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Is it possible to estimate tree height from stump/breast diameter and species?
Kindly pardon my poor knowledge, my area of expertise is not biology.
I am currently working on project where I have access to tree's stump and breast diameter and its species. We are trying to estimate tree's impact on microclimate on its surrounding.
To simulate it, we need approximation on tree height. So is there a database or textbook I can refer which provide information on estimating tree height from these features?
I understand that there would be no absolute value here but rather a distribution.

Yes and no. Allometric equations exist and are sometimes used. However, they are incredibly finicky - dependent on both species and specific growing area. With soil and water ability varying sometimes at sub-meter levels and known competitive impacts from neighboring trees  likewise depending on species, the ability to  model such allometric equations accurately and precisely is very difficult. This is further complicated by random events (e.g.wind damage, etc.). What are you trying to use this approach for? Most major journals might sneer at the approach given better methods (e.g. Lidar). ..

For southern ( USA) pines; no. In the forest they reach about 100 ft high at less than 2 ft diameter , then the diameter grows to over 4 ft. In an open area they are much shorter.

@blacksmith37 exactly -- under different competition scenarios, trees grow quite drastically different. Remember, trees are fighting for sun and nutrients -- as you alter the availability of one or more  of these resources through environmental shifts or community interactions (e.g., competition) you inherently should expect a shift in size, growth habit, etc.

@theforestecologist: For an example, I was cross-country skiing through a pine forest of mixed age this afternoon (eastern SIerra Nevada), after having read this question in the morning.  Trees with a trunk diameter about 1 ft/25 cm were around 70-80% of the height of ones with a 3 ft/1 m diameter.  And from other observations, younger trees in a dense stand will have tall trunks with few branches until the top, while those growing in an open area will be shorter and bushy, with branches down to the ground.

This is an interesting question for me because my first research internship centered pretty much entirely around this.  It got pretty deep into the weeds as this was a CS, rather than biology, internship and we were mostly analyzing the math behind the allometry (e.g. Log-transformed linear vs. nonlinear regression for fitting the curve, OLS vs. RMA regression, traditional vs. monte carlo methods for comparing curves with different numbers of parameters, etc.) but much of the work we did is applicable here.
So, what you have here is DBH, or Diameter at Breast Height, which, lucky for you, happens to be the most common method for estimating the biomasses of trees.  Here is the way that it works.  Basically, a research team will go out and measure the diameter of a bunch of trees.  Then they will cut down those trees and weigh them.  What they will end up with is a graph with a bunch of points that give you the weight of trees of particular diameters.  Then you fit a curve to this graph and, next time you want to estimate the biomass of a tree, you plug that tree's diameter into the equation for your curve.  There are a bunch of databases containing allometric equations for different tree species.  You just need to find one that contains the trees that you are interested in.  Given that you are working in New York, this might have what you need:
https://www.fs.fed.us/psw/publications/documents/psw_gtr253/psw_gtr_253.pdf
Though you are better off figuring out the species of the trees you are looking at and seeking out allometric equations for those specifically.  There might even be allometric information included with the data you are being provided.  One thing that may be an issue is that correlations between DBH and biomass are much more common than correlations between DBH and height.  Though both exist, you may have more trouble tracking down the latter for specific cases.  Additionally, these numbers are very rough estimates that vary a great deal depending on the techniques used to collect the data, fit the curve, and extract the equation.  In my own research, I found that log-transformed linear regression tended to be more successful over all (oddly enough) but that nonlinear regression was more effective on young forests dominated by stands of small trees.  We also had a rather odd finding that log-transformed linear regression of two lines with a breakpoint tended to be less accurate in both situations but more accurate overall (i.e. it did better on big trees than nonlinear regression and better on small trees than linear regression) but we weren't able to come up with a mechanism to explain why this would be the case so we scrapped the findings.  At any rate, all of this should illustrate that these numbers are very rough estimates that can be heavily influenced by environmental biases and that different research teams may even disagree on the proper allometric equations to use on a given species.  This is why databases are helpful, as they tend to average out a large number of allometric studies rather than relying on a single one, but even these should be taken with something of a grain of salt.
If you are expected to actually come up with these equations yourself, then you need to actually measure the diameter and heights of a bunch of trees, plot them, and fit a curve to them.  But from the sounds of it, you are only expected to estimate tree height based on diameter.  If that is the problem you are being asked to solve, chances are that there are allometric equations available to help solve it, perhaps even ones that were provided to you.

not only do you need to find a set of equations for your species, but these numbers very certainly vary between growth regions (and likely even at smaller scales). The equation(s) by Jenkins et al is an example of an attempt to get around this to a degree. The question, though, is: do you want to do your study, or do you want to do it well. @Jeremiah you're right that this is a common approach, but it has slowly fallen out of favor as we have developed more accurate (though more expensive) methods.

If a best-fit-model approach is being utilized, I would suggest that the models you've mentioned are all too constrained and will very likely not capture all of the (realistic) variation. Sometimes that's ok -- again, this is why I asked the OP for his/her end goal. If this model approach is used, however, I'd suggest building stronger models using mixed effects modelling or various nonparametric approaches. If the solution is a simple one (as in using a log curve), in this case, it almost certainly can be improved upon....

@theforestecologist I am aware of this.  My own work in this area, specifically, involved the use of differential evolution, genetic, and particle swarm algorithms to improve on these sorts of models.  But this is clearly not the sort of thing that one would be responsible pointing the questioner to.  He doesn't know what allometry is and started the question by apologizing for his lack of knowledge of the subject.  In this situation, one needs to start with the basics.  In this case, that means learning what an allometric equation is and how best-fit models work. He didn't ask for a better

way to estimate tree height.  He said that he had DBH and wanted to know if there were databases or anything he could use to estimate height with that.  There are hundreds of them and if  he had any business coming up with better models he would have already known that.  The questioner didn’t leave his level of knowledge of this subject ambiguous.  He was quite clear about it.  If someone in a bio 101 class asked you how metabolic rate scales with size, would you start going on about computer-aided modelling solutions that can more accurately

account for non-size related variability, or simply explain the mathematical relationship between surface area and volume to them?  You have to start somewhere and the questioner made it quite clear they are at the start line.  A useful answer should meet him there.

just fyi I'm not criticizing your answer, and I appreciate that you addressed the basics of allometry. The purpose of my comments are to provide a clear warning associated with this question/answer so that the OP and any future folks that put eyes on it know things are not so simple. The OP, specifically, might be asking a simple question that can be given an introductory answer, but the motive behind the question is still not clear -- it's always possible they're looking for a basic answer when they don't know that it'll be inadequate. Again, why I asked the OP what their goal was.

@theforestecologist I apologize if I came off as defensive.  That was not my intention.  In my experience, the best way to learn is to play around with new techniques, run up against scenarios where those techniques don't work, and then look into ways to improve them, learning new skills along the way.  A pet peeve of mine is when scientists attempt to dissuade interested parties from doing this because they don't have access to university resources.  The only actual concrete suggestion you provided was LIDAR.  If the OP had access to that sort of tech, they would be asking their research

advisor or company supervisor this question, not the stack exchange.  The same actually goes for anyone else who comes here looking for answers to this particular question.  It is, by its very nature, an intro level question.  They wouldn't be asking it if they were in an academic position where they had access to something like LIDAR.  When someone suggests that the only way to begin looking into a problem is if you have a funding source and a lab, that doesn't help them.  It just drives curious parties away.


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How can different ion channels of the same type have different cell responses?
The NMDA receptor is an ion channel and contributes to synaptic plasticity and memory. It is said that calcium ion flux through the receptor is critical for this mechanism. However, there are other ion channels that let calcium ions into the cell, how come they don't contribute to synaptic plasticity (to my knowledge)?

Can you please add references?

It is not just an ion channel. The name itself suggests that it is a receptor i.e. it responds to a ligand. Perhaps you can read a tiny bit more about NMDA receptor and the answer would become obvious.

cross posted to https://psychology.stackexchange.com/questions/21753/how-can-different-ion-channels-of-the-same-type-have-different-cell-responses although it might get a more detailed answer here

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Conjugate vaccines in the context of the original antigenic sin and antibody feedback inhibition
How come we can get an antibody response against a polysaccharide bound to a carrier protein, that we have antibodies towards, when antibody feedback inhibition exists?
If we have antibodies against the carrier protein then surely this will lead to inhibition of the B-cells that express B-cell receptors for the polysaccharide?
What's going on here?

Check out this review. Antibody feedback regulation can go both ways. Downregulation is associated with antigen masking, but that won't happen if the (new) polysaccharide antigen isn't masked by the existing Abs. So, the answer is, it depends.

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How does alternative splicing actually work?
How do two identical pre-mRNA molecules give rise to two different mRNA molecules after alternative splicing? They contain the same introns and exons and thus same splicing enhancers and silencers
Is it just a case of what proteins/snRNA happen bind to the mRNA first?

A mRNA molecule is composed of introns and exons. All introns are removed before translation occurs*. However, sometimes exons are also cut. This leads to different mRNA molecules, and therefore, different proteins. This image gives very good summaries in my opinion (source):
According the National Library of Medicine, the different mRNA strands are called transcript variants, splice variants, or isoforms. I admit that I do not understand how a cell 'decides' when to use one variant over another. This free article is on that very topic, but it is beyond me. To quote the abstract:

Regulation of alternative splicing is a complicated process in which
numerous interacting components are at work, including cis-acting
elements and trans-acting factors, and is further guided by the
functional coupling between transcription and splicing. Additional
molecular features, such as chromatin structure, RNA structure and
alternative transcription initiation or alternative transcription
termination, collaborate with these basic componentsto generate the
protein diversity due to alternative splicing.

*Some may argue that this is not true. There is a mode of alternative splicing where introns are left in called intron retention. Personally, I think that a region that is sometimes removed from the mRNA and sometimes left in should be classified as an exon, so intron retention is the results of misclassifying an exon as an intron rather than a genuine biological phenomenon.

But presumably the poster knows the part of your answer that says what alternative splicing is, and you haven’t answered his question which relates to how this is controlled, except from the quotation which you admit not to understanding. In fact the quotation says nothing of substance, but is so much hand waving.

It was not clear to me how familiar the OP was with alternative splicing, so I provided a basic overview  and a link to very detailed paper that went over the details I was not confident trying to explain. If they were new to the topic, then they have their basic answer. If they were knowledgeable in the topic already, then they have a great resource on where they can do more research. If you dislike my approach, perhaps you should leave an answer to the question.


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If DNA methylation inactivates genes, does DNA demethylation activate them?

DNA demethylation can be passive or active. The passive process takes place in the absence of methylation of newly synthesized DNA strands by DNMT1 during several replication rounds – for example, upon 5-azacytidine treatment [23]. These pharmaceutical demethylating agents act via inhibition of DNMT1 and favoring its degradation by proteosomes [24]. This approach is currently used in cancer to demethylate tumor suppressor genes [25].

If we’re demethylating a tumour suppressor gene for cancer curing doesn’t this mean that we’re activating it (to stop the tumours)? I can’t seem to understand the function of DNA demethylation. I came across it when reading about genomic imprinting and haven’t been able to wrap my head around it. Please help.

Here is a series of articles explaining DNA Demethylation from Sience Direct.
In the most broadest of senses, DNA methylation adds methyl groups to DNA preventing the transcription complex from forming and transcribing the gene into mRNA. By demethylating the DNA, it allows the transcription complex to form and mRNA to be transcribed for translation.
When it comes to cancer, Most of the tumor suppressor genes are down regulated to allow for genes like stat3 to be upregulated. Ideally, by removing the suppression of these genes, they can reduce the levels of oncogenes and slow the growth of the cancer.
Think of it like this A -| B. Cancer decreases A so B can increase in expression A↓ -| B↑. By demethylating A, we  A↑ -| B↓.


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What happens when a human ingests a large meal, and after a short time follows it up with a large amount of indigestible carbs?
A human eats a large meal and indigestible carbs (IC) with such a timing that the IC arrive to the small intestine when it is already full and busy breaking down and absorbing the meal. What would happen to the IC? Would they stay there until the digestible meal is digested, or would they somehow be moved along? Would they start fermenting if they are stuck there for some time? Would they push the unabsorbed remnants of the meal out as the body tries to excrete IC? Would they hamper absorption or aid it?

Indigestible carbs are known as dietary fiber. They slow down gastric emptying, which results in slower absorption of the absorbable nutrients in the small intestine.

Early research regarding soluble fiber demonstrated delayed gastric
  emptying and decreased absorption of macronutrients, resulting in
  lower postprandial blood glucose and insulin levels [44]. This is
  most likely due to the viscosity of soluble fibers inside the GI
  tract. Interestingly, different types of soluble fiber had varying
  effects on viscosity and nutrient absorption. Guar had the highest
  viscosity as well as the greatest effect at decreasing postprandial
  blood glucose. Therefore, it would be assumed that an increased level
  of soluble fiber would be associated with a decreased risk of
  diabetes. However, several recent studies have demonstrated the
  opposite showing no correlation between soluble fiber and a reduced
  risk of diabetes (Nutrients, 2010).

So, dietary fiber can slow down the absorption of macronutrients (carbohydrates, proteins, fats), but does not reduce the amount of macronutrients absorbed (at least not significantly).
Dietary fiber can be soluble (for example, stachyose and raffinose in legumes) or insoluble (for example, cellulose in fruit skins or grain hulls) (Linus Pauling Institute).
They are microbes, mainly in the large intestine (not in the healthy small intestine), that ferment soluble, but not insoluble fiber. Fermentation of a large amount of soluble fiber produces a lot of gas (flatulence), which typically occurs several hours after a meal.
Insoluble fiber can stimulate intestinal motility and thus help in constipation, but large amounts can be laxative, which could result in decreased absorption of nutrients; soluble fiber can trap some bile secreted by the gallbladder and may thus reduce the synthesis of cholesterol (Linus Pauling Institute).
Dietary fiber probably does not interfere significantly with the absorption of minerals and vitamins (Nutrients Review).


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Identify this plant from the Netherlands with big white flower
The picture was taken today in the Netherlands. Can you identify this plant species?

From the leaves and flower it could be a clematis.

Like @skymningen thought, this is a Clematis. However, the only wild Clematis in the Netherlands is Clematis vitalba, that has much smaller flowers (about 2 cm diameter) see "Heukels' Flora van Nederland" (the official Dutch flora) and here.
So you have photographed a plant that "escaped" from a garden. Most garden Clematis are hybrids from Chinese or Japanese origen. As there are about 300 species and new hybrids constantly being produced, the likelyhood of finding it's name is low. https://en.wikipedia.org/wiki/Clematis

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How is Vitamin D deficiency linked to multiple sclerosis?
Numbness and tingling in various parts of the body can be linked to the deficiency if vitamin D in one's diet. Also, multiple sclerosis has Vitamin D deficiency as one of its risk factors. How exactly are they related? MS is an autoimmune disorder. What exact role does Vitamin D deficiency play in here?

I don't believe this is known mechanistically to any great degree. Mayo Clinic has an easily understandable post about this.
In summary, the evidence for a relationship is that vitamin D levels correlate with occurrence of MS (high vitamin D intake is associated with less occurrence of MS in individuals; populations further from the equator have less vitamin D and more MS) and that vitamin D in individual MS patients can influence their symptoms and disease progression. Knowledge of those relationships does not require any mechanistic understanding.
The review by Sintzel et al (2018) is another source for these general epidemiological associations and evidence for a possible causal relationship of low vitamin D in MS. Mechanistically, however, they only mention general relationships between vitamin D and the immune system, not any known specific mechanism of the involvement with MS. Autoimmune disease is somewhat notoriously complicated, so I don't find this particularly surprising. The review they cite, Mora et al 2008, takes a more general look at the relationships between vitamin D and immune function, which are highly multifaceted and involve both up- and down-regulation of different cell types involved in different aspects of immune function.

Mora, J. R., Iwata, M., & Von Andrian, U. H. (2008). Vitamin effects on the immune system: vitamins A and D take centre stage. Nature Reviews Immunology, 8(9), 685-698.
Sintzel, M. B., Rametta, M., & Reder, A. T. (2018). Vitamin D and multiple sclerosis: a comprehensive review. Neurology and therapy, 7(1), 59-85.


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Why aren't mammals and reptiles considered amphibians?
We've all heard it: birds descend from dinosaurs, so they're dinosaurs too. But this got me thinking: doesn't this mean that, for instance, all terrestrial vertebrates – including humans – are technically fish? A recent video by MinuteEarth and the Wikipedia article for "Fish" confirmed my shower thought hypothesis.
Interesting. But... all amniotes, i.e. reptiles (and, by extension, birds) and mammals, descend from amphibians, right? If so, then why aren't they considered amphibians too?

It's for logical clarity. Languages aren't perfect and there can be only 1 word when 2-3 words would be useful. Amphi means both and bios is life. It means double life technically it doesn't mean water and air. the combination of AM AN and IBI in the word amphibian make it a word that has stood the test of time.

Mammals and reptiles aren't considered amphibians, because amniotes are not hypothesized to descend from Amphibia. That is to say that Amphibia did not evolve into Amniota. They are sister clades (actually Reptiliomorpha in the Tree of Life tree below).

Ah yes, this makes more sense. I must've misread something and concluded that amphibians are the ancestors of mammals and reptiles. Still though, doesn't Mammalia descend from Reptilia? If so, what about the fact that Mammalia isn't classified within Reptilia?

Follow the Amniota link on the page linked above. You will see sister clades Synapsida and Reptilia. I'm not sure what wikipedia says, but I wouldn't trust it in general.

Some named groups are not monophyletic (see this post for definition if needed). Fishes do not represent a monophyletic group. Groups like "fishes" are completely awful to define but everyone would agree that no, humans are not fish!
Now, it is important to understand for many terms, there might have a scientific and a popular definition of the term. For example, when people talk about reptiles, they talk about turtles, snakes, lizards, squamates but they don't talk about mammals. Hence by "reptile" they don't mean "Reptilia". Have a look at the post If dinosaurs could have feathers, would they still be reptiles?).

Huh. I thought the Scientific Classification of life was 100% cladistic, but since the reptilia and mammalia classes aren't contained within amphibia, I guess middle-school Biology kinda lied to me...

I think my answer was a little unclear. I edited it. Please read it again. I did not mean that in cladistic, we name groups that aren't clades (clade = monophyletic group). I mean that the terms "Reptilia" and the term "reptiles" don't mean the same thing.

Thanks, but my question remains, though: if – as you've stated yourself – cats are Amphibia, why isn't Felix catus (or any of the other amniotes, for that matter) taxonomically classified within Amphibia?

Amphibia do not contains cats though. Amphibia only contains Anura (the frogs and toads), Urodela (the salamanders), and Apoda (the caecilians) (note I corrected a mistake in my above post). Reptilia do contains cats though but you would never state that a cat is a reptile. I think you have a false belief that mammals are part of Amphibia. Amphibia are a sister lineage to Reptiliomorpha (see here) and cats are part of the Reptiliomorpha

The real - and IMHO only - reason is that some people just think it's "cool" to claim that birds are really dinosaurs.

Whether mammals are reptiles is one of those circular pointless classification arguments you sometimes get in science, that people debate endlessly. It is based on using an archaic classification in a modern system.

@jamesqf birds are dinosaurs, the clade dinosauria is defined using birds. Dinosauria itself is defined as the last common ancestor of Triceratops horridus, Passer domesticus, Diplodocus carnegii, and all of its descendants. Passer domesticus wouldbe the house sparrow.

@John: No, birds EVOLVED FROM dinosaurs (which went on being dinosaurs for many millions of years afterwards).  It is the same sort of logical confusion that would insist on saying that all vertebrates are really just fish :-)  And if your modern classification system insists on such things, perhaps the problem is with the system?

It all depends whether by dinosaurs you mean what most people mean (which exclude birds) or whether you mean Dinosauria. While it somehow makes more sense to state birds are dinosaurs, one must highlight that if you make such statement, you should also say "mammals are reptile" (or that vertebrates are fish) which is not something we would want to say. Personally I am fine with both "birds are dinosaurs" or "birds evolved from dinosaurs".

@jamesqf by that argument human are not mammals, because humans are primates, it doesn't make any sense. Imagine the only surviving mammals were bats, would bats stop being mammals?

@John Following your logic, are humans reptiles? Just accept that in the common language, people can group species in a non-phylogenetic way. I think it is as silly to attack someone that say "birds are dinosaurs" than it is to attack someone that says "birds evolved from dinosaurs".

@Remi.b what makes you think I had a problem with someone saying birds evolved from dinosaurs? I just have a problem with someone saying birds are not dinosaurs, there is no scientific definition of dinosaurs that does not include birds. biological classification is nested, which is why terms like non-avian dinosaurs exists, or non-human animals. I accept that reptiles is a bit weird because the word is so old so the lay term carries a lot of baggage, but even the original use of the word dinosaurs would include birds given what we know now.

reptiles don't work no matter what you do, crocodiles are more closely related to birds than they are snakes. It is hard to say mammals are reptiles because synapsids are likely not in crown reptilia, that is the mammal clade is not in the reptile clade, they are squarely in amniota however. going by lay usage mammoths and ichthyosaurs are dinosaurs, lay usage is generally useless.


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What is a Archival Tumor Tissue ? For What Purpose is it collected?
Over the course of Conducting trials various tissue and tumor samples are collected  from the patients.
One such sample is the Archival Tumor Tissue.
Could someone kindly clarify what is the meaning of the term archival tumor?, and what data is gleaned from it.

Welcome to Bio.SE! What attempts to answer this question have you already taken? A Google search pulls up many hits. We ask that all question posters here attempt to search for an answer to their own question & explicitly indicate research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, & it will likely be received more positively by our community. Thanks!

When a tumor is removed from a patient, it is usually send to the pathology the make sure that it has been excised completely to make sure there are no residues. Often this tumor is also used to analyze the mutation status of the tumor to determine, which further treatment is possible. For example, this is routinely done for melanoma where the mutation status excludes some drugs for further treatment.
Afterwards these tumors are important material for the scientific tumor research to isolate fresh cell lines or analyze them further. Parts of it are usually stored either frozen or as formalin fixed tissue to build tissue banks. These can be used for later research on this type of tumor and have a high value.
These tissues can then be cut and stained with antibodies or used for nucleic acid extraction (either DNA or RNA) or to test new ideas or methods which where not available to the time when the samples was archived.
Another famous case (although not from tumors) are tissues samples which have been archived from people deceased from the spanish flu in 1918, where parts of the virus was reconstructed using these samples decades later.


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What is the defining characteristics of a Gap Species?
For the following competitive exam question: A road is constructed through a tropical rain forest, following which a population of a species of butterflies declines. Which of the following is NOT  a possible explanation for the road causing a decline in the forest butterfly population?
The answer: The Road facilitates immigration of gap-loving species which compete with the forest species
What is the defining characteristics of a 'gap' species?

The previous answer from @Ark Lomas is true to the extent that gap-loving refers to preference of an open habitat. It was found that these species e.g. have improved flight abilities and are in general geographically more wide-spread.
Here is prove:
Ecology of Tropical Butterflies in Rainforest Gaps
J. K. Hill, K. C. Hamer, J. Tangah and M. Dawood
Oecologia
Vol. 128, No. 2 (Jul., 2001), pp. 294-302

Tropical forest gaps are ephemeral and patchily distributed within
forest areas and have very different light environments compared with
closed-canopy forest. We used fruit-baited traps to investigate if
gaps are exploited by more opportunistic butterfly species compared
with closed-canopy forest. Gaps supported a higher diversity of
butterflies in terms of species evenness but closed-canopy sites
contained species with more restricted geographical distributions.
There was little similarity between the assemblages of butterflies
trapped in the canopy and those in either gap or closed-canopy sites,
but the greater similarity was with gaps, and increased diversity in
gaps was partly due to canopy species turning up in gaps. Dispersal
rates (as measured by recapture rates) were higher in gaps and there
was evidence that butterflies in gaps had relatively larger and
broader thoraxes, indicating a flight morphology adapted for faster
flight. These results support the notion of a distinctive gap fauna
comprising more widespread, mobile species. Habitat modification that
opens up the canopy is likely to result in an increase in these
widespread species and a decline in understorey species with
restricted distributions.

a gap-loving species is a species that prefers existing in open spaces such as the gap that the road creates in the rain forest. I can't think of any organism native to rain forests that would be considered significantly gap-loving since most rain forest species rely on the trees and bushes etc... that the rain forest provides which therefore causes them to not prefer being exposed in the middle of a road.


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Are microbial antigens selected against?
Antigens provoke a response from the host immune system. Could selective pressures result in microbes losing their antigens? Has this been observed? Or are antigens typically so important that they are constrained from losing them?

Hiya. I find the last sentence a bit confusing and don't really know what you mean by it.. However, I interpret your question as whether there are any selective pressures that would lead microbes to lose/hide their antigenicity. If my interpretation is correct then, yes, that happens / has happened. S. aureus is probably the most famous example.. Antigenic variation as well as antigenic disguises are two "ways" a microbe can escape the host immune system.

Thanks, that answers my question! Sorry I was not clearer in the last point. What I meant was, are there certain antigens that are so functionally important to the microbe that they cannot be lost? And what would an example of such an antigen?


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What does it mean to have square brackets around a genus name?
For example [Eubacterium] rectale

The NCBI Taxonomy staff places square brackets around the genus for some species (examples: [Bacillus] aminovorans, [Candida] auris) to indicate that they are misclassified*, meaning placed incorrectly in a higher taxonomic rank.
References:
https://support.nlm.nih.gov/knowledgebase/article/KA-03379/en-us


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Why do plant leaves turn yellow?
Why do plant leaves turn yellow if they don't get enough water or get too much water? I want to know the process.
I've been searching in Google for an explanation, but none of the sites did.
Please describe the process.

Usually it is termed chlorosis, and comes about from an inability to produce chlorophyll. It can actually be determined by a whole range of things, and not just water shortage or waterlogged soil, including nutrient deficiencies, pathogen infection or unbalanced soil pH.
A lot of these factors relate to an inability of the plant root system to properly take up water. As you probably know, water enters the root system to be carried up into the shoot (through the xylem) mostly driven by transpiration, the water pressure caused by loss of water through the leaves. This water carries with it the soil-derived nutrients the plant needs to synthesise substances that can't be produced by photosynthesis. So if you change the water balance (for example by drying the soil) it becomes difficult for plants to get the nutrients they require to produce chlorophyll.
Usually this is mediated by reduced supplies of magnesium, iron or zinc, but because the precursor to chlorophyll is an amino acid, it can also be caused by shortages of nitrogen. pH comes into play because plants use a delicate balance of acidic ions to mobilise (make available to the roots) the nutrients in the soil, and if the soil pH differs too much this becomes untenable.
So in summary it relates both to shortages of key nutrients or changes in key soil characteristics, and the ability of the plant root system to uptake these key nutrients. It is mediated by these effects leading to an inability to produce enough chlorophyll, which leads to the yellowing leaves that you observe.


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Is the rate of photosynthesis higher than the rate of respiration?
In photosynthesis carbon dioxide is used up and oxygen is produced and at the same time plants respire too. So oxygen is used up and carbon dioxide is produced.
Then the net exchange of gases should be zero. If this is so, then why do we say that plants maintain the level of oxygen and carbon dioxide in the atmosphere?
So, is the rate of photosynthesis higher than the rate of respiration in plants in a year(overall)? What is the net exchange of gases annually?

The net exchange of gasses in any area will be different depending on the number of plants and what plants they are.  This is because it depends on the number and size of leaves, and because chlorophyll is essential for photosynthesis, it also depends on the amount of chlorophyll in the leaves. Therefore that part of the question is very broad.
Overall, photosynthesis (oxygen production) is higher than the rate of respiration in plants during a year.
Aerobic respiration continues all the time in plant cells (in light and in darkness), using up oxygen and making carbon dioxide. Photosynthesis, in contrast, occurs only in light and uses up carbon dioxide and makes oxygen. The more light there is, the more oxygen is produced.
There is a light intensity at which respiration and photosynthesis cancel each other out. This is called the compensation point. Below this level carbohydrates are used up and the plant cannot grow.

This and more can be read in this document from the Royal Society of Chemistry


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Which processes in the human body depend on natural selection among cells?
Are there processes in the human body which occur via natural selection among cells? Could anyone provide examples?
E.g. when tissues are conditioned to be stronger, such as a rock climber's skin getting thicker, would that be natural selection at work? What about muscle conditioning via lifting weights?

Please read about natural selection; the process requires reproduction of the organism. For that reason, it's not possible among an individual's cells. Cells have distinct purposes. They don't compete.

Cancerous tumors...

@anongoodnurse Whether we call it natural selection or not, I see no reason why cells can't compete for survival under some contexts, and become enriched in a population in virtue of particular genes. I can also imagine this process happening in the absence of higher-level regulatory / tissue-level processes, but I was just wondering if people had examples. I think Roger's example of cancerous tumours will sometimes be one such case.

Normally cells work together for the good of the whole. Cancerous cells certainly compete/outcompete, but that's not normal.

@anongoodnurse — My understanding is that natural selection can operate at multiple levels including at the cellular level. That previous source specifically mentions cancer, so I don't think the distinction you are making reflects current usage in evolutionary biology.

Yes, I thought my use of language was in line with the language of modern evolutionary biologists (as @tyersome says) and modern philosophers of biology / theoretical biologists (I'm thinking of Jablonka & Lamb's Evolution in Four Dimensions and similar work).

Arguably T cell maturation in the thymus is such a process.

That's an interesting example. +1 I'm not sure, though, that a normal process of elimination or enhancement qualifies it as natural selection. Maybe it does, but it would raise a lot of questions about what, exactly, the definition is. Are younger RBCs selected for O2 carrying because older RBCs are being picked off by the spleen?  Etc.

T cell maturation involves generating an enormous surplus of immature T cells with recombination and enhanced mutation in the receptor genes. Among those the body retains only those with binding affinity to certain molecules within a given range, killing off the majority that have too high or too low binding affinity. Thus, cells divide to form a large initial population, which is then severely winnowed by selection to produce the final population that emerges into the body. Some cells then undergo further clonal selection upon immune challenge. This seems like natural selection to me.

I understand the process. My comment stands.


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How do I reverse my insert within a plasmid?
I have a plasmid with:
...T7pro. -- RBS -- XBa1 cut site -- ProDpro. -- RBS -- AmilCP -- T -- Spe1 cut site -- T...
How do I design primers to reverse the portion in bold, such that the T7 and ProD promoters are on opposite sides of AmilCP? I am finding it difficult to understand how to design the appropriate primers.

Design your 5' primer upstream of ProDpro. with a Spe1 cut site added to the end (plus a few extra random bases to allow for better cutting). Add an Xba1 cut site to the end of the 3' primer, again with a few extra random bases on the end to allow for better cutting.
Amplify the insert, PCR cleanup, digest, cleanup again, and you should be able to easily clone into the Xba1/Spe1 digested vector that has been gel purified.

You are welcome, I hope it helps. As this seems a bit unclear on re-reading this, be sure your cut sites are on the 5' end (beginning) of each primer.

Also, if you feel an answer properly answers your question, be sure to mark it as the answer so others know that your question has been resolved.


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Exact terminology of natural selection
You don't need to explain to me what the theory of evolution is, or how it works. This question is purely about what exact meaning the word "natural selection" is ascribed to.
There seem to be multiple meanings that are given to the term "natural selection":

The process by which, in a single generation of species, the most fit individuals tend to survive. The "things that are being selected", are the individual organisms, and the "moment that selection took place", is the moment that these individuals reproduced or failed to reproduce, or alternatively, the moment that they died or survived.
The process by which, over many generations, the genotypes that result in highest fitness tend to to be selected for. The "things that are being selected" are the genes, and the "moment that selection took place" is not a single instance in time or a single generation, but a long time-span. In fact, I sometimes hear the idea that natural selection is already selecting for genes even if those particular genes don't exist in any organism. For example, if natural selection is selecting for "height", and there is a gene X that would increase height, then it is said that X is being selected for even if X does not yet exist.

Are both of these interpretations generally accepted?

Natural selection has many different nuances and interpretations different fields. A population-geneticist and an ecologist would give you vastly different answers as would the original text from Darwin. This theory has been constantly refined since its inception, in particular in response to developments in genetics and statistics. RA Fisher in particular has written about this at length. The earlier works of Dawkins also give a good summary on this topic and address common misconceptions.

Possible duplicate of What is the definition of “Natural Selection”?

"...in a single generation of species, the most fit individuals tend to survive.".  This is not correct. "Fitness" in an evolutionary context refers to how many offspring you produce. It has nothing to do with how many pushups you can do.
Yes, individual organisms are selected, and the selection process involves differential survival (to reproduce).
"The process by which, over many generations, the genotypes that result in highest fitness tend to to be selected for. "
This is largely correct.
"The "things that are being selected" are the genes..."  Yes and no. It is individuals that are selected. They live or die, depending on their traits, which are encoded by genes.
Darwin noticed the extreme physical variations that humans could create in dogs, and pigeons by selective breeding. He thought that the same process could occur in nature, and termed it "Natural selection".

I did. It seemed from the error-filled descriptions that you could use some clarification. You set up two alternative definitions, both of which were significantly flawed, as if the true definition had to be one or the other, when the true definition contains elements of both.

Biologist have a unified definition of natural selection. You presented two that no evolutionary biologist would agree with. That people outside the field are sloppy with their terminology does to mean that experts are confused.

You said the most fit survive.

Survival of the fittest lineage, not individual.

Re ""Fitness" in an evolutionary context refers to how many offspring you produce."  Not exactly.  If you produce a lot of offspring, but most or all of them die before reproducing, then you are not very fit (in the evolutionary sense).  Indeed, there are two different paths to success: have lots of offspring and hope that a few survive (like the codfish, which can lay 2.5 million eggs a year, and live 25 years or so), or like many mammals, invest lots of effort into caring for a few offspring.

That is so obvious, I did not think it needed to be stated on a biology site.

"traits, which are encoded by genes" is a little imprecise, though of course I get that we are going for simplicity here. We must accept that there is a mapping from genes to traits, but it is not a simple or linear encoding, otherwise genetic association studies would be more successful than they are; genotype-phenotype maps are complex and highly environmentally responsive (the responsiveness is sometimes encoded in the genes, of course).


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Mild introduction to selective advantage of intelligence/nervous systems in animals?
I have a general understanding of why intelligence, i.e. nervous systems in animals, is advantageous: processing information allows an animal to adapt to its environment dynamically and perform complex sequences of actions that an animal without a nervous system could not. Larger nervous systems potentially allow for more possibilities herein.
However, I am interested in a deeper understanding of the factors that cause a species to at first develop, and increase the size of, a nervous system, and different forms of cognition:

what type of environment favors the development of a nervous system in a species?
what type of environment favors life-long learning and adaptivity (neiroplasticity?) of a species (as opposed to a fixed neural structure after development in an organism)?
what type of environment favors the development of goal-oriented planning (as opposed to simple impulse-response patterns)
what type of environment favors development of "cognitive ability" in species?

Do you know of a good book that addresses questions like this?

Look at that https://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1003399

@J.A Thank you, that’s interesting. Though not precisely my question.


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Why is the anterior pituitary not considered part of the diencephalon?
According to the wikipedia page on the diencephalon, the posterior pituitary gland is considered part of the diencephalon, but the anterior is not. Is there a reason that these two lobes of the same gland are considered different enough not to be part of the same brain region?

Worth going to the wikipedia page on the pituitary:

In all animals, the fleshy, glandular anterior pituitary is distinct from the neural composition of the posterior pituitary, which is an extension of the hypothalamus.

The anterior pituitary arises from an invagination of the oral ectoderm (Rathke's pouch). This contrasts with the posterior pituitary, which originates from neuroectoderm.

The posterior lobe develops as an extension of the hypothalamus, from the floor of the third ventricle.

In other words, the different parts of the pituitary are, developmentally, entirely separate. The posterior lobe is actually part of the hypothalamus. The anterior lobe is not even part of the brain.
Lumping them together with one label happened because the anatomists who originally named the thing didn't know much about it, which is not surprising because anatomical names are quite old and understanding of the functions of any parts of the brain is quite new. Old names stick.


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Osmosis- basic questions

Hi there,
For the first picture: can someone please explain in simple terms (I started learning biology a few days ago), why the answer to this osmosis question is no?

For the second picture: The answer is left because "the tension of the balloon can resist osmosis". Can someone explain what this means?

Homework questions are off-topic on [biology.se] unless you have shown your attempt at an answer. For more information see our homework policy.

And not only is this a homework question, it is chemistry rather than biology.

Yeah, basic principles of osmosis there, but let me see if I can make it clear.  For illustration's sake, I'll take glucose as a solute and water as a solvent, but recall that the principles are true (though they can have added complexity) for other solutes and solvents (see this post on chem.SE).
Background
The basic principle behind osmosis is that conjoined systems tend toward equal concentrations.  In other words, if you have a more concentrated solution (more particles of glucose per amount of water) on one side of a membrane than the other, the solution "wants" to become equal on both sides of the membrane.
If the membrane is permeable, there's no problem: glucose can flow freely and equilibrate on both sides of the membrane.  So the solution just moves around "mixing" until there's the same concentration everywhere of solutes (ie., glucose) in the solvent (ie., water).
On the other hand, suppose that the membrane is semi-permeable, meaning that the the water can pass through but the glucose cannot.  The system still "wants" to get to equilibrium; a state of equal concentrations on either side of the membrane, but it cannot get the solute across.  What happens instead is that water starts moving from the side which is less concentrated to the side which is more concentrated.  This results in the concentration of particles on less concentrated side going up and the concentration on the more concentrated side going down, effectively equilibrating them.

Now look at Picture 1.  Intuition from all this would tell you that the concentrations would be equal.  However, there's a twist.  Osmosis can only exert so much pressure on a system, and if it has to resist a pressure, it eventually stops, even if the concentrations are not equal.
The assumption in the picture is that the balloons have the same elasticity, meaning that the balloon on the left is more stretched, and is exerting more pressure on the solution than the balloon on the right.  Therefore, it will counteract some of the osmotic pressure and push some water back onto the right side of the system.
Now look at Picture 2. Again, intuition would tell you that the balloons will have equal concentrations at the end of the scenario, but again, the pressure that the balloon on the left is exerting messes things up a bit.  Even though the balloon on the right is pushing water into the balloon on the left, it is unable to push as much as it would like to, because the pressure of the left balloon's elasticity counteracts the osmotic pressure.

Taking it to the next level
They're basically laying the foundation work for reverse osmosis in this question.  In the case of reverse osmosis, we would be artificially applying pressure to the balloon on the left, resulting in water flowing forcibly into the right container.  This can be an advantage if you want to increase the concentration of a liquid - which has hundreds of industrial usages, such as in concentrating maple syrup in Canada and the northern States.


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How do you interpret the resulting bands of gel zymography?
I would like to clear up some things for gel zymography. I understand that bright bands show proteolytic activity. But which molecular weight do these bands correspond to? Is it the weight of the active enzyme or is it the weight of the digested substrate?


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Archenteron vs Gastrocoele
What is Difference between “Archenteron” and “Gastrocoele”.
Are they same or different?
Gastrula is characterized by Archenteron or Gastrocoele or Both?


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Ploidy of Central cell in embroidery sac
In the unfertilized embryo sac in angiosperms, is the central cell considered to be haploid or diploid? though it has two polar nuclei but both of them are haploid, so I don't think it can be considered diploid.
(Actually, I encountered a question that specifically asks the number of haploid cells in an unfertilized embryo sac.)
Please help.


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Does hybridizing a specific flower affect the offspring?
If among several flowers within a plant, there is a specific flower that is slightly larger or brighter or has an extra petal, will this trait be possibly passed on to the offspring? In other words, does picking a specific flower to hybridize matter and impact the offspring or does the offspring inherit the general traits of the whole plant and any flower has the same impact? Just wondering if when hybriding a plant, I need to be selective on which flower to choose.


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Are there health benefits to donating blood?
Donating blood is typically thought of as a commensal act, benefiting the recipient at no cost beyond time and inconvenience to the donor. Some even view it as a parasitic act, wherein the recipient benefits at some health cost to the donor. But it seems reasonable to posit the opposite.
Iron has been suggested as the reason why women have notably lower incidence of cardiac events than men, until menopause that is. Why? Because some blood loss every 28 days helps to reduce iron levels in the blood. Similar logic holds with metabolic syndrome and type 2 diabetes.
Additionally, treatment-resistant high blood pressure responds — unsurprisingly — quite well to blood loss, as a bit less blood means, all other things being equal, proportionately lower pressure.
But this is speculation. Is there any legitimate evidence of the health benefits of blood donation?

I believe a number of claims in this post come across as sensationalist or false. I recommend you cite sources that support these numerous claims. For example, who is referring to blood donation as a form of parasitism?? Where did you read/hear about prevalence of cardiac events? (what exactly is a "cardiac event")? What evidence do you have for the health benefits of blood donations -- who is making those claims and based on what scientific evidence? Please update your question explicitly indicating some previous research effort regarding these points.

Simple Google searches can bring up useful and informative sources rather easily (e.g., This report from Heart.org), so please do a bit more homework to improve your question. Thanks!

@theforestecologist I was unaware that the claims in the question were controversial enough to warrant evidence-based research. The Heart.org source you supplied strongly supports at least one of the claims, feel free to edit the question :) Finally, I used the words "commensal" and "parasitic" strictly in the ecological sense, with the second implying some form of harm to the donor resulting from some aspect of the donation process. This is as opposed to parasitism in the biological sense, which isn't the meaning at all. Unfortunately, English doesn't seem to differentiate between the two.


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Increase rate of change in coding regions?
If a sequence is under selection will it acquire  more changes over time because of faster fixation than if changes were neutral? Is this true or am I missing something?

Generally speaking, there are sequences that are under purifying selection (where new mutations are often deleterious) and there are sequences that are neutral. Sequences under constant positive selection do not really exist. So, when you ask

If a sequence is under selection will it acquire more changes over time because of faster fixation than if changes were neutral?

No! If a sequence is under selection, then it is under purifying selection. As such the rate of fixation will be lower than for a neutral sequence.
If you have a sequence, where most mutations are beneficial, then it the sequence would fix new mutations at a higher rate then a neutral sequence. However such sequence don't really exist! If it were to exist, then mutations would quickly fix such that new mutations would then be deleterious again.
Of course, a single beneficial mutation has a higher chance of fixation than a neutral mutation. Also, when a mutation is under selection (whether purifying or not), the expected change in heterozygosity in the population is higher than if the mutation is neutral (the expected change in allele frequency is equal to the additive genetic variance for fitness at this locus). But those are not details you are asking about.


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Clarifying distinction between genetic recombination , translocation. and transposition
Having thought about the distinciton between these terms I have come up with the following definitions, are these correct?
Translocation describes the relocation of a chromosomal segment to a different position in the genome.
Recombination is the same except:

it usually describes a non-pathological process involving balanced, reciprocal relocation of homologous DNA segments. Translocation is its accidental counterpart.
Translocation usually related to endogenous DNA. Recombination is a broader term that can describe the incorporation of external DNA in bacteria such as transformation or transduction.
The term can be used even more broadly to include independant assortment, which also effectivley acts to "Reshuffle" genetic material.

Transposition:

essentially a special case of translocation which occurs as a result of transposase enzymes acting on mobile genetic elements.

Thanks for your help!

Translocation is a mutation . Others are not necessarily .
By the way do not confuse those 3 terms with transversion and transition mutations.
Translocation refers to 2 concepts :

In protein localizing during/after transcription

wikipedia
article

A type of mutation in a chromosome

Chromosomal Translocation
(this is about the latter)

Translocation describes the relocation of a chromosomal segment to a
different position in the genome.

To some extent yes. Also It is a type of mutation . It does not happen normally and it is a result of malfunctioning proteins, mutagens etc. More importantly Translocation happens

a) between two nonhomologous chromosomes
b) between one chromosome and itself (it moves to a different locus
of the same chromosome)

See : Campbell biology 9th.ed.2011 Chapter 15 figure 15-14
you can say that
Translocation of DNA segments between homologous chromosomes has a specific name ("duplication"). Keep in mind that most of the times we do not consider a movement of DNA to a homologous DNA a "translocation" as noted above.
Recombination is a new combination of 2 DNA . Two DNA s become one. I believe the difference between Translocation and Recombination is that Translocation usually involves a huge amount of DNA (a lot of genes) compared to Recombintation ( probably not more than 10 genes or so)
I also agree with your statements on recombination. Here's more :

it usually describes a non-pathological process

Recombination happens in several ways. We have recombination resulted from DNA repair, recombination from Cross-over during meiosis, artificial lab DNA recombination (in vitro) and also recombination by some viruses during infection ( Recall Lysogenic cycles and retroviruses) or other vectors.
Therefore recombination CAN happen in pathologic and non-pathologic procedures.
See: Molecular Cell Biology Lodish et al 8th ed Section 5.6 "DNA repair and Recombination"
See T. L. Orr-Weaver and J. W. Szostak, 1985, Microbiol. Rev. 49:33.

Transposition:
essentially a special case of translocation which occurs as a result of transposase enzymes acting on mobile genetic elements

Correct. Still I'm quite sure that we DO NOT use the term "Translocation" but instead "Recombination" for transposition.
a special case of Recombination which occurs as a result of transposase enzymes acting on mobile genetic elements.
Transposition involoves 2 or 3 genes and also it is not a type of mutation. So it is not a translocation.
See: Molecular Cell Biology Lodish et al 8th ed Section 8.3 "Transposable (Mobile) DNA Elements"

Thank you for adding some links. Please also explicitly indicate which of the sources each of your quotes comes from. Thanks

I'll keep that in mind. Still I'm not quite sure how to refer to a textbook in a correct way

Thanks, @sam, for the effort and improvements! You can refer to a textbook anyway that you deem appropriate. Just make sure when you're quoting something (in any context, really), that you include the origin of the quote in some way. Good edits :) +1


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Why don't most animals have "heads" in the middle of their bodies?
For example, humans. It would seem like, to me, if our brains and eyes, ears, etc. were situated in our stomach area they would be more protected from harm and more central than up at the top in and on a fragile skull. The same goes for other organisms. For example, horses have eyes on the sides of their heads; why wouldn't the eyes be near their stomach area? To me, it would seem like it would make it more safe and the horse could still see alot. I looked at this question, but it didn't fully answer my question.

We generally define a "head" as something that comes at the top/front of the body. I think that, we're likely to ignore examples of animals with nervous systems / sensory systems not at the top/front of their body as "animals without heads" rather than "animals whose heads are not at the top/front". For example, sponges and jellyfish.
Some animals who do, arguably, have heads, have their heads in the center of their bodies:

Image by james_michael_hill (CC BY-NC-ND 2.0)

The evolutionary - developmental roots of head position (or having a "head" at all) go very deep (although despite this, some organisms, like the starfish above, shifted evolutionarily and shift developmentally from bilateral to radial symmetry).

Regarding your concluding line: evolutionary, radial symmetry came first?

@AliceD  Developmentally, starfish and other echinoderms start out with a bilateral body plan as larvae and only become radial as adults.  So they actually evolved from a bilateral animal and developed radial symmetry secondarily.  However, some other early-branching animal lineages like cnidarians (jellyfish, sea anemones, coral) and ctenophores (comb jellies) are more or less radially symmetric.

Point 2 is a little misleading, since the oral opening of a starfish is not really homologous to the head of a human or horse.

@augurar - Thanks for explaining; I was talking evolutionary, you were talking developmentally. Glad that is sorted out:) However, removing "evolutionary" in point 2 may help to clarify. Overall, nice perspective on this question. And yes, I agree. To define the oral cavity in star fish as the head is tricky.

Animals with a "front" and a "back" are known as Bilaterians.  There is ongoing scientific debate about what the most recent common ancestor of the bilaterians, or "urbilaterian", was like.  One proposed form is a simple wormlike animal with some form of eyelike structures, a segmented body with internal organs, and a centralized nervous system.  This is contrast to animals like jellyfish which have radial symmetry with a central mouth and a network of nervous system structures distributed throughout the body.
Bilateral animals often exhibit directional motion with a defined "front" and "back" end.  Eyes and other sensory structures are positioned at the front end so the animal can sense where it is going and what it encounters.  The brain is located near the eyes because these structures require fast, intensive information processing.  This process may also have been constrained by development, since evolution occurs by gradual modifications to the existing features of an organism.  The Wikipedia article on cephalization has some more discussion of this topic.

Here is an example of two possible urbilaterians, taken from (Hejnol & Martindale 2008):

Image (a) shows a "traditional" model with segmentation, an anteriorly-located mouth (light blue), and a central nervous system (yellow).  Image (b) shows an alternate model proposed by the authors of the paper with a mouth in the middle of the body and a decentralized network of neural tissue.
Hejnol, Andreas; Martindale, Mark Q (27 April 2008). "Acoel development supports a simple planula-like urbilaterian". Phil. Trans. R. Soc. B 363: 1493–1501. doi:10.1098/rstb.2007.2239.

The brain is located near the eyes because these structures require fast, intensive information processing. The visual system is among the slowest in the body. The argument may hold for the ears though.

@AliceD It's the slowest because the information being processed is so complex.  If the brain were farther away it would be even slower.  But of course this too is speculative.

Eyes and other sensory structures are positioned at the front end so the animal can sense where it is going: In the case of insects they often have 360-degree vision. So the eyes are rostral, yes, but not because they need to see where they are going.

Small correction: bilaterian doesn't actually mean an organism with an anteroposterior/dorsiventral axis. It primarily means that these organisms exhibit bilateral symmetry i.e. symmetry across left-right axis.

@WYSIWYG True, I was being somewhat general.  Having a front/back is not at all a synapomorphy of Bilateria, just a common feature within the clade.

I think part of the reason is that our distant ancestors were aquatic - fish, for us vertebrates*.  Living in the water, fish need to be streamlined, so a long, narrow body plan works well.  Given this, and adding in the often limited visibility underwater, it makes sense to put the mouth towards the front, and sense organs near them, since they get to the food first.
This body plan got inherited by the descendants of that first fish to crawl out on land.  It would require a major re-organization of the genes to get a radically different plan, and there was no great evolutionary pressure towards some different one.  In many cases the mouth & eyes in the front works best - for predators, of course, but also think of a giraffe trying to browse on trees if its eyes were near its stomach.  For most land vertebrates, food goes directly to the mouth.  Only a few types - humans, elephants, and so on - have anything like hands to get food at a distance.  (And if you look at an elephant, they do seem partway to a mouth near the stomach plan.)
If you think about creatures like the starfish, that have a central mouth, "brain", and sense organs, their food tends to be sessile.  The starfish commonly crawls on top of its prey, and everts its stomach to digest it, so their the radially symmetric body plan works well.
*I don't know that much about arthropod evolution, but am guessing similar logic applies.

Here too is a speculative answer, but evolutionary why questions are many times speculation, as it cannot be directly scientifically tested (there are no animals with a head in their tummies), only inferred in retrospect. I will sum up a few reasons to build the eyes and ears into a solid, rotational structure and not in the torso:

The eyes are hardwired to see depth. The most important depth cue is retinal disparity, which is defined by a slight difference in the positioning of the field of view on both the retinas. This retinal disparity varies between people because it is dependent on the exact distance between the eyes. Hence, babies must learn to judge depth, as it is subjective perception deducted from a flat retinal surface. Hence, you want the two eyes to be contained in a solid, unmoldable structure and not in a bodily structure that is subject to change due to adipose tissue (belly) or breathing (rib cage).
The ears are hardwired to sense direction. The auditory nervous system does this by measuring microsecond-delays between the sound arriving in both ears to sense the azimuth. Again, along the same reasoning as for the eyes,  the ears must be contained in a solid structure.
Directional hearing is less well-developed in the vertical plane, and when a sound comes from behind it may be hard to figure out exactly where it comes from. Also, pure-tone sounds are hard to distinguish in terms of elevation. Simply turning your head helps to re-locate the source to the side, or simply being able to see it. If you have to move the whole body, you lose time and effort. In case of a T. rex running in attack modus from behind, it means the difference of life and death.
Eating needs a mouth. Consider a bat using echolocation. If the bat targets a fly using echolocation, it wants to devour it. If the ears are in the belly, it still couldn't catch its prey. The same goes for vision (birds of prey) etc.

In horses and many other prey species, the eyes are on the sides of the head and have a largely non-overlapping field of view with reduced depth perception.

@augurar, yes but the hearing arguments still count. They are examples, not fixed arguments.

Many animals do not have external ears and sense vibration in a variety of ways.  In mammals, the ear bones evolved from former jaw bones, which evolved from the gill arches in fish.  So the positioning of ears on the head is more happenstance than an inevitable outcome of the demands of hearing.

@augurar - evolution is happenstance, but a fixed position is what counts here. And hearing is sensing vibration.

Right, but in this case mammalian ears are probably positioned on the head simply because that's where the structures they came from were positioned, not necessarily because that was the best place for them.

@augurar yes but it is about them being fixated not where they are. That's my only point. On the rib cage they move about and directionality is lost in the brain due to added degrees of freedom

Let us continue this discussion in chat.

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


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Can molecular genetics make a boolean variable from a continuous variable?
In the same kind of idea than this question. Gene expression are regulated through complex interactions. The concentration of enhancers and repressors is an important aspect that dictate the level of expression of a given gene. These concentrations can take different value on a continuous scale.
Imagine a case where fitness is maximized when a given gene produce n proteins per minute if the concentration of a given protein is greater than x. If the concentration of the protein was to be lower than x, then the gene should not be expressed (0 proteins per minute are produced). In such case, it would be great if a bunch of reactants were to be able to simulate a "switch function" that would switch from "NO EXPRESSION" to "EXPRESSION" at x.
It seems to me that such switch function should be very complicated to evolve. I would suspect that all chemical reactions, including the binding of enhancer to promoter region should follow the law of Michaelis-Menten and the Michaelis-Menten function is not at all switch function. So, I have been thinking about cooperative binding. Hill's equation describes a function that is effectively a switch function given that the hill coefficient is high enough. However, seeking a bit in the literature, it's seems that the Hill coefficient never really overpass 3 (or 5 for extreme estimates). A Hill coefficient of within this range gives a logistic function but still looks quite suboptimal compared to what a perfect switch function could do.
Are there switch functions in molecular genetics that could translate a concentration into a TRUE/FALSE signal?
How well do they simulate the perfect switch function?
Are they based on cooperative binding or on some other mechanism?

References for estimate of Hill coefficients:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1435008/pdf/biophysj00200-0109.pdf
http://onlinelibrary.wiley.com/doi/10.1046/j.1537-2995.1983.23283172857.x/abstract
http://www.pnas.org/content/93/19/10078.short
http://www.ncbi.nlm.nih.gov/pubmed/8816754
http://www.fasebj.org/content/11/11/835.short
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2816740/

Positive feedbacks can be one alternative. Positive feedbacks exhibit bistability and can therefore adopt one of the two stable states depending on the initial condition. A famous example of a positive feedback switch would be that between cI and Cro in λ-phage, which repress each other. Positive feedbacks also display hysteresis: if the state of the system is dependent on an inducing ligand X such that system attains state S2 at high levels of the ligand, then to switch from S2 to S1 the concentration of X would have to be reduced below the level that was required for the S1 to S2 switch; and vice-versa. In other words, the system tries to remain in its current state.
If the transcription factors that constitute the genetic positive feedback have a co-operative behaviour then you can expect a steep switching curve.
For details see this review.

Transcription interference can also be a good mechanism to provide such switches. Transcription interference occurs between genes in close adjacency to each other. This is basically, as the term suggest, that the neighbouring genes can interfere with each others transcription (by overlapping promoters blocking transcription initiation, collision of transcription machinery on 3' ends etc). In this article all of this is well explained along with a theoretical model called Transcription Interference network.
So a switch mentioned in the question can be carried out by this mechanism. Let's take two genes (A and B) that exhibit this transcrigption interference phenomena. Also let's imagine a gene orientation where the tow genes face each other with their 3' ends like in the picture below ( part B3 but with smaller overlap at the 3' ends). The setup is that gene A is 'stronger' than gene B ( has higher transcription initiation rate), thus at the 3' prime ends it can suppress gene by knockin off the polymerase (there are many possible scenarios when two RNAP-s collide or meet one knocking off the other is just one of them). Now if gene A's activity were to be lowered then gene B could over take and nullify gene A with the same mechanism seen before. In this case transcription initiation would still occur on gene A but it could not produce viable RNA because transcription would terminate early. This results in complete shut down in gene A's expression.

(source the linked article above)
Since gene expression and transcription are 'leaky', some minimal activity is basically always present, the above mentioned mechanism can be taken care of. In the article I linked there are many other examples how such switch could be carried out by transcription interference I just took one of them. Also you'll notice that the Transcription Interference Network model is based on such switches.


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Is it possible to get a XYY genotype by the first meiotic non-disjunction?
I have read that the cause of XYY-Syndrome is a non-disjuction in the secondary non-disjunction in the meiosis. I was woundering if it is possible to get the XYY-Syndrom by the first meiotic non-disjunction? I would assume yes, since you would get XX and YY Gametes.


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Can cells show negative growth?
I know that growth is an irreversible increase in mass or overall size of a cell, organ or whole organism. I also found that growth occurs due to the net result of anabolism and catabolism.
My teacher said;
           When anabolism > catabolism - growth occurs
                 Anabolism = catabolism - no growth
                Catabolism > anabolism - negative growth
But on searching about this negative growth, I couldn't find any information. What is this negative growth? Where do you see it?

At what scale do you want to observe this 'negative growth' - cell or tissue level?

Could "negative growth" be listed as "shrinking"?

When you look at a certain mass of cells (in a petri dish, a tumor, whatever) which are in principle viable, growth can go in both directions. It can be poitive which means that the number of cells is growing over time.
It can also be negative, which results in a declining number of cells over time. We see this effect in cell growth assays, when we analyze the effect of certain treatments to our cells. Since we want to "kill" our cells with the treatment, a positive growth would indicate an unsuccessful treatment, a negative cell growth a positive treatment effect.


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Finding different Proteins with same function
Could you help me about finding two different proteins that coming from different ancestors, perform same function?
Thank you

There will be a lot!  Chromosomal dihydrofolate reductase and type II (plasmid) dihydrofolate reductase have not been derived from common  ancestor but catalyze completely the same reaction including stereochemistry by the authority of Brito.
Bacterial phenylalanine hydroxylase too is completely different in sequence of amino acids from phenylalanine hydroxylase from mammals (where plants have no such protin). The literature shows this paper Cloning and nucleotide sequencing of phenylalanine dehydrogenase gene of Bacillus sphaericus.


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Why is it beneficial for bacteria to conjugate? (Horisontal gene transfer)
Why is it beneficial for bacteria to conjugate? I would think it's more beneficial to take a plasmid from another cell, than to give yours away or "share". Not homework, I'm just curious.

I am going to try answer it. Bacteria in general has different survival tactics. In general for bacteria the best way how to surviva is as much copies as it cans. So imagine situation, when bacteria is surround with others bacteria. Then the race will bega. All bacteria wants to survive with same tactic as i mentioned. Thats mean the best way how to archived this goal is make your replication fast.
So when you take plasmid with resitantion to antibiotics its advantige to have those, but when you actually is not exhibit to that antibiotic it slow down your chance to survive (because it slows down your replication, cell division)

This article might be helpfull too here

So, it's to gain genetic variability? Because if they didn't have the ability to do HGT, the only mechanism to get genetic variability would be spontaneous mutation, which is way to slow, I guess.

@ThaleMathiassen Mutation rate is not too slow. Actually bacteria has mechanism to incries the rate. With the genetic variability you are right, HGT gets to bacteria something more, something new, what might be helpfull to survive. Good example is transduction in Griffith´s experiment.


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Is Brain Eye connections reversed in all animals or just Humans?
I know that Brain Eye connections are reversed in Humans,

Left Hemisphere controls the Right eye/Right side of the body
Right Hemisphere Controls the Left eye/Left side of the body

Is it true in other animals like Birds,Cephalopods and other creatures?
Are the optic nerves physically connected in reverse or is it internally mapped ?

The premise with which this question starts is incorrect. It is not true that the left cerebral hemisphere exclusively 'controls' the right eye, or the other way round, in humans. (See https://www.kenhub.com/en/library/anatomy/the-visual-pathway for details.)

According to Wikipedia, the nerves cross in all the vertebrates:
In vertebrates with a large overlap of the visual fields of the two eyes, i.e., most mammals and birds, but also amphibians, reptilians such as chameleons, the two optic nerves merge in the optic chiasm. Part of the nerve fibres do not cross the midline, but continue towards the optic tract of the same side. The purpose is so that the part of the visual field that is covered by both eyes is joined so that the processing of binocular depth perception by Stereopsis is enabled.
https://en.wikipedia.org/wiki/Optic_chiasm


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What happens to blood after a person dies?
After a human dies, what happens to their blood?  I know that it tends to accumulate in the lower areas of the body, whichever parts are closest to the ground, but I am wondering about coagulation.  Does the blood always coagulate?  How long does this take?  Does it ever "de-coagulate"?  If so, how long does that take?  If it coagulates, then "de-coagulates", does it "re-coagulate"?  How long does that take?
Note:  I'm asking this question because I am a fan of The Walking Dead, but I have always been a bit puzzled by the fact that on that show, the blood of zombies (who are dead) is consistently depicted as being fluid, dark red, and not coagulated at all.  I'm obviously not asking about the particulars of zombie blood, because zombies don't exist (yet).  I'm just curious as to whether it is possible for blood to remain liquid, and similar in appearance to the blood of living people, after death has occurred.  You can see my related question, on SF&F.SE, by clicking here.

Related: http://scifi.stackexchange.com/questions/106691/why-doesnt-zombie-blood-coagulate

Typical bodies in routine postmortem practice (i.e. refrigerated after being found dead, though the time interval between death and being found/transfer to the mortuary varies) tend to have at least some liquid blood (which is helpful for collecting samples for postmortem analysis), but there tend to be at least some focal areas where the blood has clotted (but the appearances of antemortem and postmortem clots are different).
The postmortem literature is generally quite scarce, but it appears that it has been noted that the degree of blood coagulation is really quite variable, with some cases at either extreme (completely coagulated blood vs completely liquid blood). Some reasons for this could relate to the mechanism of death and whether the clotting cascades were activated (and depleted) in the immediate period before death.
Malone, P. Colm, and Paul S. Agutter. "Cadaver Clots or Agonal Thrombi?." The Aetiology of Deep Venous Thrombosis: A Critical, Historical and Epistemological Survey (2008): 221-232.
https://doi.org/10.1007/978-1-4020-6650-4_13
Müllertz, Sten. "Fibrinolytic activity of human blood after death." Acta Physiologica Scandinavica 27.2‐3 (1953): 265-271.
https://doi.org/10.1111/j.1748-1716.1953.tb00942.x


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What is this fish?! Is it even real?
According to a guy in a Facebook group I belong to, this fish was caught in the Missouri River near Omaha, NE, US. I have never seen one like it in my life, not in person or photo or anywhere. What on earth is this fish?! Is it even real? I've not seen it in person, only the photo below, but he says its real.

Welcome to Biology.SE. I added a small coma to make sure you don't "belong to the fish" but to the "Facebook group". To ESL like me ponctuation is appreciable!

@Remi.b I hope it was a comma instead of a coma ;)

I thought it looked a lot like a sea robin which didn't make sense in context. Glad to find out sculpins and sea robins are very close in appearance indeed!

@Andy, we're discussing a different fish down in chauxvive's answer, and we may need a change of best answer!

Original Answer

It looks to me like a species of sculpin, for example, the "short-horned sculpin" Myoxocephalus scorpius.

http://www.luontoportti.com/suomi/en/kalat/short-horn-sculpin

Best answer

After some deliberation, and it appears the other very good answer was for some reason removed: the OP fish appears to be a northern sea robin Prionotus carolinus.

This conclusion comes from the aid of user chauxvive, so much thanks for the identification, though his answer is oddly gone. The conclusion is based off of (1) the morphology of the head and face plate, (2) the longer and tapered pectoral fins, (3) the distinguishing long feelers at the sides anterior to the pectoral fin, and (4) the more probable distribution.

It indeed looks like a sculpin +1 However, would you expect to find this species in the Missouri river? (Caution: very bad naturalist and bad ichthyologist is commenting!)

You know, my background doesn't give me any expertise here either, I'm just particularly good at acquiring information as needed. So to answer you, I'm really not sure out of experience. You definitely find sculpin in the Missouri River, but the distribution for the short-horned sculpin is certainly further north, which is why i could only provide it as an example, rather a clear-cut ID.

It definitely looks like what your answer says it might be, but I looked that up and it says its habitat is arctic coast! how would it have gotten to the Missouri River?! https://en.wikipedia.org/wiki/Myoxocephalus_scorpius

It's a really good question. I added a link to some info on sculpins, and there's a query to geographic distributions, you can use it to find a distribution for the specimen above and related. None seem to be endemic to the Missouri river if we're considering spiny sculpins, based on information I can find here

I think this is most likely it. Maybe it was an aquarium fish someone let go. Very odd though!

I think this is probably the mottled sculpin (Cottus bairdii) which is found in freshwater in NA, including the Missouri river.
http://www.fishbase.us/Summary/SpeciesSummary.php?ID=4065&AT=sculpin
https://en.wikipedia.org/wiki/Mottled_sculpin

Sculpins are a good candidate at this point, but I hadn't considered the sea robins at first. Taking a look at Prionotus carolinus, this fish is in my opinion a better fit than a sculpin. The morphology of the face and mouth, and the presence of what appear to be feelers at the bottom of the fish (as opposed to horns) confirm this, I believe.

I'm glad to see it may be indeed be a sea robin. Please vote for my answer here, if you don't mind, since my other post is gone. The pectoral fins were what I noticed first- robins have such unusual fins!
here's a great image, looks much like our fish here.
here's another anatomy of the sea robin. As you can see, it has pectoral fins much closer to this mystery fish than the sculpin.
This is an interesting discussion of the sea robin types and habitat The common sea robin is much larger than the northern and apparently the northern can stand much fresher water. Obviously this is outside of their range (which is along the coast and up brackish rivers of the Eastern US) but mystery fish could be a release. This isn't a popular tank fish, but you can buy and order them online (reference) They are pretty common in new england, apparently.

Your answer still looks like a comment and in its current form deserve being converted into a comment. You should edit it to include a picture and the reasons that make you think it is a sea robin and not something else. You can consider @kendall's answer as an example. Not however, that it is a little worthless to repost an answer that already exist (even though I understand you were first to suggest it a sea robin but again your answer just looked like a comment).

Also you should not use answers to complain about how the StackExchange sites work. You can use the meta-sites (either Meta-Biology.SE or the more general meta.SE) to ask question about how the SE sites work and suggest improvements.

I looked your strange fish and I think that it is a short horned sculpin because of its spikes.So, don't imagine that it is a sea robin because sea robins live in very deep waters (500 meters depth aproximately).In fact, I think that this sculpin was trapped in the river while it was going to the sea and the fishermen caught it.


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What exactly is extreme heterozygosity and how does it work?
What does the concept of "extreme heterozygosity" mean?
I first encountered this concept in "The Drunken Botanist". They describe that when planting a seed from, say, a 'red delicious' which was pollinated by another 'red delicious' does not guarantee growing another 'red delicious' tree. The author goes so far to say that the new tree may have almost none of its parent traits, and may barely resemble any other breed whatsoever. They argue this is caused by extreme heterozygosity.
I later found the concept of extreme heterozygosity the Wiki page for "apple"

This is because seedling apples are an example of "extreme heterozygotes", in that rather than inheriting DNA from their parents to create a new apple with those characteristics, they are instead significantly different from their parents.

On a PNAs article on Extreme genomic variation referencing extreme heterozygosity

We conclude that the extreme heterozygosity in C. savignyi is caused by a large effective population size and not an elevated mutation rate.

My understanding of population genetics (allele frequencies and patterns of dominance)
I understand homozygous diploid pairs, like pp or PP, and heterozygous pairs like pP and Pp, and hetero/homozygous dominance and recession. I also found an interesting paper on sea squirts to work through later that suggests why extreme heterozygousity is popular in large population sizes.
What I can't seem to find is exactly how "extreme heterozygousity" works. How is this different than ordinary heterozygous? Is there an entirely different context I'm missing out on? The only way I can imagine a more "extreme" heterozygosity is with triploid mismatched pairs, which can't be right. So how does the process work and what exactly defines it?

Can you please link to your article? I have never heard of "extreme heterozygosity" and it is pretty hard to say anything without seeing the paper.

Large population size tend to have higher heterozygosity and there is less drift to wipe out genetic variance. I guess this is what your paper is refering to given that you say extreme heterozygousity is popular in large population sizes. The term popular seems a little inappropriate though. You should cite correctly.

I am voting to close as you're asking to comment on a claim and a concept without providing the claim or the context in which you found this concept. Of course, I'll remove my vote close as soon as you link to the article.

Please take a look at my edits.

Thank you! That is much better with the links. I am surprised that even in the PNAs paper, they don't seem to offer any good working definition.  I voted to reopen. I also made important edits to your post. Feel free to roll back or make any further modifications.

I appreciate your edits as I'm new to the site and do want to make positive contributions. Although I've read the faqs, these changes are helpful in context, thank you.

@yingw response was right, but I will try to explain it a bit better.
Say that you had a gene, let's call it the plumb gene. This presents two alleles: P and p. Those alleles behave in a way that gives three different phenotypes depending on the genotype: PP, Pp and pp all have different phenotypes, for example, yellow, green and blue color.
If the P and p frequencies are each 0.5 on the total gene pool of the population you would expect a Hardey-Weimberg equilibrium if the reproduction and survival was random (there would be no selection).

$0.5^2=0.25$ of homozygous (PP and pp are each a 1/4 of the total population)
$2*0.5^2=0.5$ of heterozygous (Pp would be 1/2 of the population)

For what you say, extreme heterozygous would mean that the rate of heterozygosity in the population would be much higher. For example, if we found 90% of green and only 5% of blue and 5% of yellow, that would mean that there is a selective advantadge for the green individuals.

It is also my intuition that "extreme heterozygosity" would refer to any heterozygosity higher than $0.5$. That'd be great if you'd have a reference for this definition!

From the article the OP linked: extreme heterozygosity in C. savignyi is caused by a large effective population size and not an elevated mutation rate.. It doesn't seem to match your definition as large population size and (reasonably) high mutation rate won't cause a heterozygosity that is greater than 0.5.

Without reading the article, given the context that you have mentioned, I think extreme heterozygousity means that most of the individuals in the population are heterozygous (much higher than 50%). So there might be some kind of selection pressure that gives heterozygous individuals a reproductive benefit.

Great insight- So the likelihood of homozygous pairs would be highly unlikely? But in diploid pairs, would that mean that rather than two options like r and R, there would be more alternatives, like say r, R, d, and D for one spot? so you would be less likely to get rr, and more likely to get rD or something? The article isn't relevant to my question. I had heard of extreme heterozygousity in apples and couldn't find any other explanations of exactly what that meant in Punett square vocab.

I think you might be confusing a couple of things. r and R would be two different alleles. Alleles can often be thought of as different mutations (ex. R represents the original A allele, r represents an A->T mutation, D represents an A->C mutation. Its possible that the A base pair is dominant to T and codominant with C). If you find that R allele appears in 0.5 fraction of individuals, r in 0.2 and D in 0.3 then if population is in equilibrium you expect RD = (2* 0.5 * 0.3), RR = (0.5 * 0.5), Rr (2* 0.5 * 0.2), etc. If you observe fewer RR/rr/DD then there is some selection for heterozygous

According the this article: Extreme genomic variation in a natural population

There is increasing evidence that many animal species exhibit high levels of heterozygosity (1–4), which, according to the Neutral Theory, should be caused by elevated mutation rates or large effective population sizes (5).

This would imply in addition to the fact that even in a single genetically homogeneous orchard the offsprings are still very heterozygotous, that apple trees have a high mutation rate from the parents to the children.


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What is the average volume of the human Psychic tear? ("emotional tear")
My goal is to find out the volume of the average human "emotional tear" (Psychic tear - sadness, happiness), specifically when crying. I found a lot of information about Basal tears (constant lubrication), as well as Reflex tears (when slicing onions), but nothing about the volume of Psychic tears.
I should mention that in a 2016 study Is it possible to cry a river by the University of Leicester, the volume of one average tear that was used is the same as the volume of the average Basal tear - 6.2 micro liters. (Volume of Basal tears was also determined to be 6.2 micro liters in another study I found online)
I have a slight doubt that the average Psychic tear has the same volume as the average Basal tear, which is approximately 6.2  micro liters plus/minus 2 micro liters.
Could it be that both types of tears have the same average volume, and it is only the flow intensity that is different?
There seems to be nothing about this online after several hours of research. Any help would be greatly appreciated. Thank you.

Are you asking about the volume of a single tear drop or the total volume of the 'available' tear?

Yes, I'm interested in the volume of the average tear drop.