, but I'll have to read the paper you found.

Note that there is 10 mM Mg and 5 mM Ca, so you may need to add in excess of 15 mM EDTA.

I diluted the TKMC/DNA 1:1 when adding the 10 mM EDTA (keeping the Tris-HCl @ 10 mM) this dilutes the Mg2+ (5 mM) and Ca2+ (2.5 mM).

Could you use a spun column to exchange the buffer? Some sort of gel filtration column; equilibrate column in TE; add your DNA sample, spin through excluded DNA. TKMC components will be included in the column and thus retained.
Update
Have a look at this paper, and references therein. Apparently magnesium ions influence the flexibility of DNA. Clearly if the shape of your DNA in the two buffers is different this would impact upon the effects of shearing forces.


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phylogenetics and substitution ratios for positive selection
So very new to phylogenetics!. I've been scrambling and reading so much to get this done!!.
I would like to see if one or more of the sequences I have (from a gene family) are under positive selection using the dN/dS ratio. The conceptual parts are clear to me, however, practically speaking i have found several problems/questions along the way.
My most important question would be: I have four related organisms (insects), and their full sets of genes in a gene family. I have reconstructed trees to delineate their evolutionary story (duplications and losses). What would be the input for the calculation of dN/dS ratios when a single gene has several possible orthologs in the other organisms?, like gene A in species 1 has gene B and C and D in species 2 and E, F, G, H in species 3 etc... Do I need to align only the orthologs for each species? all of them?, or just align all the sequences form the subfamily including all paralogs and orthologs?, wouldnt that overestimate the ratio?
I have tried PAML yn00 package and got a result for a small "test" set of sequences, which were not codon aligned. Results are pairwise, how can I interpret this?, do I want to get "overall" omega values instead of pairwise? what would be the most interpretation on each case?
Second question is how I get codon alignments for these sequences?. I saw a couple of free software on th internet but they wouldn't work.
thanks a lot!


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Is this a leafhopper? (Italy)
I'm located in Bologna, Italy, in the city center. I found this insect on by bean plants, I think it's feeding on their leaves.

What is it? The answer to this question suggests that it is a leafhopper, but I can't find the exact species. When approached, they seem to jump away.

 Altough related to the question I linked, I don't think it's a crosspost, because in that question I want to know primarily what's the solution to the problem of white spots on bean leaves, while here I ask for the exact species in the photo.


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Are there any viruses that integrate their DNA into organellar DNA?
It is known that many viruses (e.g. retroviridae) integrate in the nuclear genome of their host as part of their cycle. However, I'd like to know if integration can happen in organellar DNA (cpDNA and mtDNA) as well.
I've found a paper proposing that some chloroplast genes have a viral origin; however, the virus would have been present into the ancestral alpha-proteobacterium that later became the chloroplast, so no direct chloroplast infection is involved.
There is also this almost identical question on ResearchGate, but frankly the answers there are not satisfactory.

Mitoviruses have been reported to replicate within the mitochondria of certain fungi, though integration was not observed.
https://www.sciencedirect.com/science/article/pii/B9780123943156000064?via%3Dihub

Oh, I forgot the juicy tidbit here about DNA!  The virologists have this theory about Mimi?  This massive huge virus...that came from asteroids and meteors.  That this virus caused life to start (some used to call this the God virus but I gag) and inserted some basic DNA.  How else would we share DNA with plants?  Hello?  Fascinating stuff!

I'm only aware of one paper that claims to show regular viral integration into mitochondrial DNA, and even there they suggest it might be a host defense rather than a viral life cycle thing:

Interestingly, 69.4% (50/72) of HBV integration sites were observed in human mitochondrial DNA (mtDNA) (Supplementary Table 2). ... However, 32% of HBV integration sites in mtDNA (16/50) were in the displacement loop (D-loop) region, which is known as the major control site for mtDNA expression as it contains the origin of replication for the heavy DNA strand and the major promoters of transcription (Figure 1B). Of note, we repeatedly detected mtDNA integration events through the same micro-homology site in independent mice, indicating the hotspot for HBV integration in mtDNA, which is probably related to replication or transcription. ...
We found that HBV integrations were mediated through MMEJ, which is known as an alternative DNA double-strand break (DSB) repair system and reported as a principal mediator during mitochondrial DNA lesions. This suggests that early-phase HBV integration occurred in mtDNA. Damage in mtDNA is known to induce autophagy and was removed in C. elegans, therefore it is possible that integration of HBV DNA into mtDNA might be a defensive mechanism to protect the nucleus from HBV integration.

--Characterization of HBV integration patterns and timing in liver cancer and HBV-infected livers
I would like to see this replicated and extended before I spent too much time wondering about functions and mechanisms.


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What is this whitish jelly incrustation on a plastic tube?
I found this plastic tube hanging in the seawater from a pier in the haven of Taranto, Ionian sea, southern Italy. I'm wondering what is the whitish jelly in the lowest part of the photo next to the yellow Botrylloides violaceus. It didn't seem to come off easily (I didn't insist much though) and it didn't have any macroscopic reaction when touched (no contraction or similar).

The photo was taken on the first days of January. The water was shallow in that point (no more than 2m deep) but close to deeper water, as expected from a haven, and rather polluted.

The orange/yellow jelly organism is very likely a colonial tunicate (sea squirt) similar to the one from this post. I welcome you to do some of your own research to determine more species specifics :)

Possible duplicate of What strange jelly-like thing is shown in the photo?

Can a photo identification post really be a duplicate if it's a different photograph? I guess that's a topic we could pick up on meta.

Thanks @theforestecologist! I hadn't see the question (I sent mine from a cellphone so I didn't see the suggestion) - it's actually Botrylloides violaceus, an alien invasive species. I'll edit my question and make the side quest the main one :)

@TimonG. I don't think it's a duplicate, since it's a different species. However, it's true that I could determine the species basing the research on the similarity to that one. I guess it can or cannot be a duplicate depending on OP's ability to search for similar species. I agree that it's worth raising the issue on meta.

No worries, LinuxBlanket -- just linking up the two questions. You're right that it's a different species and that closing it as a duplicate could easily be voted against. Generally with this type of question, the OP doesn't care about the actual species and knowing the type of organism alone suffices, which is why I voted to close. Interest in the specific species would be fair game for me to rescind my close vote. Regardless, I'll rescind the vote due to your edit. Thanks!

@TimonG. Yes for sure. This happens all the time, especially with common ID questions such as for bed bugs, psocids, carpet beetles, etc. Sure it's not the "same" question, but it serves no benefit to litter the site with IDs of the same species. In these cases, closing isn't a bad thing or form of punishment; it's simply a way to keep the site tidy and allow future visitors ease of finding info they need. But please by all means, start a meta post about it and we'll see how the community feels about that current approach. Thanks