text:
Why are sugars in whole fruits not digested the same way sugars in juice are?
In this paper of the WHO, it is claimed that we should limit our consumption of free sugars:

WHO recommends a reduced intake of free sugars throughout the
  lifecourse. [...]  Free sugars include monosaccharides and
  disaccharides added to foods and beverages by the manufacturer, cook
  or consumer, and sugars naturally present in honey, syrups, fruit
  juices and fruit juice concentrates.

At first, I was wondering if the sugars in a fruit can be different from sugars in a juice. According to the answer to my question here, the sugar molecules are exactly the same in both (in the case of a 100% pure juice).
So, why this recommendation? Why doesn't our body digest sugars from fresh fruit the same way as sugars from juice? To make it simple, my question only concerns 100% pure juice with no added sugars.
I tried to find an answer and, according to the answers of this question, because our body is slow to digest sugars from a fruit, it assimilates it better. Is it right? And, if it is the case, if we eat fiber and starch with our fruit juice, it should be the same as a fresh fruit, right?

Sugars in 100% natural fruit juices are chemically the same as in whole fruits. They mainly include glucose, fructose and sucrose:

Apple nutrition data (expand the carbohydrate section)
Apple juice nutrition data

Sugars in whole fruits are "incorporated" into the fruit, which means the digestive system first needs to physically decompose the fruit and then extract and absorb sugars, which takes some time. In fruit juices, sugars are "free," so they are absorbed quicker than from whole fruits, which results in higher blood glucose levels, which is a risk factor for diabetes type 2 (Defeatdiabetes, Diabetes.co.uk).
Also, fruit juices are liquid, so they pass through the stomach quicker than whole fruits, so they fill the stomach for a shorter time and may be therefore less satiating. This can make you drink more juice than you intended, which can result in unwanted weight gain.
If you eat foods high in fiber along with juice, the fiber will slow down the absorption of sugars from the juice (Nutrients). If you eat foods that contain mainly plain starch (white bread, cookies or rice, or potatoes) along with juice, the starch will be quickly digested and absorbed as glucose and will raise the blood glucose even quicker than the sugar from the juice.
The effect of nutrients from foods on blood glucose level after meals is expressed as glycemic index (GI): the higher the GI, the higher blood glucose (Harvard):

Glucose = 100
Cornflakes (mainly plain starch) = 81
Potato, boiled (mainly plain starch) = 78
White bread (mainly plain starch) = 75
White rice (mainly plain starch) = 73
Sucrose = 65
Honey = 61
Apple juice = 41
Apple: = 36
Kidney beans (high in fiber) = 24
Fructose = 15

In conclusion, natural sugars from whole fruits, fruit juices and artificially added sugars are all digested in the same way, but sugars from juices are absorbed quicker, which can result in higher blood glucose levels. Foods that contain mainly plain starch can raise the blood glucose levels much more than fruits and fruit juices.

It's interesting that Fructose has such a low GI... considering that honey is basically made of fructose (low GI) and glucose (high GI) it falls roughly in the middle of the two.  And for reference HFCS which is always mentioned as bad maxes out at 68 which is still lower than four of the foods on that list.

It's also interesting the apple juice is only about 10% higher than apple - probably not far off the difference between apples.

@ChrisH Yes, we've bred apples for a long time to make them the easily digestable sugars they are today (though evolution did it's fair bit even before us - fruits are carriages for seeds, "designed" as easy sugar) :) It's funny how thousands of years of breeding are now essentially being reversed, because we're no longer energy deficient by default. But there's still that one difference between juice and an apple - you usually eat one or two apples, but drinking a bottle of juice is something you easily do without even noticing (though I know people who eat apples the same way :D ).

Drinking the juice without the fruit can easily lead to over-consumption. It is after all harder to eat four apples than drinking 500ml apple juice.
As the liver breaks the fructose through lipogenesis it creates fat and can cause non-alcoholic fatty liver and obesity.
Since sugar (fructose/glucose/sucrose et al.) can be absorbed already through the mucus membrane, it also causes a rapid elevation in insulin levels leading to insulin-resistance. Insulin-resistance has an impact on depositing white adipose fat which in turn has several harmful effects on the hormone production of the body. Leptin resistance from insulin-resistance alone will cause you to be unable to regulate hunger properly, even further elevating excess fat storage in adipose fat.
You may notice you don't feel full when drinking sugars, but you do much more readily when eating them. WHO is recomending against all sugar beverages and juice is just as unhealthy as soda in this regard.

"You may notice you don't feel full when drinking sugars" I'd be quite interested in some numbers about this; I certainly do feel just as full when drinking sugars as when eating the corresponding amount of fruit (which is to say, "not much"). The main difference is that you're more likely to drink juice at the same time as eating your main meal, while you'd probably eat the apples as either a snack or a dessert after a meal. Insulin resistance is a real risk, but rather than sugar from apples and juice being different, I'd expect frequency has more blame - you can sip juice for hours.

@Luaan Liquids are readily absorbed by the body. "Sip" the same volume of carrots or similar fibers and you certainly will feel full. Sipping a liter of carrots will certainly not result in the same sensation as sipping a liter of juice.

Jan's answer is great, but I'm just going to quote the paper you reference:

The systematic review of the effect of intake of free sugars on body weight
  included 30 of the 7895 RCTs and 38 of the 9445 cohort studies initially identified
  as meeting the inclusion criteria. Meta-analysis of the five trials in adults with ad
  libitum diets (i.e. no strict control on food intake) found that reduced intake of free
  sugars was associated with a decrease in body weight (–0.80 kg; 95% confidence
  interval [CI]: –1.21, –0.39). Meta-analysis of the 10 trials that involved increasing
  sugars intake (mostly sugar-sweetened beverages) suggested a comparable weight
  increase (0.75 kg; 95% CI: 0.30, 1.19). Meta-analysis of the 11 trials that examined
  isoenergetic exchanges of free sugars with other carbohydrates showed no change
  in body weight (0.04 kg; 95% CI: –0.04, 0.13).

TL; DR:

If you keep the same energy intake, free sugars have no effect on body weight
If you eat without energy controls, reducing free sugar intake has a large effect on body weight

So in other words, it's not really that free sugars are easier to digest or anything; it's just that if your food has more free sugars, you're more likely to increase your overall energy consumption. This might have relation to feelings of satiation, blood sugar levels etc., but in the end, it's that simple - if you don't watch your energy intake, limiting free sugars in your diet will likely decrease your daily energy intake.

I guess this is the link to the paper https://www.ncbi.nlm.nih.gov/pubmed/23321486 ; would you include it in your answer? There are several other systematic reviews that conclude pretty much the same: nutrients (sugars or other carbs, fats) are not fattening by themselves but only when they contribute to excessive calorie intake.

I'd challenge that "If you keep the same energy intake, free sugars have no effect on body weight". The liver has specific response to fructose through lipogenesis, so even if keeping the same energy intake, fructose has an impact on body weight. In fact, you have to have an energy depleted liver for fructose in isolation to have the same characteristics as other carbohydrates.

@PebermynteLars You can challenge that, but it's not my claim. I'm just quoting the WHO meta-analysis that the OP has a misunderstanding about.

@Luaan Have a read at the Harward Health letter quoted in my answer for an updated understanding of lipogenesis. The section "From fructose to fat" is quite clear on the mechanics. Not all sugars are equal.

@PebermynteLars I didn't claim all sugars are equal. The case the OP is asking about is about the same sugars, and regardless, my answer doesn't touch on that subject at all, because irrespective of the various mechanisms at play, the quoted meta-analysis found just one thing of statistical significance - free sugars make you more likely to increase your total energy intake. In the end, your answer says pretty much the same thing, just with an explanation of one of the mechanisms involved.


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Does the minimum spanning tree tell us anything useful about evolutionary ancestry?
Question migrated from bioinformatics stackexchange due to lack of interest.
I'm new to bioinformatics and have been reading through a bioinformatics book, and it seems calculating a phylogenetic tree is quite a complicated process.
I'm wondering if generating the minimum spanning tree (MST) from a similarity matrix would provide a decent approximation to the actual phylogenetic tree, i.e. provide some information on the evolutionary ancestry of a collection of organisms?  My thinking is that animals diverging from ancient ancestors will always be farther away than animals that diverged recently, so the MST will at least show me what animals are genetically related and which are genetically distant.
I realize this is not quite the same thing as a phylogenetic tree, but it seems to give me some of the same information provided by a phylogenetic tree, namely which animals are closely genetically related and which are distant relatives.
For reference, I'm measuring similarity based on the normalized compression distance (NCD) metric.  The metric is defined in "Clustering by Compression" by Cilibrasi and Vitanyi.
Here is an example MST using the dataset from the referenced paper.  Some parts make sense from my rudimentary knowledge of biology, like the clustering of primates.  Other parts are new to me, and I'm not sure if the relationships are just an accidental feature of the metric, MST, or if real.  For instance, cows are more related to whales instead of horses according to the MST, cats and dogs appear to have evolved from seals or visa versa, and pigs are related to a wide variety of animals: ranging from bats to rabbits to whales.
Note, the 'randgen' nodes are randomly generated DNA sequences that I added to the dataset as a sanity check.  As expected, they are off on a branch by themselves instead of mixed into the population of real animal DNA sequences.  The reason why they are clustered is because I repeat each DNA sequence 40 times to amplify the signal, and repeated short random subsequences become compressible.  The random DNA sequences are probably clustered because they tend to share random subsequences, while the mammal DNA sequences are orderly and have fewer random subsequences.
Here is the repo to reproduce the tree.
https://github.com/yters/ncd

If i search for anything as distant as a mouse and a seal i get 5000 results. I did an OTT parser but i dont know what a similarity matrix is... Dont know why or how to apply similarity to phylogeny!

Have you tried comparing your tree to phylogeny? From a cursory look the answer seems to obviously be "no".

Whales are artiodactyls just like cows and pigs, so that actually makes sense. but from looking at it they must be using a really shallow dataset because they have some strange clustering. Also the fact all your randoms are clustering makes me wonder if they are really random.

@John the reason the randoms are clustering is because I have to repeat each string 40 times to get enough compression.  So, the repetition causes the randoms to cluster, because most other sequences don't have as many random subsequences.  Their subsequences are more orderly.

@com.prehensible similarity matrix is created by measuring similarity between each unordered pair using the NCD metric I reference.  I repeat each sequence 40 times before measuring similarity to get enough of a signal for the metric to work.

@BryanKrause that is a good suggestion, but I'm also wondering about the informativeness of a minimum spanning tree in general.  It would seem the MST should show how closely/distantly related different organisms are.  Hence my question about the weird clusterings that John mentioned.  Basically, the MST seems to be much simpler than the tree construction algorithms I've read about, so it'd be great if the MST is phylogenetically meaningful.

Well, for a start, it shows nothing about ancestry. A phylogenetic tree shows where modern species exist relative to their most recent common ancestors. That concept is completely missing here.

I agree with @BryanKrause. For species relationships, this is absolutely meaningless, showing nothing about common ancestry. It could perhaps be interpretable as, for example, an unrooted haplotype network, but if there is no explicit interpretation in number of inferred differences (and of course, given the level of divergence summarised here) this doesn't make much sense either.

@NatWH if I have organisms A, B and C, and A and B are linked on the tree, while A and C are far away, can't I infer that A and B have a recent common ancestor and A and C have an ancient common ancestor?  I think this is valid reasoning because the MST is formed from the shortest edges, i.e. most genetically similar organisms, and two organisms that share a recent common ancestor should be more genetically similar than two organisms that have an ancient common ancestor.  Is there a flaw in this logic?

@yters Take an example where A and B are closely related, and C is more distant from A and B (let's say A is a tiger, B is a lion, and C is a gorilla). In your map, A and B will be connected, sure, but where is C? It should be equally far from A and B. In your map it will instead connect to either A or B. That connection is not meaningful. It should connect hierarchically to (A and B). Phylogeny has this, your map does not.

Well yes, because rates of evolution frequently vary between lineages, and genetic (dis)similarity may not cleanly map to species relationships. So you might get some signal, but most of it is probably meaningless. For example, your figure above is telling me that fin whales are as closely related to blue whales as blue whales are to Hippopotami, but it's fairly uncontroversial that cetaceans are monophyletic. We already have fast algorithms to infer inaccurate trees.

For another example from your actual example, it looks like a chimp is connected to a platypus through a rhino? What does that even mean?

Even worse, to get from guinea pig to mouse we go through blue whale and pig?

@BryanKrause Yes, it seems to only give me one directional inferences.  If C is far away from A and B then I can infer it is from a more distant common ancestor.  But, if B and C are both connected to A, then I cannot infer much about the distance of the common ancestor in that case.  I also agree my tree has a bunch of weird paths, but I'm not sure if this means MST is meaningless or that evolution is much weirder than I first suspected.

@NatWH the branch lengths are not meaningful in my graph, so I can only make inferences based on number of nodes on the path.  This means my graph says a dormouse is more closely related to a cow than to a mouse, but it does not say a blue whale is as closely related to a fin whale as to a cow.

Actually yes, it does - because you're confusing distances for relationships. Relationships are only ever discrete, defined in terms of degrees of common ancestry. The branch lengths do not matter in terms of statements of relatedness. So your graph explicitly does say that a blue whale is as closely related to a fin whale as it is to a cow, because they each are separated by one edge. If you wanted it to say otherwise, you would have to introduce a node representing the hypothetical ancestor to the tree, and @BryanKrause points out.

Basically, any algorithm that places an extant taxon on a node, not a tip, is probably not inferring a phylogeny.

@NatWH great point.  I have updated my question to not be so attached to the phylogenetic tree aspect, but whether a MST tells us anything about the evolutionary ancestry.  The reason I'm focused on the MST is 1) it's easy, fast, understandable algorithm and 2) seems to hypothetically provide some information about evolutionary ancestry.  But, your point that evolution rates can vary dramatically would imply that the MST is meaningless.  However, then I wonder how is it possible to infer anything about lineage based on DNA sequences if the rates are so variable?

@yters there are already fast, distant-based approximations for phylogenetic trees - look up Neighbour-Joining. But they are weak for the reasons we have discussed. Instead, we use more sophisticated models which can account for variable patterns of substitutions, rates across sites, and even rates across lineages, implemented via maximum likelihood or Bayesian inference. The reason that phylogenetic inference is frequently slow is precisely because the process we are attempting to understand is intensely complicated, and short cuts are often suboptimal.

I think @NatWh has explained this very well. I also think the updated question title is a bit worthless. Can it be useful? Well, maybe if you only have a group of closely related species it could give you some hints but it's not particularly efficient and there are other better tools. I'm not sure why you are reinventing this wheel.

@NatWH simplicity is also a reason I was looking at MST because the problem with an extremely complex process is that it is easy to bake in a lot of assumptions about how evolution works.  The more complex the reconstruction the more likely we are making the data fit our model instead of the other way around.  I will look into the neighbor joining method.  A bit more complicated, but it seems straightforward to implement and the wiki page has a worked example.  Thanks!

That would be all well and good if we didn't already have solid demonstrations that attempting to oversimplify this process leads to totally erroneous results (like the ones in your network). Why are you trying to reinvent the wheel?

@NatWH mostly b/c barrier to entry and understanding for standard approaches looks quite high, and they seem to have a whole lot of assumptions built into them.  Given how frequently and significantly evolutionary theory keeps changing, the built in assumptions seem like premature optimization.  I don't want to spend months and possibly years learning an outdated theory of evolution.  And, as I mentioned, just thinking about the logic of evolutionary lineage, the simple MST seems like it should provide some insight.  At any rate, the current answer provides a good way to check the MST.

I am not sure that you have thought about the logic of evolutionary lineage, or you have fundamentally misunderstood what I and other commenters have been saying. Your diagram is not a phylogeny, and doesn't show anything about evolutionary history or even lineage, because it implies that extant taxa evolved from other extant taxa, which is false.

@NatWH the main sticking point is the rate of evolution.  But, even if there is high variance in rate, there are still certain patterns in the MST.  For instance, organisms with the highest rates should be farthest from everything else, and organisms with the slowest rates and common ancestor should be closest to each other.  Organisms like bacteria will have extremely high evolution rates, and organisms with long lifespans and few children like humans and elephants have very low evolution rates.  Thus, an MST with humans, elephants and bacteria will form three unmixed clusters.

@yters If you think the main sticking point is the rate of evolution you are definitely not understanding the criticism. The main sticking point is that you've generated something that is nothing like a phylogeny. I'm also uncertain what you mean about evolutionary theory changing...the major principles have been constant for decades. All that has changed recently are minor nitpicks.

@BryanKrause the problem is I'm not a very clear communicator :)  Yes, the MST is not a phylogenetic tree.  The initial phrasing caused this confusion, which I've corrected.  The MST seems to tell us something about evolutionary lineage, based on the simple mathematical reasoning I've offered.  My understanding of modern evolution comes from a couple books, such as the bioinformatics book I linked in my question.  I've also been reading through Koonin's 'Logic of Chance' and Kauffman's 'The Origins of Order'.  The evolution they describe is not the kind I read about in 'Origin of Species'.

Your graphic is omitting nodes of the tree, branching points, which are essential for trees and phylogeny.
When you read the data file, you should count the brackets ((( ))) because they signify where the tree has nodes, common ancestors.
You should generate simple phylogeny trees, prior to doing complex data mining for similarity. The names are in latin? there are genetic distance numbers? What format and data are you using? You have given the common animal names. you may have to use a database of common-and-latin-names to be ables to search "tiger"... that database will return "panthera tigris tigris"... And then you can start crawling up and down the tree branches to search for animals related to tigris tigris, by counting brackets and marking species close to that name.
To prevent the tree exploding to 5000 animals, you can
1/define a search depth. Depth 5, Five, will not go further than five brackets: (((((panthera_tigris_tigris)(lion)(cheetah)))))
2/represent a random fraction of the species (1/100 gives 50 animals from a 5000 tree)
3/use statistics measures to select certain animals based on data mining.
If you want to travel from whales to monkeys, you will have most of the mammalian family, and you will be able to count nodes and brackets by the dozens.
Not that parsing 5000 species has a big computational load that can take 1 hour to read through once, let alone 40 times!
Whichever statistics you are using to measure similarity, number of brackets / genetic distance numbers, you should have once represented trees as branches, nodes and leaves, because that is what tree data is meant to represent.
I'd recommend that you draw a tree using nodes and random animal selection, like 1% chance the animal is drawn in the final tree. When your tree has branches and is drawing OK, change the 1% selection line for the complex MST / MCD selection.

This is a great suggestion to run the MST on a known phylogenetic tree.  Currently, I am just using a collection of DNA sequences.  If you could provide a link to a database that has both the tree and the DNA sequences for comparison, I'll mark this as accepted.

source: Stack Exchange

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

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What is ApoCas9 in the CRISPR-Cas9 system?
I am currently reading an article about a particular assay of Cas9 nucleases. In one of the experiments, they have used ApoCas9 (Apo variants of other CRISPR nucleases) as some sort of control.
But the whole article they have not defined ApoCas9? I did check online of definition and activity of ApoCas9, but came across without any fruitful results.
A universal method for sensitive and cell-free
detection of CRISPR-associated nucleases

In general, "apo" is used to indicate an apoenzyme — that is the protein part of an enzyme without essential cofactor(s).
This is actually defined in the Experimental section of the paper:

Cas9/Cpf1 without gRNA (ApoCas9/Cpf1)

So, in this case ApoCas9 is Cas9 endonuclease that is not bound to a guide RNA.

Thank you. I clearly missed that from the experimental section.

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


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Is bacillus strain 2-9-3 really 250 million year old?
I've read that in the last decade (I believe) some scientists discovered a microorganism, which they dubbed bacillus strain 2-9-3, in a crystal of salt that they think is 250 million years old and that started replicating when put in favorable conditions.
Is this really an example of the longest surviving life form?
Could someone confirm this is true and scientifically validated and provide some info and references that can be understood by non specialists. I'm a telecommunications engineer so I can understand general scientific approach and I have a basic understanding of chemistry and biology, but no formal or specific training on the subject.

Disclaimer
I was unaware of 2-9-3, but performed a simple internet search which brought up a an open-access paper from 2001 refuting the claim, and nothing more recent, suggesting that the refutation was valid. I mention this both to make it clear that although, like the poster, I am not an expert in the topic one can get considerable mileage through standard search techniques. (I do acknowledge that it does help if you know you can get access to papers through a University Library, open-access or not.)
Refutation
The claim was actually made nearly two decades ago in a paper by Vreeland et al. in Nature 407, 897-900. The date is relevant because at that time full-length sequences of bacterial genomes were only just appearing.
The paper refuting the claim is entitled “The Permium Bacterium that Isn’t” by D.Graur and T.Pupko and was published in the journal, Molecular Biology and Evolution 18 1143–46 (2001).
The authors put forward various indirect arguments for doubting the claim but they based their refutation on sequence comparison between so-called Bacillus permeans (2-9-3) and other bacteria. The first argument was that the 99% similarity of B. permeans to a contemporary halophilic bacterium, previously known as Bacillus marismortui, subsequently renamed Salibacillus marismortui, implied a relatively recent divergence from the latter. To rebut the argument that S. marismortui had also been trapped in salt for millions of years until recently a comprehensive comparison with other bacteria was conducted resulting in the phylogenetic tree shown below which was incompatible with the bacterium having not evolved in the last 250 MYr:

An independent analysis by Nickle et al. in Journal of Molecular Evolution 54, 134 (2002) came to a similar conclusion.
I am not expert enough to judge the methods of determining rates of evolution and relative distances between species, but it would appear that they are accepted by those in the field.


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What kind of spider is this, please?
I've found this spider in my bathroom today, never seen one like this, especially since I'm living in part of Europe ( Bosnia, Balkans ) that isn't known for being promised land for spiders. This one was somehow aggressive, when I touched him with an object, he immediately launched himself from the roof using his net, and when landed, he raised his "bottom"?! I've sprayed him with some water, and removed him as seen on picture, didn't want to kill him, but I'm interested if this is some venomous kind, because his head was blood red, and I've never seen this in my region

To me it seems to be an Araniella Cucurbitina ,also called a cucumber spider. It grows upto 4mm to 6mm. This type is native to the UK and they have venom which is not considered dangerous to humans.

Welcome to Biology.SE! When answering identification questions inclusion of an uploaded image for comparison will help you get a more favorable response to your posting. If you can provide details (ideally with references) for what characters led you to this identification that would be even better. ——— You may also wish to take the tour: biology.stackexchange.com/tour and then consult the help pages on the standards for how to effectively provide answers — see: biology.stackexchange.com/help/how-to-answer. Thanks!

looks more like a kind of sac spider to me


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Why haven't humans been able to make blood producing vats?
There are people in hospitals in life threatening circumstances that need blood packages, and they fully depend on blood donors' blood.
With our current technology, we have been able to "persuade" stem cells to differentiate into many kinds of cells or to replicate themselves, and even modified bacterial DNA to produce insulin. Why haven't we still made something that produces blood?

It's more difficult and expensive than expected. There are some prototype artificial blood, but they don't work as well as real blood. https://en.wikipedia.org/wiki/Blood_substitute One umbilical cord can provide 20 units of blood... but the research has hit a technical hitch. Search NEWS for artificial blood and blood pharming to find what has happened lately in the field.

Here is a history of artificial blood from 2019: https://www.popsci.com/artificial-blood-history-science/

Welcome to SE Biology. Please take the Tour to find out what the site is about and what questions are relevant. You will see that this is a question and answer site about specific biological problems, not a discussion site about why medical science has not advanced further.


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Is the Lucy fossil really what scientists claim it is?
The New Scientist has an article talking about how a baboon bone was found in the Lucy skeleton.
Creationist sites like this, https://christiannews.net/2015/04/23/evolutionary-embarrassment-part-of-famous-ape-man-skeleton-actually-came-from-baboon/, and Dr. David Menton are claiming that the Lucy fossil is another hoax like Nebraska man.
Are we sure that the Lucy fossil is not a hoax? (I am not trolling, I really want to know the truth, and when I search, I get mostly creationist sites).

Creationist websites are not a source of information. You can read the paper which the news article is referring to, or at least its abstract, and see that none of the scientists involved are claiming that Lucy is a "hoax".

Although evolution concerns biology, your question is one of palaeontology requiring expert knowledge and familiarity with the particular fossil. It is not on topic here, and you are unlikely to find anyone here more knowledgeable than the professional experts who have analysed it. If someone here with a doctorate told you it was true or untrue, why would you believe them? You have to make your own choice whether to trust the published work of generations of scientists or believe the conspiracy theorists. We can’t make it for you.

I'm voting to close this question as off-topic because it is about palaeontology not biology in terms of SE Biology.

There's dozens of other australopithecus in better condition that Lucy's bones, so there are literally 100's of times more heavy evidence than Lucy. If you want very interesting reading, check out the Homo Naledi discovery. You can read about the circumstances of Lucy's discovery on Wiki, and there are 100'ds of references where scientists have argued the finer points of the discovery.

@David paleontology is completely withing acceptable biological topics.

Per the comments, the actual paper seems pretty like a pretty straightforward operation of normal science:

Somebody noticed something that looked off about one of the bones and decided they'd look into it more carefully.
They found that yes, that bone appears to have been an accidental inclusion, and in fact the rest of the skeleton makes more sense without it.
The original conclusions are not weakened in any way, but are in fact strengthened by cleaning up a minor mistake.

It might have come out otherwise, but in this case, as in most cases, careful criticism and examination of scientific work ends up making the whole enterprise more coherent.
It's frankly not even very interesting, scientifically, which is probably why you're finding discussion of it mostly on creationist sites.  Note also that the creationist article linked uses sloppy language like "proof" and "part ape, part human" that tend to indicate a massive lack of understanding of both science in general and evolution in particular.

It is also worth mentioning the historic hoax anthropoids were discovered by scientists basically as soon as scientists were allowed to see the specimens. They are what happens when people try to circumvent the scientific process and go dirrectly to the media instead.


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Why are hydathodes called hydathodes and not hydrothodes?
I can't seem to find any etymological root for the hyda- in hydathode.  I expected the water-relater structure to be called a hydrothode, but it just isn't!

I'm voting to close this question as off-topic because it is about etymology and Greek language.

This may possibly be okay for [hsm.se] or [latin.se] but please verify in their meta/chat first. You may be asked to provide more background.

@WYSIWYG You are correct. However, those studying biology (with a similarly limited knowledge of Greek and Latin) might have a similar question when first learning about hydathodes.  Additionally, the answer given by LinuxBlanket describes the hydathode etymology as being directly related to hydathode physiology, which I think justifies its place in Biology.

The etymology of hydathode, according to the Collins dictionary, is "way (hodos) of water (hydat-)". So the correct way of dividing the word is not hyda-thode, but hydat-hode.
Also, "hydat-" is the genitive of the Greek word for water, "hydor" (literally "of water"), whereas "hodos" is in its nominative form ("the way"). If you want to say "water way" in ancient Greek, you have to use nominative+genitive, not nominative+nominative, but there might be also euphonic reasons to why is not *hydrohode.

Dictionaries are your friend.  American heritage says "Greek hudōr, hudat-, water; see wed-1 in the Appendix of Indo-European roots + hodos, way, road."  Merriam-Webster says "International Scientific Vocabulary, from Greek hydat-, hydōr water + hodos road"


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Mammal Statistics about Natural Death Versus Being Killed?
Is there data determining what percentage of mammals die a natural death (disease, old age) and what percentage die due to being killed and/or eaten by other mammals?
In watching wildlife documentaries over the years I'm accustomed to footage of mammals killing each other. So it makes me curious if wildlife mammals are more or less likely to be "murdered" by other mammals than humans are to be murdered by humans.

Incidentally I posted the question here, as there's no SE site for wildlife, and this thread directed me here.

This question is wrong on meta, I move it accordingly.

I think this question is very broad because "mammals" are a very diverse group, and because predators often target the weak and sick: do you count their predation as a natural death or not? "Murder" is also not a concept that should be applied to animals in the natural world because murder is a human social construct.


text:
Why has reproduction evolved as a choice?
From an evolutionary perspective, the purpose of an organism is to pass along its genes through reproduction. However, as humans we have a choice if we want to reproduce or not. The good feeling from climax hardly seems to be a strong enough incentive to make people want to have sex, especially when that good feeling can be achieved in many other ways.
So why did we evolve to have a choice whether we want to reproduce or not, when it's defeating our biological purpose? Why didn't we evolve a different "reward system" than a climax to goad us to have sex, and is it likely that in the far future we will acquire a different, stronger reward system?

All organisms have some level of control over reproduction. Nothing unique to humans. There are many conditions in which reproduction is costly (for e.g. food shortage). Even bacteria won't reproduce if the conditions are not favourable. The word "choice" is a very anthropocentric term.

I've voted to close your question as off-topic as any answer to either question "Why didn't we evolve (some other way)" or "Is it likely in the future…" can only be speculative. This is not a discussion site, it is a question and answer site about (single) "practical detailed questions in biology". And in any case your premise seems false — if it hadn't worked we wouldn't be here.

Ask a typical parent how they feel about their children and I think you'd realize there is more than just one reward system... If it was only orgasm, babies wouldn't survive long enough to care for themselves.

@David All hypotheses are speculative at first. My premise, that an organism's biological purpose (from an evolutionary standpoint) is to pass on its genes, is not false.

I had thought your premise was that there was a problem with the way we had evolved because it risked the survival of the species.

Possible duplicate of Why do some bad traits evolve, and good ones don't?

@P.SN, Evolution does not have a purpose or intent, it is just a description of how some structures tend to make similar replicas of themselves in certain situations that have occurred in the past.  There is no intent or purpose that an organism reproduce, it's just that some organisms inherit structures that lead to replication if conditions it finds itself in are suitable, as happened for its ancestors.

Why has eating evolved as a choice, because it is not always advantageous to eat something.

I'm actually quite curious about the many other ways to reach a good feeling equivalent to an orgasm. That is certainly interesting academically as well as practically.

Evolution happens also on the level of social groups: It may be an advantage for the survival of  a group when many of the individuals do not have own children, but support the parents of other children, leading to few strong children instead of many starving children.

Your fundamental mistake is this statement:

the purpose of an organism is to pass along its genes through reproduction

Evolution does not actually involve "purpose" in any way.  Rather, it is just the observation that populations with traits that more reliably produce descendants end up with more descendants.
With regards to humans, being really smart and flexible creatures has been extremely advantageous for us as a population (so far at least). One of the side effects of that intelligence is that we have a lot more agency in our choices than many other forms of life---and also a maddeningly huge amount of variation in our world-views and preferences (whether consciously chosen or otherwise).
That includes one's attitude toward sex and reproduction, and so it's entirely unsurprising that there are many people who choose not to have sex, or who choose to have sex but not to reproduce.
At the same time, no matter what your personal opinion on the sufficiency of our drives may be, it seems to be enough to motivate most others to have sex and children. As such, there doesn't seem to be anything selecting for that motivation to change, because the people who are insufficiently motivated to have children will not tend to have descendants, while those who are sufficiently motivated will.
Bottom line: humans are reproducing effectively and those who reproduce are evolutionary selecting for the status quo---the same drives that already motivate them to reproduce.


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What are the evolutionary reasons behind men being taller than women?
Human men and women are sexually dimorphic: there are some phenotypic differences between men and women.
Men being taller than women is an accurate stereotype. Overall, men are on average 13 centimeters taller than women. The most extreme example is Macedonia, where the average man is 18.5 cm taller than the average woman.
When you look at animals, I think it's pretty intuitive to think that females are often larger than males from the same species. Spiders, fish, insects, some birds, there's an endless list of examples of bigger females than males. This is explained by a variety of different reasons depending on the species, from mate competition to the ability to bear children. So why would human males be so much bigger than women?
We all know that there are a lot of factors behind the height - and, on a related subject, strength - differences between the sexes. There are some genetic factors, as pointed out in this interesting Quora post about the topic. We also know that nutrition has a large impact in growth. In a word, we know what causes the height difference between men and women. There is a great post about it here. But I couldn't find any conclusive evidence as to why men are taller than women.
Is this because women naturally like tall men? Did prehistoric men have to be taller than women in order to thrive? Or is it just genetic drifting that, more or less randomly, led to this height difference?

The motivation behind my curiosity is feelings-driven. A while ago, my dad said during a conversation that he once "saw a documentary in which they explained that early men stole all the good proteins from the women, so they could grow taller and stronger unlike the poor females." As much as I love and respect my dad, I have a hard time believing that men are natural culprits and thieves. I am by no way making this post just to "prove him wrong" - I am absolutely interested by the topic and would love to know more. Also, if anyone knows the documentary he was talking about, I would be glad to give it a watch.
All apologies for any bad English you might find. Please tell me if I make recurring grammar mistakes.

In many mammalian species, the male is larger than the female. It is not a special case in humans.

I assume by asking why, you are asking about the distal evolutionary causes, and not the molecular mechanisms that account for these things.
(Important disclaimer: these causes are difficult to be certain about; they require a fair amount of informed speculation.)
With that said: it is widely agreed upon in evolutionary biology that human males, as in other mammals, are thought to be larger mostly due to sexual selection. In other words, size is sexy, and sexy individuals fare better with respect to mate choice, on average. Sexual selection can also work via male-male competition. There may be other causes that are relatively minor contributors compared to this one.
Notice, however, that in humans, females evidently do not remain tiny with respect to males, but they get 'dragged along' in terms of their height, so that males are not drastically different in height (unlike, for instance, in elephant seals). This too may be a result of sexual selection, quirks of physiology across the sexes (e.g. genetics of dimorphism), or even natural selection. Think hip size and the size of human skulls.
Additionally, differences in development time (e.g. length and onset of puberty) can skew body size. Humans certainly exhibit dimorphism with respect to development.

Thank you for this very interesting answer. Indeed, my question was about distal evolutionary causes, and not molecular things. The example of the elephant seal is great, I was not familiar with this.
I can't vote on your answer due to low rep but I greatly appreciate it.

Women do not get dragged along, more extreme sexual dimorphism exists in other great apes. Differences in sexual dimorphism is well predicted by levels of competition and cooperation.

Sexual selection isn't an arbitrary process, it's generally based on objective evolutionary qualities. So shouldn't it rather be: Size is better, so size is sexy. But then this answer is really missing the point?

Certainly sexual selection can be a completely arbitrary process and in many (in many clades, most) species it is completely arbitrary and devoid of any real hallmark of signal of fitness. Sometimes, things just become sexy and this drives traits for that sexiness to be selected, and it often also sometimes drives species to extinction due to the trait rendering individuals unfit for competition in their habitats. Beetle weaponry and bird coloration and generally all sorts of ornamentations come to mind.

Sexual selection would explain tall people. But it doesn't explain taller MEN. Because the same tall men would produce both sons and daughters. Unless the argument is that tall men would produce more sons (e.g. the children of Presidents of the United States), while short men produce more daughters.

More details to support @SPr's answer, from the abstract of Plavcan (2012): "Sexual Size Dimorphism, Canine Dimorphism, and Male-Male Competition in Primates: Where Do Humans Fit In?"

While dimorphism in primates is associated with agonistic male mate competition, a variety of factors can affect male and female size, and thereby dimorphism. The causes of human sexual size dimorphism are uncertain, and could involve several non-mutually-exclusive mechanisms, such as mate competition, resource competition, intergroup violence, and female choice. A phylogenetic reconstruction of the evolution of dimorphism, including fossil hominins, indicates that the modern human condition is derived. This suggests that at least some behavioral similarities with Pan associated with dimorphism may have arisen independently, and not directly from a common ancestor.

mate competition: bigger males can beat up smaller males to gain access to females
resource competition: bigger males can beat up smaller males to gain access to resources (and hence survive better/gain access to females/have their offspring survive better/etc.)
intergroup violence: bigger males are more likely to survive & win when fighting with smaller males in other groups
female choice: as @SPr says: "size is sexy, and sexy individuals fare better with respect to mate choice, on average"

And "the modern human condition is derived": that means that our best guess is that human dimorphism and behaviour have evolved since we split off from the rest of the primates; this makes it slightly harder to use non-human primates as a model.


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Figure out which is the risk allele from SNP in GWAS article
I do neuroimaging research, and am interested in dabbling in genetics. I am trying to create an anxiety risk profile score from several SNPs shown to correlate with measures of anxiety in past GWAS studies. However, many of the GWAS studies, such as this one (https://www.biorxiv.org/content/10.1101/540245v1) don't seem to explicitly state which allele was the risk allele (i.e. which allele was positively correlated with anxiety). It's likely that in most cases the minor allele is the risk allele, but I don't want to assume this. Am I missing something in the text of the example manuscript, or would I need to contact the author to find this out?

I suggest you contact the authors, because they do not show the direction of effect. They should share this information, otherwise you will never be able to tell which one is the allele that gives risk and which one is protective. And, as you said, it is better if you do not assume that the risk allele is the minor allele. There is no reason to be like this.


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Is there a name for survival of the fittest in a single family?
Imagine a case where the children of a bird each have a 50% chance of being born blind.
But the bird always has on average 4 chicks. So on average 2 will be blind and 2 sighted.
(Perhaps this could evolve if the energy needed to create a chick with 100% probability of being sighted is more than the energy needed to create two chicks each with 50% probability of being sighted. The eye being a very complicated organ).
Now, the mother brings food to the chicks and only the sighted children eat the food. The blind chicks (the 'runts') are thrown out of the nest. (It is common there being a 'runt' of the litter. So this scenario has some truth in it.)
Thus all adult birds of this species are sighted. (The 'fittest' birds).
(This is a kind of surival of the fittest but in a family setting.)
Is there a name for this kind of process? This could happen in any animal that has on average more than 2 children. Where it might be cost effective not to make sure that 100% of the children are fit, because the weakest will die anyway.
Secondly, imagine a scenario, where there is a surplus of food one year, so that even the 'runts' make it to adulthood. Now, 50% of the adult birds will be blind. And people might say "There is an epidemic of blind birds". Can we make comparrisons with the theory that there is "an epidemic of myopia" in modern human populations, possibly due to modern medicine decreasing childhood mortality?

"Survival of the fittest" is a flawed summary of natural selection that covers up some nuance in the theory (and was not originally used by Darwin but rather a phrase used to try to explain the theory, and then, probably unfortunately, edited into Darwin's own work). Your question seems to lack a basic understanding of heritability and evolution. In particular, your model seems to not involve a heritable trait.

Is there a name for this kind of process? You described a non-heritable lethal trait with a prevalence of 0.5 (which is very unlikely). Does this answer your first question? I don't understand what you mean by Where it might be cost effective not to make sure that 100% of the children are fit, because the weakest will die anyway.. Can you please clarify what is on your mind?

Your second question starts with Can we make comparrisons. One can only compare whatever they want to compare. One can even make analogies. But that does not mean there is much to be taken from it. Can you please write a clearly defined question or, otherwise, maybe just remove this second point.

@Remi.b Yes, the biology needed to grow a bird with 50% likely of being blind might cost 3 units of energy. But the biology needed to grow a bird with excellent vision might cost 500 units of energy. (Think of buying two cheap cameras vs buying one expensive one.) It might be more cost effective to buy the cheap cameras even though they are likely to be defective. As long as you buy enough of them so that at least some of them work.

@Bryan. Yes I understand evolution. That is why I asked is there a name for this process. Which is not standard evolution.

@zooby I understand evolution Take no offense but the phrasing of everything in your post strongly suggests that you don't have much knowledge in evolutionary biology.

@zooby You will probably want to have a look at wikipedia > siblicide. A famous example of siblicide (not listed in the wikipedia article) is the case of shark that kill each other in the mother's womb (see this popular article)

@Remi Of course i'm no expert. I will look at the shark thing. sounds intriguing.

I've read The Selfish Gene and Darwin's book. I don't know what else you want from me? Since I wasn't talking about evolutionary biology I don't know how you came to that conclusion.

This competitive relationship often goes by the simple and intuitive name of sibling rivalry, and its closely related idea of parent-offspring conflict.  While it may seem counter-intuitive for evolution, you must remember that while it's better for the parents to have multiple surviving chicks, it's better for the chick to have less siblings to compete with for insufficient food.
We do in fact, see this type of behavior amongst humans as well: who amongst us with a sibling has not competed for parental resources and affection? Fatalities, though, are much rarer than in birds that routinely have more chicks than they can support, because our species are different.

Yes, "sibling rivalry" is probably the right phrase. By question is really, whether there is a name for an animal deliberately making children compete in order to weed out the most fittest or healthiest and discard the runts of the litter. (And also since humans used to have lots of children, whether this sibling rivalry is good for health of a population.)

Also, I make a side point, that if an animal was to stop having lots of children and so there was less sibling rivalry, would this be bad for the health of the species?

@zooby In general, there's no "deliberately" involved, since you're not talking about animals with sufficient cognitive faculties to make such a choice.  Even with humans, how often do you think that a parent deliberately makes their children compete, vs. falling into it as a side effect of their own choices and patterns?  As for whether it's "good" for the population---it doesn't have to be, it just has to be a stable equilibrium.

Well I mean deliberate in the sense of a stable equilibrium, like you say, that has evolved over thousands of years. Perhaps birds evolved under the assumption their chicks compete. Perhaps humans evolved to have their children compete, and stopping the children compete will upset the equilibrium and be bad for the population's health however one might define it. Perhaps it is "natural" for humans to have 10 children who fight to the death leaving only the two fittest to reproduce.

What I'm trying to say is, whether there is reasearch into how much "sibling rivalry" is essential for maintaing the health of a population. Or having enough children incase some of them are weak is important vs having only two children and hoping they are both strong.

@zooby It's a spectrum, and species can end up at different set-points along it.  See, for example the notion of r-selection vs k-selection: https://en.wikipedia.org/wiki/R/K_selection_theory

I think "r-selection vs k-selection" is pretty much an answer to the question.


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How do cone cells underneath capillaries receive light?
Came across this image of retina's cross section:
1) How do the cone cells directly underneath the blood vessel ('demarcated in the picture') receive a spectrally correct representation of the incident light? Wouldn't the blood absorb most of the spectrum, leaving only red behind. Is it because the blood vessel is too thin?
2) The fovea region seems to be void of any such capillaries, how do the cells then receive nutrition and oxygen?

1) The photoreceptors in fact don't receive all the light because some of it is absorbed by the blod vessels and nerve cells above the photoreceptors. The Wikipedia article on the retina states:

Although the overlying tissue is partly transparent, and the accompanying glial cells have been shown to act as fibre-optic channels to transport photons directly to the photoreceptors, light scattering does occur.

Here is the direct link to the article describing the fiber-optic effects.
The red blood cells in the capillaries do absorb some light but the brain corrects for the color distortion. The most notable effect of the capillaries is that you can actually see white blood cells moving across your retina when looking into the skye:

The white blood cells in the capillaries in front of the photoreceptors can be perceived as tiny bright moving dots when looking into blue light. This is known as the blue field entoptic phenomenon (or Scheerer's phenomenon).

However, our eyes are still extremely sensitive:

A rod cell is sensitive enough to respond to a single photon of light.

Furthermore, the inverted retina actually protects the light sensitive cells from overexposure and damage by UV light.
Interestingly, cephalopods (e.g. squid, octopus, nautilus) have their photoreceptors on top of the retina, making their eyes more sensitive and better adapted to the low light conditions of the deep sea.
2) While blood circulation is necessary to maintain nutrient concentrations in large tissues, small distances can be covered pretty well by diffusion of the nutrients through the tissue. The fovea is only 5.5 mm in diameter which is small enough for diffusive nutrient supply.


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Is presence of air necessary for silica gel to absorb moisture?
I am a biologist currently doing field work where I need to quickly dry leaf samples using silica gel crystals.  I use the orange indicating kind that are 2-4mm in size.  The setup is like this.  I stuff 1-2 leaves in a manila paper envelop which I drop in a ziplock bag containing ~1/8th cup of silica gel.  Then I squeeze out most of the air before sealing the ziplock.  The end goal here is to extract DNA from dried leaves when I am back in the lab.
I have had varied results in terms of drying and looking to achieve the maximum efficiency.  Recently it occurred to me whether squeezing air out is actually counterproductive to fast drying.
So my question is, whether presence of sufficient air necessary for silica gel to absorb moisture from leaves?  Essentially I am creating partial vacuum inside the ziplock.  Is that keeping silica from doing its job?

Welcome to Biology.SE!  I don't think you can create any sort of vacuum by squeezing the air out of a bag — the pressure inside and outside will be identical.  What you have done is minimized the volume of air inside the bag.  I would guess that the placement of the silica gel relative to the leaf and the porosity of the paper would be the most important factors in how rapidly the moisture would be transferred.

@tyersome I agree, the proximity of beads to leaf seems to be pretty important for drying.  It was mainly for this reason that I started squeezing air out so the beads wouldn't move as much.  I try to get them to cover the envelop.  Next, I will try using tea bags which should allow much rapid exchange of vapor.

That sounds like a good strategy — making sure the leaves are covered by silica gel on both sides should also help.  The waxiness of the leaf cuticle could also be a significant barrier — could you try crushing the leaves or dipping them in solvent?

@tyersome Crushing leaves is quite impractical as I am often collecting upwards of 60 specimen on a given day.  Moreover, contamination between samples is an important concern.  The less contact I make with leaves, the better.  I work with poplar species in the mountain west USA which tend to have sticky balsam on cuticle, which likely is also slowing the drying process down.


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What are the best plants to cultivate yeast from?
I know that cultivating yeast from potatoes yields a good brewing yeast and that forms of wheat make good baking yeast, however; I have not seen much information on other useful plant yeast cultures. What are some of the other plants that offer potentially useful yeast cultures?
*edit : corrected my error in thinking yeast was produced by plants due to a answer given

Are the wine-producing yeasts that live on grapes too obvious?  (FWIW, the plants do not produce the yeast.  Yeasts are independent organisms which colonize the surface of some plants, among many other things.  But they, and other fermentation-producing organisms, can be found elsewhere.  See for instance sourdough bread.)

Grapes are a bit obvious but it follows the main idea of my question. I'm curious about plants that are not commonly used. There isn't a directory that I could find that lists yeast cells commonly fond on specific types of flora

Yeast colonize the surface of many plants — for example they are a typical part of the normal surface flora (microbiome) of fruits such as grapes1 and pears2.
As you can see from the second reference, yeast can compete with other microorganisms to delay rotting of the fruit.
You might also find the "Uses" section of the wikipedia article on yeast and this article on winemaking to be of interest.
References:
1: Zahavi, T., Droby, S., Cohen, L., Weiss, B., & Ben-Arie, R. (2002). Characterization of the yeast flora on the surface of grape berries in Israel. VITIS-GEILWEILERHOF-, 41(4), 203-208.
2: Benbow, J. M., & Sugar, D. (1999). Fruit surface colonization and biological control of postharvest diseases of pear by preharvest yeast applications. Plant Disease, 83(9), 839-844.


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Do bacteria exist which live exclusively on non-organic matter?
Are there bacteria which consume exclusively non-organic matter? Meaning that they do not require organic matter from other organisms to stay alive and reproduce? A completely pacifistic bacterium.
Or phrased differently, are there bacteria which can stay alive and reproduce indefinitely with only non-organic matter present (plus sunlight or thermal vents etc.)?
I'm asking specifically, to name one or more bacteria species which can do this.

Welcome to Biology.SE!  It is expected that you will do research on your own before asking questions here — in particular you would benefit from reading up on bacterial ecology — there are hundreds if not thousands of examples of such organisms easily found.  For example you could start with the wikipedia article on autotrophs: https://en.wikipedia.org/wiki/Autotroph. –––––––– For details on how to use this site, please check out the tour: biology.stackexchange.com/tour and then the help pages on how to ask questions on this site: biology.stackexchange.com/help/how-to-ask. Thanks!

Could you clarify your question. What do you mean by non-organic? A chemical definition would be compounds that contain carbon. However, all organisms contain carbon which ultimately comes from carbon dioxide. Do you include photosynthetic bacteria? If so, just look them up on Wikipedia etc. And what on earth do you mean by pacifistic? Are you under the impression that most bacteria survive by killing and eating other bacteria? This is a science site — you need to choose your words carefully so they convey precisely what you mean.

Sulfate reducing bacteria get their energy converting sulfate to hydrogen sulfide. They are relatively common and may have been the source to turn some oil/gas deposits "sour". Specifics in Wikipedia.

But that’s answering only half the question. How do they get the C to use the energy to build their myriad C-containing structural components?


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Are there any known plesiomorphies of all living mammals relative to a newer trait state in all living reptiles?
If I understand how a "trait" is defined, a turtle's shell is a synapomorphy relative to mammals and the common ancestor of living amniotes. The same would go for a snake's limblessness, etc. But are there any synapomorphies all living reptiles have in common relative to an older trait state found in most or all modern mammals? Traits modern mammals share with the common ancestor of living amniotes which reptiles do not also possess?

What do you mean by reptiles? Do you mean "Reptilia" or do you mean " turtles, crocodilians, snakes, amphisbaenians, lizards, tuatara". See this post and that post.

"living reptiles" so what you listed plus birds.

So not reptilia, that would be Sauropsida or possibly diapsids, in which case the answer is no, since mammals fall outside the clade.

What your asking is really unclear, especially when you use terms like "relative" Are you asking for a plesiomorphy uniting mammals and early amniotes but excluding Sauropsids? You may want to read this so you can use the right terminology. https://upload.wikimedia.org/wikipedia/commons/thumb/b/bb/Reptilia-Sauropsida.jpg/800px-Reptilia-Sauropsida.jpg

Yes, that is my question. I don't see how my terminology is incorrect. Is "living reptiles" not a correct description of a subgroup of sauropsids? Do "living reptiles" not constitute a monophyletic clade in contrast to things like reptillomorphs that gave rise to mammals and modern reptiles? Is the term "reptile" just not used at all anymore despite common usage?   That was my question, traits that unite mammals with the reptillomorph common ancestor of living amniotes, in relation to a synapomorphic trait in living sauropsids.

No living reptiles do not constitute a monophyletic clade, neither does reptile by itself.

Early mammals and early reptiles are both anapsides but modern mammals are synapsids while modern reptiles are diapsids (or at least ancestorally diapsids in the case of turtles).

Modern reptiles aren't monophyletic if you include birds?

modern reptiles is monophyletic if you include birds, but it does not include the ancestors of mammals nor the common ancestor of amniotes.

The following article lists some distinctive skeletal differences in synapsids and sauropsids, and reptilia and non-reptilian amniotes:

Sauropsida is defined as "reptiles plus all other amniotes more closely related to them than they are to mammals" (Gauthier, 1994). The characters supporting Sauropsida include the following:

Presence of a single coronoid. Synapsids and the diadectomorph Limnoscelis have two coronoid elements. The coronoids are bones on the dorsomedial surface of the lower jaw.
Supinator process parallel to humeral shaft and separated from it by a groove. In synapsids and diadectomorphs, the supinator process is strongly angled relative to the shaft.
Presence of a single pedal centrale. Two centralia were present in the tarsus (ankle) of synapsids and diadectomorphs.

Reptilia is defined as "the most recent common ancestor of extant turtles and saurians, and all of its descendants" (Gauthier et al., 1988). Characters supporting Reptilia include:

Tabular small. The tabular (a bone on the posterolateral corner of the skull table) of early synapsids and diadectomorphs is large, but reptiles have only a small tabular, when it is present.
Suborbital foramen present (Fig. 1B-D). The suborbital foramen is a small hole near the lateral edge of the palate, between the pterygoid, palatine, and ectopterygoid (or jugal, when the ectopterygoid is absent). This structure was not found in early synapsids and diadectomorphs (Fig. 1A).
Supraoccipital anterior crista present. The supraoccipital of mesosaurs, synapsids, and diadectomoprhs lacks anterior parasagittal flanges. The supraoccipital of reptiles has a paired anterior parasagittal flange called an anterior crista.
Supraoccipital plate narrow. The supraoccipital is a bone in the back of the braincase. The supraoccipital plate of mesosaurs, synapsids, and diadectomorphs is broad and extends farther laterally than the postparietal.

Phylogeny and Classification of Amniotes, Michel Laurin and Jacques A. Gauthier


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(How) do horizontal pupils dialate?
I was looking at mongoose eyes in particular, but my understanding is:

Circular (human-like) pupils simply get larger/smaller depending on light levels, no change in "shape"
Vertical slit (cat-like) eyes get wider or narrower, from "almost a line" to "almost a circle".
Goats, mongooses, etc. have horizontal "bar" pupils — more-or-less straight edged across the top and bottom, with rounded (semicircular?) sides.

Do horizontal bar pupils, like those of a mongoose, change size in varying light levels? If so, how does their shape change? Do they get taller or narrower? Do the top and bottom become convex or concave? Does the radius of the sides increase? Does anyone have good reference pictures or diagrams?

There is a large variety of pupil shapes and ability to contract pupils in animals. The vast majority of animals can contract their pupils, including goats and mongooses. Prey animals tend to have horizontally slit pupil, like goats. Mongooses (carnivores) seem to be an exception in that respect. Here is a picture of a sheep's pupil fully dilated and fully contracted:

As you are particularly interested in mongooses, the paper "Characteristics of  the eye of the Indian mongoose (Herpestes auropunctatus)" reports the following concerning pupils dilation induced by topical application of pilocarpine: "The dilated pupil is approximately 3.80 mm in diameter and  slightly oval,  the long  axis  being  horizontal. [...] The constricted pupil is teardrop-shaped, with horizontal  and  vertical  dimensions of 2.5 and 1.1 mm, respectively,  the  narrow end of the  aperture being the nasal end." However that shape seems specific to Indian mongooses because if you search for images of mongooses you'll see that most of them have oblong pupils when contracted. But all of them seem to have almost circular pupils when dilated. Here you can compare the pupil of a mongoose during the day (strongly contracted) and at night (mostly dilated, the color comes from the night photograph):

Nellis, D. W., Sivak, J. G., McFarland, W. N., & Howland, H. C. (1989). Characteristics of the eye of the Indian mongoose (Herpestes auropunctatus). Canadian journal of zoology, 67(11), 2814-2820.


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Are there completely self-sufficient autotrophs?
Are there completely self-sufficient autotrophs which can survive and reproduce indefinitely by consuming exclusively non-organic matter (plus energy from sunlight or thermal vents etc.)? I'm asking specifically.

This is essentially the same question you already asked, but expressed in a more scientifc manner. Please delete the previous question.

It really depends on what you mean by "organic matter".  No cell is going to be able to grow and reproduce without an appropriate source of CHON atoms (plus lesser amounts of the other necessary elements).
So, if by organic matter you mean CHON+, then no, everything needs organic matter to grow and reproduce.
If by organic matter, however, you mean natural organic materials like soil or groundwater, then yes, there are lots of things that can live on chemical mixtures that can be produced by purely synthetic means.  A simple example is M9 media, which is a commonly used bacterial culture medium.

@user1136 You should not answer in the comments: if you have an answer prepared, please post it as an answer and not as a comment.

@user1136 — Re your last sentence. This is not a discussion site so don’t embark on one. Just write an answer of your own to the question as an answer. (I have already flagged for deletion the answer you posted as a comment, which ignored the explicit injunction not to answer questions in comments. I’d advice you to copy it into an answer before it disappears.)

Why would groundwater be considered an organic material?

@jamesqf Natural water sources are typically full of dissolved or suspended organic materials https://en.wikipedia.org/wiki/Organic_matter#Aquatic

@jakebeal: Natural water sources, yes, if you include lakes & streams.  But at least in my experience, most groundwater has little or no organic material.


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Modern views on the correspondence of moles
In his Memoirs, Casanova wrote:

In the midst of the dimple which added such a charm to her chin Esther had a little dark mole, garnished with three or four extremely fine hairs. These moles, which we call in Italian ‘neo, nei’, and which are usually an improvement to the prettiest face, when they occur on the face, the neck, the arms, or the hands, are duplicated on the corresponding parts of the body. I concluded, therefore, that Esther had a mole like that on her chin in a certain place which a virtuous girl does not shew [...]
I then explained to her the theory of the correspondence of moles on the various parts of the human body, and to convince her I ended by saying that her governess who had a large mark on her right cheek ought to have one very like it on her left thigh.

Does contemporary biology/medicine support this law? Are there publications on it?

Law? If you go around looking for moles on women’s thighs you are certainly likely to end up with the law after you. Come on, are you as gullible as the women who fell for Casanova’s nonsense?

There are a lot of different types of moles out there, and while there are correlations in locations of some classes based on their nature, there is nothing like the correspondence described.
There is, however, a long history of attempting to attribute meanings and patterns to moles, however, since essentially random phenomena like this tend to engage our human biases for pattern-making.


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semantic similarity measurement for cell line ontologies
I have a set of cell line pairs and I want to know to what extent the pairs are similar based on their ontologies.
The problem I have is that I have found a Python library called Fastsemsim, but it has many similarity measurements. Or to be exact, there are actually many ontology similarity measurements. And I want to know which similarity measurement is best suited for my case (cell line ontologies similarities). There might be a couple of good ones that are good for cells ontologies.
These are a set of similarity measurements that are available in Fastsemsim.
Semantic Similarity

SemSim.TermSemSim
SemSim.ObjSemSim
SemSim.ObjSetSemSim
SemSim.SetSemSim
Specific Semantic Similarity measures
SemSim.MixSemSim
SemSim.avgSemSim
SemSim.maxSemSim
SemSim.BMASemSim
SemSim.SemSimUtils

Source:
https://fastsemsim.readthedocs.io/en/latest/library.html

If your question is about python libraries, it would probably fit better (and get more answers) on SE Bioinformatics.

Yes, as it's about algorithm selection SE Bioinformatics is likely better. Also, I think you are using "ontologies" to refer to the terms/classes, when the ontology is in fact the collection of such terms. E.g. CLO and Cellosaurus are ontologies, and they have terms representing particular cell lines.


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Blinded sphinx first instar caterpillars not eating
I've got several freshly-hatched Blinded Sphinx Moth caterpillars (ID'd the mother), but they don't seem interested in any of the host plants I've offered. I had birch and basswood ready, and so far it's only basswood that's even gotten a nibble. I have access to cottonwood, willow, and aspen, and will probably go pick some up soon.
My question is-- is there a reason a caterpillar would ignore a plant that is a known host for the species?
Thanks!
Cal


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What is the percentage of food that goes to a lamb fetus?
Does any one know the percentage of food eaten by a pregnant ewe that goes to the lamb fetus?
Specifically how much does the mother take for her body from every one kilo of food
and how much does the fetus take?

Welcome to Biology.SE! It is expected that you will do research on your own before asking questions here — for example you could start with this: https://extension.oregonstate.edu/animals-livestock/sheep-goats/nutrition-lambing. –––––––– For details on how to use this site, please check out the tour: biology.stackexchange.com/tour and then the help pages on how to ask questions on this site: biology.stackexchange.com/help/how-to-ask. Thanks!

In addition, since the answer to this question will vary considerably by gestational stage please edit your question to clarify what you want — e.g. an average over the entire pregnancy.


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Xylem vessels, lignin, wood

I learnt that lignin impregnates xylem cells, causing the cytoplasm to die due to the inability of water and nutrients to pass freely, hence creating hollow tubes adapted to transport materials. This means that in order for the cytoplasm to die and the tubes to be hollow, lignin needs always be present.. However lignin is not present in all xylem vessels... Lignin is the woody tissue that only forms the trunk of a tree. So how do these cells hollow out in other parts of the plant/tree to create empty transport vessels..??

Welcome to SE.Biology!  For details on how to use this site, please check out the tour: biology.stackexchange.com/tour and then the help pages on how to ask questions on this site: biology.stackexchange.com/help/how-to-ask. Thanks!

In particular, you have correctly deduced that what you were taught can't be completely correct.  The next step is to do some research!  A quick search for "protoxylem vessel formation plants" turned up this review: https://nph.onlinelibrary.wiley.com/doi/full/10.1111/nph.13383

I did my research... of course I dont like to wait for answers on forums.. but I didnt find what answers my question. And the info I quoted is not wrong since it is from a Cambridge University book. And why do people have these forums if members constantly assume people love asking them questions instead of "doing some reaearch"?! I obviously didnt find an answer and wanted to ask a person my question. So in case you dont like the question, dont answer it, but kindly do not patronisingly guide people to research. And if u didnt read the question, my ans is still not in the source u suggested!

Your question is much better now!  I'm sorry you felt patronized by my comments, but if you stick around (please do) you will see that many questions are posted by people who clearly haven't made even a minimal attempt at working out an answer.  Since there was no indication in your original post that you had tried to do any research I assumed that was likely to be true in your case as well.  I guess that whoever voted your question down felt the same way ...

Based on the passage you highlighted I think you are misinterpreting what is written — it does not say lignification is necessary only that it is sufficient.  I had another look at the article I suggested and from the summary "We also summarize the processes which have been shown to be instrumental during xylem maturation. This includes mechanisms of cell wall formation and cell death which collectively complete xylem cell fate." — I don't have time right now to read through the whole article, but that sounds directly relevant to your question to me ...

Just as u feel people dont do their research, the opp is true for questioners cux people constantly, instead of answering a Q, tell them to use the internet.. I or anyone might have 100's of questions while we study, we dont have the need or time to post all 100 here... but upon being unable to find a clear ans, just as we might ask a teacher/friend, we pose qs to the virtual community. So i think its only fair to give the benefit of the doubt and answer qs which is what the Q&A forum was meant for. In case one is against the institution of asking a q, lets not have these forums, is my point.

Yes but how does that death take place??? If not by lignin how does a cell lose its cytoplasm is what I dont know. PS The problem i highlighted above is what I encountered mainly on stack exchange. Nobody "assumes" things or tells u not to ask on other QnA forums like Yahoo Answers. Cux that beats the point of having a forum. Anybody, whether they have researched or not, can ask a question without community members downvoting qs they dont "approve" of for a reason like this.Thats how forums become databases for info. YA search results are mostly top of the list in frequency n content quality.

Thanks for the article.. I dont understand it clearly enough but thanks..

Please do not post text as graphics. It doesn’t index and discriminates against people with sight defects.

I may be wrong but I knew that lignin is found in all xylem, both primary and secondary xylem.


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The Evolutionary significance of Coelom
What is the evolutionary significance of coelom formation?

Welcome to Biology.SE! It is expected that you will demonstrate that you have done research on your own before asking questions here — for example you could start with this: https://en.wikipedia.org/wiki/Coelom …. –––––––– For details on how to use this site, please check out the tour: biology.stackexchange.com/tour and then the help pages on how to ask questions on this site: biology.stackexchange.com/help/how-to-ask. Thanks!


text:
Why don't we speak of medial and lateral rotation of the forearm? And pronation and supination of the upper arm?
Why don't we speak of medial and lateral rotation of the forearm?
I notice we speak of forearm supination and forearm pronation, but why not medial and lateral rotation.
It seems to me that if we take the diagram of the human with palms forward, which I understand to be the neutral position one is meant to start from.. then forearm pronation looks to me like a medial movement. So why not medial rotation?
And similarly with upper arm.. why don't we speak of pronation and supination of the upper arm?  We speak of medial and lateral rotation of it..

Pronation and supination involve a change in relationship between the ulna and radius.

When you rotate your hand from palm ventrally (as in anatomical
  position) to palm facing dorsally you have moved your hand from a
  supinated position to a pronated one. This movement of supination to
  pronation occurs when the distal head of the radius rotates on the
  capitulum , the bone rotates along its long axis, and the proximal
  head of the radius flips over the ulna. (Duke Medicine)

and:

Pronation and supination are rotational motions that exist exclusively
  in the forearm. The mechanical bases for these movements are the
  existence of two forearm bones and the presence of two coupled
  trochoid joints—the proximal and distal radioulnar joints (PRUJ and
  DRUJ). (Clinical Gate)

Image source: Wikimedia, CC licence
During medial or lateral rotation of the upper arm (without additional rotation of the forearm), the humerus rotates, but the relation between the ulna and radius does not change, so there is no pronation/supination.
It is more practical to use supination/pronation for the forearm/hand, because you can have a forearm/hand in various positions where medial/lateral or internal/external does not make sense: for example, when you rotate your forearm/hand with your arm extended toward the side. Saying that, medial/lateral and internal/external rotation of the forearm is also commonly used (search: "medial rotation of the forearm"). So, you can use any of these terns according to what's more practical and less confusing in a given context.

ok, that answers for the terms supnation and pronation being forearm only. What about medial/internal and lateral/external rotation, why we don't say that of the forearm, or do we? maybe we do https://exrx.net/Articulations/Forearm

@barlop, I added that at the bottom of my answer. It's mainly to prevent confusion.

I think this line "It is more practical to use supination/pronation for the forearm/hand, because you can have a forearm/hand in various positions where medial/lateral or internal/external does not make sense: for example, when you rotate your forearm/hand with your arm extended in front of you or toward the side or placed on the table. "  <-- is incorrect, because the same applies to the upper arm , it can be out sideways, and they speak of medial and lateral there / internal and external rotation.

And your next thing "medial/lateral and internal/external rotation of the forearm is also commonly used "  is correct I think and proves that the previous thing was incorrect.

Also your last line "So, you can use any of these terns according to what's more practical and less confusing in a given context."  is I think unclear. The terms medial and lateral rotation can be applied to either. But as you showed, the terms pronation and supination only apply to the forearm

When you have your arm extended toward the side (lateral extension) and you supinate or pronate the forearm, you can't say if you medially or laterally rotated it. It is true that the same issue applies for medial/lateral rotation of the upper arm, but in this case is not really confusing. In summary: you can use all the mentioned terms for both the forearm and upper arm, except supination/pronation for the upper arm.

I think you've answered it I think I could possibly make it a bit clearer..  BTW you can say you medially or laterally rotate it because the terms apply because they're done with the human anatomy diagram of a person with arms down palms out, so you look at it from the perspective of arms down palms out when using those terms, even if the arm is out to the side.

Do you have any idea about question of mine on a similar subject? https://biology.stackexchange.com/questions/52346/confusion-regarding-degrees-of-flexion-and-a-goniometer

I'll look at it.

Supinus and pronus are latin words which mean lying face/body/palm downw and lying face/body/palm up. The hand clearly has a front and a back, and everyone knows where the back of the hand is compared to the front. It's a very clear medical word for describing the hand. Supinator and pronator muscles are also clear groups that action the hand to a prone/supine position.
If you ask which is the front and back of your forearm, not everyone will reply the same. The upper arm doesn't have a clear front and back, so it's not the best way to describe the forearm and the upper arm.


text:
Non-nucleated cell-like population with RNA
We're working on invertebrate hemolymph (blood) and we have found with flow cytometry (staining with DRAQ5) a cell-like population without nucleus but it has RNA production.
Does anyone any experience with something similar? May anyone recommend any publication with something like that?
More information:
1) We don't know the real population size because we have identified it by flow cytometry, future experiments we wish to use TEM to characterize it better.
2) We know that this "population" produces RNA because we have extracted total RNA using low input RNA kit and run the result in Bioanalyzer.
3) We "know"/suspected this population doesn't have cell-nucleus because DRAQ5 is a DNA staining and this population is DRAQ5-. We wish study that by confocal microscopy ASAP.

Welcome to Biology.SE!  Will you please edit your question to include more information – including: 1) size of these putative "cells", 2) how you know they produce RNA, and 3) how you know they don't have a nucleus?

My first inclination is to suspect some sort of prokaryote — can you rule that out?

Hi! Thanks so much for your contribution but I might not be a prokaryotic population because it's producing 18S and 28S rRNA, instead of 16S and 23S.

This is a bit outside my wheelhouse so forgive me if I am ignorant of something, but does (2) actually mean RNA is being produced? Or could it just be that some RNA is still present? For example immature RBCs have RNA and make proteins despite lacking a nucleus.

Maybe you are seeing extracellular vesicles1?
At least might be worth checking out since extracellular vesicles containing RNA have been reported within the hemolymph of mosquitos2.
References:
1: Van der Pol, E., Böing, A. N., Harrison, P., Sturk, A., & Nieuwland, R. (2012). Classification, functions, and clinical relevance of extracellular vesicles. Pharmacological reviews, 64(3), 676-705.
2: Severo, M. S., Landry, J. J., Lindquist, R. L., Goosmann, C., Brinkmann, V., Collier, P., ... & Levashina, E. A. (2018). Unbiased classification of mosquito blood cells by single-cell genomics and high-content imaging. Proceedings of the National Academy of Sciences, 115(32), E7568-E7577.


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Are there any documented cases of extinction of a species of fungus?
Are there any documented cases of extinction of a species of fungus? I imagine it would be hard to detect something like this.
Edit: documented by humans when it happened and/or induced by humans.

Why should it be hard to detect?

@Jam Fungi are composed of soft tissue, which breaks down easily and quickly. The conditions to preserve such tissue occur even more rarely than the already rare conditions for fossilizing bone.

@Jam 99 % or so of funguses are below ground and more or less microscopic.

According to the International Union for Conservation of Nature’s Red List there are many endangered fungi, but none that are documented to have become extinct within the time frame of interest to you.
However, it seems likely that some fungi have gone extinct with their plant hosts — according to the IUCN there have been 133 documented extinctions of plant species. In particular, mycorrhizal1 (and other) associations between plants and fungi are prevalent and some of these associations appear to be specific (i.e. the fungus only associates with one plant species). For example, there are reported to be 28 species of fungi that only associate with the shrub Lantana camara.2
References:
1: Hoeksema, J. D., Bever, J. D., Chakraborty, S., Chaudhary, V. B., Gardes, M., Gehring, C. A., ... & Lajeunesse, M. J. (2018). Evolutionary history of plant hosts and fungal symbionts predicts the strength of mycorrhizal mutualism. Communications biology, 1(1), 116.
2: Hawksworth, D. L., & Rossman, A. Y. (1997). Where are all the undescribed fungi?. Phytopathology, 87(9), 888-891.

Yes. One example is of a fungus named Prototaxites. It was originally thought to be a tree, but it was a massive, tree-like fungus.

"documented by humans when it happened and/or induced by humans" does not really match with "approximately 430 to 360 million years ago" though

@eis I believe that the OP added that in an edit to their question after I provided my answer.

I don't think that is true - based on timestamps, edit was made 20:11:08 and you answered 22:43:23.

@eis Well, I must have missed the edit... ::shrugs::


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What do bones need to grow outside the body?
In what environment outside of a living organism can bones grow?
If I were to put an arbitrary human bone in a room and attach a bunch of tubes to it, or dunk it in some kind of solution, where would I have to connect the tubes and what stuff would have to be in the tubes/solution to make the bone grow as if it were inside a living organism?

Are you counting being sheathed in velvet like an antler as "inside" the body?

@swbarnes2 Yeah, I forgot to think about antlers, but since they're attached to a body I'm counting them as "inside" the body. I mean I want these bones to grow independent from an animal.


text:
Examples of environmentally influenced gene-expression in humans?
In discussions of the relevant importance of genetic and environmental influences on the development of the individual, it's often stated that the genetic and environmental influences interact.
An example that is often given is a certain kind of rabbit (usually white), carrying a particular gene for fur color. When the proper allele is present, AND the rabbit is exposed to cold, it will a dark spot on its fur. When the allele is present, the dark spot does not develop without the cold, and when the rabbit has the opposite allele, the spot will not develop even with cold exposure.
This is fine, but when I want to explain genes and environment to people, it has two pedagogical flaws:
(1) it's about rabbits
(2) it's about a trait people don't really care about
Is there a human example of this phenomenon?
That is, a phenotype which requires BOTH a certain genetic background and particular environmental influences in order to be expressed?

Not answering your question but if you want to read a small introduction in the theory describing how the environment, genetics and other things affect phenotype, you should definitely give a read to this post

The rabbit example seems to have at least three pedagogical benefits: (1) it's a simple Mendelian gene (I presume), (2) it's easily and ethically inducible (cold exposure), (3) it's a visible and obvious example of a phenotype: fur color. There are many many human gene-environment interactions but most are studied in the context of disease and are far more complex.

Could you please give an example? Relevance to human health is exactly what I am looking for.

@Maringo7 There are so many examples of health related traits that have a non-zero (and non-one) heritability in humans (lung, breast and ovarian cancer, schizophrenia, depression, back pain, sensitivity to common cold, ...) but I can't think of anyone that particularly stand up as a classical example for kids.

Would carcinogen exposure (an environmental influence) and cancer be a good example for you?

What about skin pigmentation? It is influenced by genes and by the exposure to UV. http://www.jbc.org/content/282/38/27557.full.html and https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3093193/ may be a good place to start.

How about entire sections of the X chromosome in males, various active parts of the immune system, or everything involved in pregnancy.

I think your question is interesting, though the use of "expression" is misleading in context of your rabbit example.

Examples of environmentally influenced gene-expression in humans?
...
That is, a phenotype which requires BOTH a certain genetic background and particular environmental influences in order to be expressed?

In the example you give, the color-changing phenotype is not due to changes in gene expression but rather a conformational change in a tyrosinase variant at low temperatures that leads to decoupling of an inhibitor from the enzyme.  This is not to say that there aren't any changes in expression with changes in temperature -- only that the phenomenon you describe is ultimately a change in enzyme activity and not the induction of a specific allele.  See Kidson and Fabian, 1981 [1] --

It is proposed that at the normal body temperature of 37 degree C, tyrosinase from Himalayan skin is strongly bound to an inhibitor. At lower body temperatures, the affinity of the enzyme for the inhibitor decreases, thus allowing the synthesis of melanin to increase. This change in affinity of the enzyme for the inhibitor could be regulated by temperature-induced conformational changes in either the enzyme or the inhibitor or both.

Note that this study was conducted in "Himalayan" mice, not rabbits, though the authors do reference an earlier rabbit study [2] --

These results are in support of Danneel's visual observations ('41) that "ferment" activity of Himalayan rabbit skin is absent at temperatures above 25 degree C.

the full text of which can be found, in German, on Google Books.

Concerning a human example of allele-environment interactions, look no further! The same temperature-sensitive tyrosinase mutation has been reported in people with oculocutaneous albinism (OCA) [3], albeit with a slightly different phenotype.  From the abstract:

In this paper, we report a new type of OCA that results from a tyrosinase allele producing a temperature-sensitive enzyme. The proband had white hair in the warmer areas (scalp and axilla) and progressively darker hair in the cooler areas (extremities) of her body. Melanocyte and melanosome architecture were normal. Quantitative hairbulb tyrosinase (dopa oxidase) assay demonstrated a loss of activity above 35-37 degrees C. Plasma pheomelanin and urine eumelanin intermediates were reduced and correlated with hair melanin content. This is the first temperature-sensitive tyrosinase mutation to be reported in humans and is analogous to the Siamese mutation in the cat and the Himalayan mutation in the mouse.

References

Kidson SH, Fabian BC. The effect of temperature on tyrosinase activity in Himalayan mouse skin. J Exp Zool. 1981 Jan;215(1):91-7.
Frisch KV, Goldschmidt R, Ruhland W, Winterstein H. Ergebnisse der Biologie. Eighteenth Volume.
King RA, Townsend D, Oetting W, et al. Temperature-sensitive tyrosinase associated with peripheral pigmentation in oculocutaneous albinism. J Clin Invest. 1991;87(3):1046-1053.

This answer is almost too perfect.

I did not read this carefully enough on the first pass... agreed! Good frame challenge.

The breadth of examples of environmental exposure directly influencing changes in gene expression in humans is astonishing, occurring at every developmental stage from conception  to death.
As an example, consider the environmental exposure to a reasonably high dose of a gram negative bacteria with lipopolysaccharide. Immune cells recognize this very particular environmental exposure as a danger signal, triggering a signaling cascade that includes activation of nuclear factor kappa beta, or NFKB.  A series of changes in gene expression begins, including transcription, translation, and release of interleukin-1 and TNF-alpha, which are responsible for a host of externally observable changes, not the least of which is an increase in your body temperature.  You can read about this generally in any introductory clinical microbiology or immunology text. One example is Murray Medical Microbiology, Ch. 2.
In this example, exposure to an infectious agent is analogous to cold weather in the rabbit. Fever is analogous to the change in the rabbit's fur color.
As acvill’s answer indicates, the color change in rabbits is not mediated by gene expression. In the case of fever, though, it is, and may be a useful teaching example. Everyone has experience with fever and understands that fever is not the basal state, but a response to the environment. It is not hard to make the leap from that personal experience to the idea that the signaling molecules that cause fever are not typically present, but are in response to very particular environmental cues, and that change (from the absence of circulating IL-1 and TNF-alpha to the presence of IL-1 and TNF-alpha) is controlled by a famous and fun to say transcription factor, NF-kappa beta.