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Is the barcode COI sequence the sense or antisense strand of DNA?
Is the COI sequence commonly used for DNA barcoding the sense or the antisense strand of DNA?

You could use either with the same results. I imagine researchers would refer to the sense strand.

When the barcode sequence is generated by Sanger sequencing, it is sequenced in both strands, and presented in sense strand.

Thank you very much for your answer, which I will accept. But it raises two further questions:

Is it always the case (at least for phylogenetics) that the sequence reported for a gene is the sense strand?
(i.e. the strand which reads the same as the mRNA).

I was a bit confused when you said that both strands are sequenced in Sanger sequencing. I thought that just one of the complementary strands was sequenced?

Careful workers ALWAYS sequence both strands, because some nucleotides are hard to read. Especially at the beginning and the end (the first 35 nucleotides or so, and anything out past 500 from the primers). So you sequence both strands so that one confirms the other. As one strand extends out past the easy to read "sweet spot", between 35 and 300 nucleotides from the primer, the other strand picks up with higher quality reads. Then you put the two together, carefully edit, and report the sense stand to GenBank.


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Alpha-gamma co-activation
I am having trouble visualizing/grasping the necessity of alpha-gamma co-activation. My understanding is the following:
When an external load causes stretching of the sensory muscle spindles, the 1a afferent fibers travel via the DRG and synapse on both alpha and gamma motor neurons in the anterior horn of the spinal cord. The alpha motor neuron then relays an efferent signal to the extrafusal muscle fibers and induces a contraction. Almost simultaneously, the gamma motor neuron relays an efferent signal to muscle spindles, causing the contraction of the intrafusal muscle fibers at their polar regions, and stretching at their equatorial regions. The stretching of the equatorial regions is what causes the 1a sensory fiber afferents to relay signals to the spinal cord.
Herein lies my problem. If muscle spindles can only relay their afferent signals to the spinal cord AFTER gamma activation, but gamma activation requires muscle spindle afferent signals, wouldn't this be a catch 22? Also, I read from a few sources that gamma activation, while almost simultaneous, occurs after alpha activation. Wouldn't the converse make more sense as gamma activation would trigger higher alpha firing frequency?
I hope my question makes sense. This is my first time making a post on this forum so I do apologize if the syntax of my question is not in accordance with proper question formatting.

source: Stack Exchange

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

sort: votes


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How could this molecule affect the body? (Lysergic acid derivative)

First of all, could you please help me name this molecule? I think the name of it is something like this: N,N-pentamethylene lysergic acid. Secondly, my main question is what could be the pharmacology / mechanism of action (eg the target receptors, etc.) of this molecule? I couldn't find any info on DrugBank, so I'm all ears to your ideas. Please help me on this; it is quite a burning question.
P.S.: If there are any mistakes in my English, please excuse me.

That is lysergic acid piperidide, an analog of lysergic acid diethylamide (LSD). According to Wikipedia, it is an agonist of the 5-HT2A receptor, but is much less potent than LSD.

@ostal123 You're welcome. Please consider accepting the answer if it has, in fact, answered your question.

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


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What kind of fruit is this? It is the size of a small avocado or a plum

The flesh inside them seems ripe as it is squishy, and it gives off a strange odor. The smell at first reminded me of menthol. It's about the size of a small avocado, or a plum. A coworker of mine left a few on my desk before he left, but he didn't say what they were.

My cat definitely hates the smell. She reacted more strongly to this than to citrus.

Were did you find them? On a tree, on the market? Which country? Etc.

And please add an approximate size.

Might be a Kwini. Mangifera odorata

Please add more information about where this fruit comes from. (I upvoted your answer and downvoted your question)

After doing a bit more research and asking a few friends, I found out that it was a feijoa, or pineapple guava. I think the ones in the picture aren't fully ripe yet, though.


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What Animal is This Skin From? A Wooly Mammoth?
I was at the American Museum of Natural History in New York City today, and I saw the skin pictured below. Because it was next to stuff about wooly mammoths, I thought it might be a mammoth skin. However, there was no sign accompanying the skin. What is it from?

its looks like an elephant's leg on the right. close enough to be a mammoth then.

Yes, this is the remains of a wooly mammoth. Many mammoths have been found frozen and well preserved in Siberia.


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what kind of bonds join the okazaki fragments
During DNA replication, the synthesized okazaki fragments adjacent to each other are joined up directly by DNA ligase-catalyzed phosphodiester bond formation. Can someone point out to me which part of this statement says it's false? All I know is that the fragments are joined together by DNA ligase, which can only mean the part about the phosphodiester bond is wrong, but arent the 2 nucleotides joined by a phosphodiester aka nucleotide bond?

This seems to be a garbled version of a trick MCQ which is of no interest to anyone. Rather than vote for the half answer, vote to close it.

I'm pretty sure the "phosphodiester bond" part is correct.
The only thing I can think of that might be questionable is the word "directly". If directly = immediately, then the sentence could be termed false, because they aren't joined immediately.
Even then, it seems like that's just grasping at straws, so I wouldn't worry too much about it. It sounds like you understand the concept, which is what matters.

The best guess I could make is "directly". Okazaki fragments also contain RNA primers, which need to be replaced by DNA fragments. This is why joining Okazaki fragments together is a bit longer process. In short, the RNA primers are first removed by Flap endonuclease I and replaced by DNA Polymerase $\ce{\delta}$, after which these fragments are joined by DNA ligase I. I would suggest you read the Wikipedia article about Okazaki fragments.

You're most welcome :) If my post really answers your question, please consider selecting it as correct. It gives points to both the answerer (me) and the asker (you) ;)

Okazaki fragment maturation involves a gap-filling (between adjacent Okazaki fragments) and strand-displacement (5'-end of the downstream Okazaki fragment) DNA synthesis by DNA polymerase δ (Polδ) which produces a ligatable nick; the nicked DNA is the substrate for DNA ligase.

http://www.jbc.org/content/278/3/1626.long
http://www.jbc.org/content/286/9/6865.full

Okazaki fragments do not attach to the lagging strand adjacent to one-another, but rather, attach randomly, some distance from one-another.

My answer is correct. Okazaki fragments do NOT line up adjacent to one another. They are some distance apart, and the distance between them must be filled in. That was the error in the question.


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What kind of tree is this — why do its huge leaves change shape and "grow fingers"?
Edit 2: Confirmation that it's one tree!
Surrounding trees on either side along the sidewalk are completely different, and the ones on the other side of the fence are short and have rounded but far smaller, as well as thicker, dark leaves.
I've taken a 180 degree vertical "panoramic" photograph to show that there are no encroachments from trees with large leaves from behind. I've also included a few more photos of small clusters of leaves coming from a single large branch, again showing all three types of leaves.
Note some of the photos are large, and if you open them in a separate tab or window you can zoom in for additional detail.

I was riding a bike in Taipei recently (November 2017, location in google maps - more views of trees: https://goo.gl/oXPHr3) and I saw two huge leaves on the sidewalk. I stopped to photograph them and realized that they were very different shapes but otherwise looked quite similar. They are both over 40 cm long broad leaves, but while one has smooth edges and is "leaf-shaped", the other has long serrations (roughly 10 cm deep, 5-7cm spacing) on each edge.
I took some more photos of the leaves and branches of this very large tree, and one of the trunk, which looks quite gnarly.
Edit 1: I've cropped and lightened sections of two of the photos where I believe I can show examples where leaves on the same branch exhibit continuous change from smoothed edges to serrated edges. I've used 1 to denote smooth-edged leaves, 2 to denote leaves that show a few "digits" at the far end of the leaf, and 3 to denote leaves that exhibit full "digitization". In each case I think it's pretty clear that they connect to the same branch, and are not from different trees as suggested in the answer. This is strongly (if superficially) reminiscent of the sassafras leave differences.
Question: What kind of tree is this, and why do its huge leaves change shape and "grow fingers"?
It was pointed out to me that Sassafras leaves also come in different shapes with "fingers", I've included one image of those below as well for comparison.

For comparison, here's an image of Sassafras leaves with "fingers", from Landscape Plants, Oregon State University.

It looks to me that one of your pictures (the third) shows an entry to something like a botanical garden. Maybe they even are involved with the planting or care of the trees in front of their doorsteps. It wouldn't hurt to ask there directly. (Assuming this is one of the pictures you took yourself.)

Having different shapes of leaves is called heterophylly. I noticed this in Ficus carica (common fig tree), Hedera helix (Ivy), some Eucalyptus, and, I think, Paulownia. I assume this is something quite common.

@skymningen Oh my gosh! I ride by there often but I've never stopped to see what's actually there. You are right!! There's a botanical garden and a herbarium and things related. Thank you for pointing that out! OK I will have to spend some time in that area and see what I can find out.

@Glorfindel your edit adding a link to Seaworld is not appreciated. https://i.stack.imgur.com/JaN1Q.png

I'm going to take a stab here.  It looks a lot like Artocarpus altilis or breadfruit.  However, the trunk is a bit gnarly for breadfruit, but maybe that is the result of being a street tree.  Also, I can't find any reliable information about the variation in the leaves (heterophylly) for this species.  However, other species in the genus have entire leaves, so perhaps this is hybrid.  Also, Artocarpus chaplasha does show heterophylly related to light intensity and leaf position (online images suggest your tree is not A. chaplasha however).  I think the climate in Taipei is consistent with Artocarpus too.  If it's not breadfruit, I imagine it is a species from the Moraceae.  Finally, in some of your pictures it looks like there is an adjacent tree (possibly a Ficus or Clusia) mixing in -- those leaves are obtuse rather than acute at the tip.
EDIT:
I'm including one of your photos with the leaves of the tree in question circled in yellow, and what I believe to be the leaves of a different tree circled in red (in case my earlier comments were too cryptic).

EDIT 2:
Here is an excerpt of Fig 1 from Jones et al. "Morphological diversity in breadfruit (Artocarpus, Moraceae): insights into domestication, conservation, and cultivar identification" Genetic Resources and Crop Evolution vol 60 no 1 pgs 175-192 (2013) which shows the diversity of leaf morphology in Artocarpus including some hybrids.  I'm convinced you are looking at one of the species in this genus or a hybrid, and looking at the leaves in the panel for A. altilis there is considerable diversity (phenotypic plasticity) w/i that species, so that may be as close as it can be nailed down.
Finally, I can't run it but apparently there is graphical key to Artocarpus species which might be fun to try.

EDIT 3:
@uhoh has verified that all the leaves in the pictures belong to the same tree, so, it's likely we are seeing heterophylly based on the age of the leaves.  I went back to the reference above, and found this sentence would would seem to be consistent with the young leaves being entire and obtuse (and we've already established that the more mature leaves show a lot of variation): "Leaf characteristics, such as the number of lobes, degree of dissection, size, and shape can vary between young shoots and older branches".  So I think all the observations and literature point in the same direction, namely good 'ol breadfruit.

Sounds good, I'll await your additional impressions once you get the chance.

Added an annotated version of one of the original pictures to show what I believe to be a different tree.

I looked at the Google street view but one can't zoom in that much.  However, the different leaves I marked in red appear to be from the trees behind the fence at the back of the side walk.  I'm sure it will be clear when you can inspect again in person.  Fun puzzle, thanks for asking the question.

Did you have a chance to re-inspect these trees and make a final determination?

I think maybe you took my comment that there appeared to be a different set of leaves in the one pic as a personal affront.  It was not intended that way -- it was just speculation ("... it looks like...") based on a single image (it's not uncommon for trees to be intermixed).  Thanks for re-visiting and affirming your original observation that all the leaves belong to the same tree.  Is it your impression that the leaves with entire edges and obtuse tips are young leaves?  Perhaps that is how they emerge and the serrated edges and mitten-features grow in over time. 1/2

2/2 I noticed the following statement in the article referenced above: "Leaf characteristics, such as the number of lobes, degree of dissection, size, and shape can vary between young shoots and older branches" suggesting they do change over time.

Ah, the persistent trauma of grade school... I edited my answer to include the additional info from the literature reference.

Continuity of the thread... there is a discussion that evolved over time here, and removing parts of it would leave future visitors confused.

Stackexchange answers are not conversations or threads.


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Albino elephants
How many albino elephants are there across the world? There is no information on the total number of albino elephants across the world except for the few albino elephants captured by people.

According to this howstuffworks.com article who itself poorly cite a paper with a broken link (!), albinism in mammals occur in typically about 1 in every 10,000 births. The claim is quite definitely not trustworthy but that's all I found!
There are an estimated 450,000 - 700,000 African elephants and between 35,000 - 40,000 wild Asian elephants. So, if we believe that about 1 birth in 100,000 is an albino, then there are between 30 and 100 albino elephants in the world.
See also this quora post

This is the website/magazine howstuffworks.com is referring to. They don't cite anything but "some researchers".


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How do biologists determine the parents of a child
I am not well-versed in biology so this question might be wrong. As far as I understand meiosis, two germ line cells with 23 chromosomes each (one cell from the father and another from the mother) combine and after meiosis we get recombined chromosomes from the haploid cells with 23 chromosomes that will develop into an embryo. So, the child has different chromosomes than the ones of his father and mother. Then how can we know, by analyzing the child's DNA, who are the parents?
My simple question comes, in part, from this video about meiosis
I apologize for any errors.

Your description is not totally correct (or understandable). There is plenty of source of information online so, I won't repeat the whole thing here. In very short and very simplified, talking about humans...
Ploidy, meiosis and fecundation
Both parents are diploid (2N=46). Both parents have specific cells that are undergoing meiosis (in testis and in ovaries). After meiosis, the cells (spermatozoids and ovules) are haploid (1N = 23). The spermatozoid and the ovule fuse (fecundation) to make another diploid (2N = 46) individual. This diploid individual will grow for about 9 months in the mother's uterus before coming out!
Crossover
Now, during meiosis, cross-over occurs. It is a mechanism where the two chromosomes mix up their material. When the cross-over occurs in the father for example, it is the chromosome that the father receive from his father and the chromosome that he received from his mother that mix-up their genetic material.
Possible chromosomes
Let's say the maternally inherited chromosome of the dad is
AAAAAAAAAAAAAA

Let's say the paternally inherited chromosome of the dad is
BBBBBBBBBBBBBB

Then, in the meiosis (where spermatozoids are produced), the two chromosome might mix up and the haploid spermatzoid can end up with something like
BBBBBBBBBBBAAA

Now, on the mother's side, her two chromosomes are, say,
CCCCCCCCCCCCCC

and
DDDDDDDDDDDDDD

The mother might therefore transmit
DDDDDDDCCCCCCC

The (diploid) baby would then be
BBBBBBBBBBBAAA
DDDDDDDCCCCCCC

So of course, the chromosomes present in the baby are a bit different form the ones present in the parents but we can still recognize them. If there is doubt who the father is, a genetic analysis of another father might return the chromosomes
BBBBBBBBBBBBBB
FFFFFFFFFFFFFF

, then we would know this individual cannot be the father because he could have not transmitted the AAA part of the chromosome found in the kid.

So their parents have the DNA very much like the son but not equal..that was the point in the question..

@santimirandarp I am not sure by your comment if you feel like the question has been answered. If not, can you please explain why?

I was waiting for another good answer. It was good. I will accept.

To solve this mystery or get the answer by a well known technology even to a lamen called DNA fingerprinting. This technique is applied to the DNA which is extracted from the parents and the child, then these will be analyzed simultaneously and the result would be like of they are really the child's parents the all 3 have many equality and if they are not then all 3 DNA are widely distinct.


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Is it possible to have sleep paralysis while sleepwalking?
At least from a conceptual level, these two disorders don't conflict. The effect of sleep paralysis is being conscious while having the inability to consciously direct motor functions. Sleepwalking is the unconscious direction of motor functions. So combining the two, the effect would be that you are consciously aware of yourself and your surroundings while you are also unconsciously moving about, outside of your conscious control.
Therefore the only way the two wouldn't be possible together is if their activation conditions were mutually exclusive.
From wikipedia

Sleepwalking occurs during slow-wave sleep (N3) of non-rapid eye movement sleep (NREM sleep) cycles. It typically occurs within the first third of the night when slow-wave sleep is most prominent. Usually, it will occur once in a night, if at all.

https://en.wikipedia.org/wiki/Sleepwalking#Causes

The first of these stems from the understanding that sleep paralysis is a parasomnia resulting from dysfunctional overlap of the REM and waking stages of sleep.

https://en.wikipedia.org/wiki/Sleep_paralysis#Pathophysiology
So from a small amount of searching it seems it is not possible, unless SWS, REM, and the waking stages of sleep can all be overlapped.

Dissociative states are not the same as sleep paralysis, which means paralysis upon waking from sleep, not sleepwalking or combining it with other movement. There are a number of sleep disorders. You can't be paralyzed while walking. You can be sleepwalking. It might be something else.

While it is hard to completely rule out this convergence ever happening (perhaps cases haven't been reported), it is highly unlikely due to the specific stages of the ultradian sleep cycle at which sleep walking and sleep paralysis occur [Ref. 1]. Sleep walking during non-REM sleep would have to continue through the REM stage in order to see intrusion of sleep paralysis that occurs at the exit of REM to wake [Ref. 2].
A key feature of REM sleep is deep muscle atonia that paralyzes the body and prevents among other things one from acting out dreams [Ref .3]. Thus, if a person sleep walking were able to enter REM before returning to bed, the sleep walking / other unconscious motion itself would cease.
I do question your reasoning that the combination of these two parasomnias would result in being:

consciously aware of yourself and
  your surroundings while you are also unconsciously moving about,
  outside of your conscious control.

because the intrusion of sleep paralysis would in fact lead to muscle atonia and prevent one moving about. This is not to say that terrible things have not occurred where muscle atonia has failed while the subject remains asleep/unconscious; this falls under the fascinating category of REM-behavior disorders (where people act our their dreams - including violently hurting themselves and their partners), which judging by your question I think you will find interesting! [Ref. 4].
References:
[Ref. 1]: sleep stages
[Ref. 2]: sleep paralysis
[Ref. 3]: muscle atonia
[Ref. 4]: rem-behavior disorder


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Do DNA footprints vanish in generations?
Consider humans (or really any creature with sufficiently complex set of genes).  If person $A_0$ has an offspring, say $A_1$, we can without a doubt find markers in $A_1$ that we can definitely say indicate that $A_1$ is the progeny of $A_0$.  Likewise, for any generation $n$ we can say that $A_{n+1}$ has markers that indicate that generation $A_n$ is their parent.  Presumably (and maybe this is where I'm heavily mistaken), as $n$ grows large there are fewer "direct signs" that $A_n$ has $A_0$ in their ancestry.  I mention "direct signs" (although this isn't an official term) because obviously if one can prove $A_{n-1}$ is the parent generation to $A_n$ and $A_{n-2}$ proceeds $A_{n-1}$ and so on ... then one can deduce the relation between $A_0$ and $A_n$.  That's not my point.  My question is this:  Do the genes of $A_0$ "dilute" so that after so many generations it is possible or probable that none of the genes from $A_0$ are present in $A_n$ for some large $n$ (where by "none" I mean "no genes that give us a high warrant for believing $A_n$ is related to $A_0$ in the absence of evidence about $A_j$ for $2\le j \le n-1$").  Obviously if $A_0$ is human and $A_n$ is human then they share a great deal of their genes with one another (something like $99.99\%$)
If there is such an $n$, how large does $n$ need to be so that say $90\%$ of what makes $A_0$ unique is no longer present in $A_n$ (with a high probability of confidence), what about $95\%$ no longer being present, or $99\%?$
Please let me know if my question isn't sufficiently clear (I'm trying to convey the heart of my question, even if it isn't perfectly worded).

You seem to be figuring that since $A_1$ has half the genes of $A_0$, and $A_2$ has half the genes of $A_1$, etc throughout the generations, we quickly get to a point where $A_n$ has none of the genes $A_0$ had.
This would be correct, if we assumed no inbreeding among the descendants. And by "inbreeding" I don't mean siblings or first-degree cousins breeding, but any of $A_0$'s $n^{th}$ descendants breeding with another. Which is clearly absurd; at some point you're going to run out of breeding partners who aren't also a descendant of $A_0$, unless the lineage isn't very prolific and the number of descendants $A_0$ has is always a small proportion of the total population. And in that case, sure, those genes are probably going extinct.
The same thing happens the other way around by the way; we (most of us) have two grandparents, four great-grandparents, etc. As we go back in time this exponential growth quickly outstrips the amount of humans that were alive at the time our $n^{th}$ great-grandparents were around. That's because that exponential growth assumes no inbreeding, which there is. There is a point in time in the past beyond which everybody alive today is the descendant of everybody back then who has any descendant at all; that's called the Identical Ancestors Point. See for example:
https://www.nature.com/news/2004/040929/full/news040927-10.html
The end result is that there are really two outcomes for $A_0$'s descendance: either they increase over the long term faster that the overall population grows, or they increase at the same rate or slower. In the first case, we'll reach a point where the whole population is part of $A_0$'s descendance. In the second, unless population growth is huge then $A_0$'s line is probably going extinct. Even if not, and if we assume individuals are breeding randomly throughout the population (not a good assumption, but no gene dilution without it), then the original assumption that $A_0$'s descendants have fewer and fewer of $A_0$'s genes every generation is correct, and $A_0$'s genes will likely go extinct even if their descendants don't.
On the other hand if $A_0$'s descendance end up consisting of the whole population, then no more "dilution" can occur. Say at that point every individual has 1% of $A_0$'s alleles; their offspring will also have 1% of $A_0$'s alleles on average, and same goes for all later generations.
Note that at that point $A_0$'s alleles are distributed throughout the population; even if everyone has 1% of them, they don't all have the same 1%. So the question of whether "what makes $A_0$ unique" is present in the descendants is really hard to interpret. Some of $A_0$'s alleles may be present in everybody at that point (they have become fixed in the population), some may be present in X% of the population, some may have gone extinct. The specific combination of alleles that made $A_0$ is gone, but then it was gone when $A_0$ died. As for the question of whether scientists can investigate the descendants and find traces of $A_0$ after all those generations, the answer is "sure": see the aforelinkedto nature article.
More to the point, consider this sentence you wrote:

Obviously if $A_0$ is human and $A_n$ is human then they share a great deal of their genes with one another (something like $99.99\%$)

Do you not see how this factoid relates to your question? You are asking whether human $A_n$ still shares some genes with its ancestor human $A_0$, and caveat that "obviously" they already share most of their genes, what with being human. You mean, what with both descending from the common ancestor to all humans. That those $99.99\%$ of identical genes come from. Except of course that not even, given $99.99\%$ of that $99.99\%$ comes from our common ancestors with chimpanzees, and so on. Most of "what made the common ancestor to all life unique" is still in our genes today! So yeah, it will take more than a human-scale $n$ generations for all traces of a human ancestor to be predictably erased from its human descendants (keyword "predictably"; in practice many lineages and alleles do go extinct, but not all do and you can't really tell which in advance). More than that, on those evolutionary timescales natural selection is a strong force and you get phenomena like conserved genes - that is, genes that are important to the organism and are thus selected for to stay the same. At that point there is no "random dilution" phenomenon happening: there are specific forces at work to maintain the gene in all descendants in a more-or-less unchanged state.

We can reconstruct the pretty much the entire tree of life from genetic data! Of course, the further you go, the harder it becomes to know the exact relationship between individuals.
The false concept of gene dilution
I think most of your misunderstanding comes from the idea that genes "dilute". Genes are particular. An allele  (=gene variant) is either transmitted or it is not. But it is not like it would be a little bit transmitted. Consider the classical (historically important and obviously racist) "bad" argument of Jenkins

Jenkins supposed that a white man was wrecked on a desert island inhabited by Africans. The shipwrecked European would kill many black men in struggle for existence. He would have many wives and children. Many of his subjects would live and die as bachelors. In the F1, there will be some intelligent young men who are mulattoes (mixed race) more intelligent than negroes. Eventually instead of the beneficial white characteristic rising in frequency through natural selection acting on intermediates, Jenkins said that the European alleles and genes will be diluted out.

Putting aside the obviously racist and false assumption that whites are superior to blacks (such extreme racism was standard at that time in England), the argument does not sound so silly. Why would not the beneficial characteristic of an individual just dilute into the majority unadapted population? This concept was called blending inheritence and was the major way of thinking during the 19th century until the rediscovery of Gregor Mendel's work.
Individual characteristics are not 'fluid'. Characteristic of parent don't just average to give the characteristic of the offspring. There are actually particular unit of heredity (a gene) which has some 'atomic' property in the sense that it will be transmitted or it will not but nothing in between.

Assuming no inbreeding, you have 4 grandparents, 8 great-great grandparents, 16 great-great-great grandparents, 32 great-great-great-great grandparents, 64 great-great-great-great-great grandparents.
So sure, 98.4% of your genome came from someone other than that one great-great-great-great-great grandparent.  And most of that 1.5% is shared by every single person.  If that 1.5% doesn't contain any mutations unique to that ancestor, then sure, I guess it's lost.


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Can mutation rate be selected for?
Can the mutability of DNA be selected for in a population? I don’t mean selection for the phenotype that is the result of a mutation. Rather, can the rate of mutations in a population be increased by natural selection?

You might be interested in this question and answer.

The short answer is yes. There is quite a bit of work, theory and empirical on the evolution of mutation rate. To nicely answer, one would need to make a good review, probably inspired by some existing review. Such answer would take some time but I think is worth it.

You may like this reference. It clearly makes the case for the selection of an "ideal" mutation rate in the HIV virus.

Yes.

Evolutionary success of bacteria relies on the constant fine-tuning of
  their mutation rates, which optimizes their adaptability to constantly
  changing environmental conditions. When adaptation is limited by the
  mutation supply rate, under some conditions, natural selection favours
  increased mutation rates by acting on allelic variation of the genetic
  systems that control fidelity of DNA replication and repair. Mutator
  alleles are carried to high frequency through hitchhiking with the
  adaptive mutations they generate. However, when fitness gain no longer
  counterbalances the fitness loss due to continuous generation of
  deleterious mutations, natural selection favours reduction of mutation
  rates. Selection and counter-selection of high mutation rates depends
  on many factors: the number of mutations required for adaptation, the
  strength of mutator alleles, bacterial population size, competition
  with other strains, migration, and spatial and temporal environmental
  heterogeneity. Such modulations of mutation rates may also play a role
  in the evolution of antibiotic resistance.

https://www.ncbi.nlm.nih.gov/pubmed/16677295

Large differences in mutation rates can be found among viruses: 10^-3 mutations per nucleotide per replication in RNA bacteriophage Qβ versus 10^-8 mutations per nucleotide per replication in DNA Herpes simplex virus. Generally, RNA viruses have higher mutation rate because RNA-dependent RNA polymerases lack the proof-reading capacity present in DNA polymerases. However, both increasing and decreasing these typical mutation rates leads to reduced virulence of the virus population.
https://www.ncbi.nlm.nih.gov/pubmed/16220146
https://www.ncbi.nlm.nih.gov/pubmed/16327776

The answer is yes and your nice question was answered several decades ago by Luria and Delbruck. Take few minutes to read their experiment that gives them the Nobel prize:
https://en.wikipedia.org/wiki/Luria%E2%80%93Delbr%C3%BCck_experiment

I think the OP is not asking about wether the trait "mutation rate" is affected by selection on the mutation rate and not whether mutations appear as a response to a selection pressure for a given trait. I understood the question as you did at first (and got four downvotes in a few hours!) and ended up deleting my answer.

Well partially I think that can be answered by their experiment. This because in their experiment they show that bacteria have already all the possible mutations that can be "selected" in a particular environment. The selection of a mutation can happen randomly or as evolutionary biologist think it is selected by "natural selection". But what is natural selection? Are there specific mechanisms that can explain natural selection? I think this is still an open question nowadays. Please tell me what you think am open for this discussion :)


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What is intercalary mitosis in bacteria?
According to Wikipedia, in vegetative reproduction fragmentation takes place, and Spirogyra simply undergoes intercalary mitosis to form new filaments.
How is 'intercalary' defined in a bacterial context, does have to do anything blank or dead cells of Spirogyra?

To define, intercalary differentiation or mitosis applies to any cytogenesis through mitosis which arises between different specialised tissues or cells. Spirogyra may undertake either sexual reproduction, should conditions prove to be adverse, or asexual. The latter involves an 'intercalary mitosis'. This entails a fragmentation in the original filament in order to produce additional filaments.
Within bacteria, a good analogy may be the 'Blue-Green algae', a deceptive misnomer for phototrophic cyanobacteria. Thus, in the context of filamentous bacterial colonies, you may consider intercalary binary fission, cell division within the filament.
More information available from: http://bioweb.uwlax.edu/bio203/2010/fenske_megh/reproduction.htm


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How did Shulgin take cognizance of the dosage of a new substance?
We know that Alexander Shulgin synthesized MDMA, 2C compounds and several other tryptamine derivatives and phenethylamines. But how did he find out that the average dosage of an unknown compound is X mg? For instance, if I synthesized a new psychoactive compound, how could I find out the dosage?

He didn't.
It was basically a matter of trial and error. Of course, having previous experience with other psychotropics of the same class helped him to have a rough estimate: in the case of MDMA, Shulgin was neither the first one to synthesize it nor the first one to use it, and he knew beforehand that the psychoactive dose was between 100 and 200 mg. Besides that, being a rational chemist, he started by what he supposed to be the smallest, safe dose.

Alexander Shulgin
For instance, regarding MDMA, Shulgin (2010) describes the following dosages (I'm copy/pasting only the start of each paragraph):

(with 100 mg) Beforehand, I was aware of a dull, uncaring tiredness that might have reflected too little sleep, and I took a modest level of MDMA to see if it might serve me as a stimulant...
(with 120 mg) I feel absolutely clean inside, and there is nothing but pure euphoria...
(with 100 mg of the "R" isomer) There were the slightest of effects noted at about an hour (a couple of paresthetic twinges) and then nothing at all...
(with 160 mg of the "R" isomer) A disturbance of baseline at about forty minutes and this lasts for about another hour...
(with 200 mg of the "R" isomer) A progression from an alert at thirty minutes to a soft and light intoxication that did not persist...
(with 60 mg of the "S" isomer) The effects began developing in a smooth, friendly way at about a half-hour....
(with 100 mg of the "S" isomer) I feel the onset is slower than with the racemate...
(with 120 mg of the "S" isomer) A rapid development, and both writing and typing are impossible before the end of the first hour...

Unfortunately, he doesn't explicitly say what was the sequence of the dosages he took... I can only assume it was the sequence of the paragraphs.
However, by far, the best example of how "blind" the chemist is regarding the adequate dosage of a unknown psychotropic is the famous case of Albert Hofmann, who invented LSD (not as a psychotropic) in 1938.

Albert Hofmann
When he decided to test LSD, in 1943, he ingested 250 micrograms... well, that's almost ten times a typical "street" dose of LSD nowadays, which is around 20 micrograms. Luckily for him, overdose of LSD (up to more than 100 times the amount he used) is not lethal.

Source: Shulgin, A. and Shulgin, A. (2010). Pihkal: A Chemical Love Story. Berkeley: Transform.

Phenetylamines I Have Known And Loved +1. The late Alexander Shulgin (Shura) did have a certain protocol, basically starting off with the tiniest trickle of the compound and slowly increasing it until effects were noted. By then he would decrease the dose increment and continue up until the point where substantial effects were noted, if any.

@AliceD Indeed, a very peculiar book! I also like Hofmann's "My problem child".

That sounds like an interesting read! I should get my hands on it somehow. Lovely to see references to these books :) +1'd already, can't give you another, unfortunately :)

If you like reading ebooks instead of paper books (I don't), both Shulgin and Hofmann's books are available online, at Erowid: https://erowid.org/library/books_online/lsd_my_problem_child/


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Contribution of major nutrients to energy in the human body
What is the contribution of the major nutrients -- glucose, fat and protein -- to the human body's energy requirements, in normal conditions?
For some tissues, the fuel preference is known qualitatively -- the brain runs on glucose, the heart preferentially oxidizes fatty acids, etc. I'm looking for quantitative data on the consumption (oxidation) rate of the major nutrients, on the whole-body level. Molar amounts per unit time, or energy per unit time, or relative contributions to the total.
To get a rough idea, I looked at glucose and triglyceride turnover in blood. This article estimates blood glucose turnover at about 8 g / hour, or 190 g / day. If we assume that blood glucose transport equals amount of oxidized glucose, then this corresponds to 3200 kJ / day, or about 1/3 of the daily energy requirement. Similarly, this article estimates blood triglyceride half-life at about 1h; with a blood triglyceride content about 5 g, this yields about 90 g / day, or 3300 kJ / day from fat.
So with this rough estimate, sugar and fat appears about equally important, but about 1/3 of the daily energy requirement is missing. And I would imagine my quick calculation is inaccurate in many ways... Anyone know of better estimates? Some literature on the subject?
(I'm aware of the the dietary reference intake data, but diet composition may not equal the proportions of nutrients oxidized due to all sorts of interconversions.)

Good question... depends on what "normal conditions" is defined as... even during a 'normal day' the transition from prandial to post-prandial changes the fuel utilization for different tissues of the body

@VanceLAlbaugh  Yes, I realize it may differ with feeding.  I would be happy to learn of any quantitative data, in fed and/or fasted conditions.  Haven't found anything besides by own home-cooked estimates ...


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What causes the human body to “jump” when we get a shock?
At a Remembrance parade today, a cannon was set off to mark the beginning of a two minute silence. As it went off, the crowds quite comically jumped in sync, from the shock it gave them. I’ve seen very similar reactions in other scenarios, such as a jump-scare in a horror film.
Seeing the in-sync crowd jump today made me wonder.. what is it, in the human body, that make us jump when we get a shock?

This is similar to many other reactions humans have when scared, such as freezing, feeling like as if your heart is beating out of your chest, shaky legs, or the feeling that hair stands up on the back of your neck.
Fear starts with a trigger, and in your example, it is the sudden loud sound of the cannon. That stimulus signals to your brain that you might be in danger. Whether the stimulus is touch, sight, or sound, the scary signal quickly reaches the thalamus at the center of the brain and travels down to the amygdala, at the base of the brain.
From here a neurotransmitter called glutamate then carries the signal even deeper into the brain. This is what causes us to freeze, or involuntarily jump, and put humans through what is know as the "fight or flight" response.
These two reactions are automatic and involuntary because the deep brain is ancient in terms of evolution. We have little control over it. The reason is because a fight-or-flight response unleashes powerful hormones that affect the entire body.
When frightened, your body floods with the hormone adrenaline, skyrocketing your heart rate and blood pressure. The hormonal surge also causes your heart to pump blood more forcefully to the muscles. That's why you might feel a little shaky or unsteady when you're scared — the extra blood is getting your body ready to sprint away from the danger or stand and fight if you need to; hence the name fight or flight response.
Our bodies can reverse the fear response fairly quickly, though. If it turns out we aren't in a life-threatening situation, the parasympathetic nervous system (PSNS) kicks in to counter the fight-or-flight instinct, primarily by stopping the flood of adrenaline and lowering our heart rate back to normal. That's why every time we jump during a scary movie, or in your case a cannon sound, we don't run out of the theater/parade screaming; after the initial reaction, our PSNS helps us recognize the threat is not real and calms us down.
On a side note, part of the reason the PSNS exists is because adrenaline can actually be toxic in large amounts. If too much adrenaline floods into the heart, it can lead to the failure of that organ and death. You cannot control the fight or flight response, however you can limit it through meditation.
Hope that helps <3,
Jess


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Help identifying this bird from Southern Brazil

I've seen a few of these birds at my university located in the extreme south of Brazil.
I noticed they usually stay on wet areas and like to eat small critters, such as worms and young tadpoles (I'm not completely sure about the last one).
I also noticed they usually stay alone in a particular area or, at maximum, two in the same location.
Also, here we also have many Southern Lapwings, which are in the breeding season, and one of them sometimes attacks the bird in the picture (for apparently no reason). When attacked by the Lapwing, this bird bristles the feathers of his neck and just dodges the Lapwing's attacks.
Does someone know what bird is this?
P.S.: Sorry for the bad picture. I couldn't get closer to it.

That is Syrigma sibilatrix, the whistling heron. In Brazil we call it "maria-faceira".

Here is Syrigma sibilatrix page in Wiki Aves ("aves" is birds in Portuguese): http://www.wikiaves.com.br/maria-faceira
Wiki Aves is by far the best source for birds in Brazil. It is a very well documented and reliable source, maintained by great ornithologists.
PS: Regarding the Southern lapwings: they are not really attacking, they are just trying to drive off the intruder. And there is a reason: the lapwings nest on the ground. I was "attacked" by them several times (I'm from the Southern Brazil), when I inadvertently approached their nest.

Maria-Faceira. I laughed hard at this one :P. I'm quite familiar with the behavior of the Lapwings too. I just though a little strange that their offsprings are already quite grown up and the Maria-Faceira isn't too close to them. I guess the Lapwings are just a little short-tempered ^-^ Thanks!

Yes, the lapwings (or "quero-quero") are very short-tempered!

@PhelypeOleinik What's the meaning of "faceira"?

It's something between 'happy' and 'in a good mood'. For example, when a kid receives a christmas gift and stays happy all day long about it, we say that the kid is "faceira" (nor very usual though).

@PhelypeOleinik do you speak Portuguese? Faceira also means coquettish and flirtatious.

@GerardoFurtado Yes, I'm Brazilian, but I can assure you I have never heard anyone using this word with this meaning.

They do in the northeast, where it has a more sexual meaning. I lived in Floripa and I never heard this word there.


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Since the matter in the brain is recycled every few days how does consciousnesses work?
Since parts of the brain are recycled every few days does that mean that materialistic theories of consciousness don't work?

How does any other body part work, when the actual matter is generally recycled over shorter or longer periods?  FTM, how does your car keep running when you have to keep filling the gas tank, replacing tires, batteries, & other parts?  If you kept it long enough that you eventually had to replace every single part, wouldn't it still be a running car?

Notice that the link you provide concerns development, where plenty of things change. You have added a tag for proteins but do not really discuss the implication of protein turnover given the prominent role that modern neuroscience gives to translation-dependent synaptic plasticity. @jamesqf The question is not how can the brain work given the turnover, but if we can for example claim that a person is the same over time. Or put differently, how much of this turnover is critical for "consciousness". If none of it is, then "consciousness" cannot reside in matter, or so the argument goes.

@vkehayas: The turnover/consciousness argument is, at least to me, so obviously false ("not even wrong" comes to mind :-) that it's actually hard to think of how to refute it.  But consider a computer as an analogy.  With RAID storage, you can replace one of the hard drives (often hot-swapping while the computer is running), and all the data will remain unchanged.  Over time, you could replace all the disks.  With a largish cluster, you can swap out CPU nodes while programs are running, and (if properly designed) they'll continue working just fine.  (Continued...)

... The programs (and presumably consciousness - not that I'm claiming to know what that is) are PROCESSES that aren't tied to specific bits of matter. You can replace the underlying hardware, whether it's silicon chips or proteins, and the process continues unaffected.

What is consciousness?

That was an interesting read, and I saw nothing to support your statement that "brain parts die every few days".
Neural plasticity demands that some synapses degrade as new ones are formed. But there are (an estimated) 100+ trillion synapses (some put it an order of magnitude higher) so, really, a few here and there means little. It's when there is wholesale loss that problems arise.
A strong argument for a materialist theory of consciousness is that as neurons involved with memory die, so does memory. This is evident in the transition that occurs in early childhood allowing for the formation of long term memory as well as the degradation of short-term memory and other brain functions in people with, say, Alzheimers.
Hippocampal Neurogenesis Regulates Forgetting During Adulthood and Infancy Science 9 May 2014


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This is the bone of which animal? And which bone?

so this bone was found on a construction site in Paris and I was wondering from which animal does it come from?

Not really a bone guy, but it does have a sortof tibial/carpal look to it. Some kind of ungulate maybe?

This looks quite large. I don't think it belongs to current french Fauna. Do you know in what geological layer this bone was found? Is it petrified?

It might be interesting to have information about the history of the site.

I don't really have any info about the geological layer and whether if it's petrified or not. My only guess is that it's a femur...I'm not really good with bones

looks like a femur to me. You can see the head and paired distal condyles

Related? https://biology.stackexchange.com/questions/62871/identifying-a-lone-bone-found-newar-rowena-crest-oregon-usa?rq=1

@LinuxBlanket. Thanks for bringing attention to that other bone ID question. However, the bone in your linked question is a forelimb bone (the humerus) while the bone in this post looks much more like a femur (a hind-limb bone). The sizes are also drastically different.


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Does the right ventricle affect blood pressure in pulmonary veins?
Now, I know there are multiple things that push the blood through the entire pulmonary circulation like the contraction of arterial muscular walls... But what I want to know is whether the right ventricle pumps the blood even through the pulmonary veins, or whether its effect stops at the arteries.
This may not be of significance to be honest, but I got into a debate with a friend over this and thought people here would end this debate :)


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Horizontal gene transfer and Botulinum toxin
Is it theoretically possible that any aerobic bacterium becomes able to produce Botulinum toxin as a result of horizontal gene transfer from Clostridium botulinum to that bacterium?


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What is the easiest way to measure a human body surface area?
Looking for accuracy, cost-efficiency, and speed: this could provide useful information for determining individual bioinformatic calculations, pertaining to, for example cell type estimation, for personalized medicine regimens. I'm not sure why this question was marked as off-topic and closed.  The biological implications are grandioso.

I am wondering whether enginneering.SE would be better suited for your question.

Walsberg & King (1978) came up with a method for estimating the surface area of an organism fairly cheaply. They were interested in birds, but it would work on people as well. Is this the sort of solution you were after?
http://jeb.biologists.org/content/76/1/185

@kmm - Wouldn't that measure the entire mass of the body? The OP wants just surface area.

If you do a Google search, there are a few models that will estimate your BSA (Body Surface Area) based on a few measurements. The degree of their accuracy though is something to be slightly weary of, however, I think they do good as a rough estimation. Google "Du Bois and Do Bios BSA formula", and then consider this publication, which revisits that previously mentioned formula for more accurate constants.

I think nomogram method

I think nomogram.I

How cost efficient does it has to be? Do you want these data to be comparable to another study?
Fundamental issues
What do you call surface area?
The interior of the guts (interior of the mouth, stomach, intestins, ...) are typically considered as exterior to the body. I would assume you don't want to consider these things in your measurements, right?
Coastline paradox
By aware of the coastline paradox

The coastline paradox is the counterintuitive observation that the coastline of a landmass does not have a well-defined length. This results from the fractal-like properties of coastlines.

Similarly, for the surface of the human body, the results will be drastically different depending upon the scale of measurement you want to consider. If you want to measure the small bumps of each atom or if you're happy to consider the the skin is a perfectly flat surface, the answer will vary a lot (numerous order of magnitudes)!
So, if you want to make your results comparable to those of another study, then you should definitely copy their methodology. If all that matters is that you can compare the different individual you measure, then you can pick a methodology that works well for you.
Methods
Those are in no way an exhaustive list.
3D scanner
3D scanner is probably the way to go for accuracy.
Approximation of body shape into cylinder and spheres
If you want cheap and inaccurate, you can assume each body part is a cylinder. Consider for example reducing the human body to 4 limbs (which you could further split in two separated by the knee and the elbow), a torso and a head. Just measure the perimeter of each body part and and approximate the surface area.
It might sound like a silly technic but it might well be good enough for your purpose (esp. if you're not comparing your results with another study).
Polyethylene film
Following Walsberg & King (1978) (thanks to @bshane for pointing this paper out), you can wrap people in a polyethylene film and then measure the area of the film. When measuring the area of the polyethylene film, you are going to have to make some approximation into some simplified (or series of simplified) shapes just like I suggested above. Walsberg & King (1978), when measuring birds, assumed the overall shaped was a prolate spheroid with a hemispherical head. You're going to have to try to find what simplified shape ressembles most to the polyethylene film.
Of cours, you might want to eventually consider other fabrics than polyethylene film and you might want to consider different number of fabrics.
You could prepare pre-measured rectangles and triangles of a given fabrics with colors matching a known size. Then you can just stick those fabrics on the individual body and simply add up the size of the shape you add on the body. This sounds like a difficult solution as you will have a hard time to correctly place the fabrics to avoid wrinkles, overlaps and gaps.
Test reliability of your measure
Reliability of your measure
Do not forget to repeat measurement on a few individuals to measure the accuracy of your measure.
inter-raters reliability
If several people are going to work on this project, you should also make sure to test the inter-raters reliability

i would:

wrap my body in non-overlapping pieces of fabric* and adhesive tape;
unwrap my body and "ouch";
measure the area of each piece;
sum these areas.

*Body-fitting tights, long-sleeved T-shirt, mask, and gloves would cover most of my body quite quickly. The problem is only that i would have to destroy the clothes by cutting them into pieces between the steps 2 and 3.

I would recommend against any type of elastic clothing, since its surface area isn't rigid once taken off the wearer.

i edited my answer: "Compression" >>> "Body-fitting"

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


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Why do some trees hold their leaves through fall and winter?
Why do some species of oak (Quercus spp.) retain their leaves through fall and winter?  I've found that these leaves are called marcescent leaves. There must be some benefit that the tree gains from this because it seems like it would increase the possibility of limb damage due to snow accumulation on the leaves.

Some trees only grow in places where there is no snow.

The trait might not necessarily allow for an advantage, but a few possibilities have been proposed:

Nutrient return to the soil when needed in the spring
Less palatability to grazing animals

Source:
 http://northernwoodlands.org/articles/article/why-do-some-leaves-persist-on-beech-and-oak-trees-well-into-winter


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What is this rather large insect in northwestern USA?
As you can see from the ants in the first picture, this insect is peculiarly large - over an inch long. I thought it was dead in the first picture, but it started moving around the next day. A couple of days later I found it again, dead. I have two dead specimens and other pictures if desired.

I think I've seen a shedded exoskeleton of one on a forest trail and another dead one from months earlier.
What species is it?
Location: Oregon, USA.

I just edited your question's title, changing the state for the country.

This is a Jerusalem cricket, an insect from the Genus Stenopelmatus.
Here is an image of Stenopelmatus fuscus for comparison:

PS: I was almost sure that this was a duplicate, I remember seeing this insect before on Bio SE. However, I searched "Jerusalem" and "Stenopelmatus" and found nothing.

Stopping at genus here is the best course; I misremember where I read this, but the genus Stenopelmatus is known to have upwards of fifty species that have not yet been named, with the more widely distributed species (of which fuscus is one) recognized as composite (there's more than one species hiding in the published records of that name).

@ArthurJFrost In reading articles on "Jerusalem cricket", I saw it was mentioned in a few that there were quite a few similar species not entirely documented or studied yet.


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Why do humans transport glucose but not sucrose like plants?
The reason why plants transport sucrose rather than glucose is due to the fact that it is more efficient and that nearby cells would not take up all the glucose too quickly.
Hence the plant convert glucose to sucrose before transporting them throughout the plant.
However, why is that humans and other animals all transport glucose in their bloodstreams? Why is it that they do not convert glucose to sucrose before transporting them since, as mentioned above, it would be more efficient?

Short answer digestion and absorption.
Animals have to digest sucrose into it's component sugars before it can be absorbed. Turning it back into sucrose afterwards would take energy and have no real benefit so it has had no reason to evolve.
The real question is why do plants make sucrose, and the answer is by living at a much slower pace,As you mentioned it is has slower uptake on the cellular level which is fine for plants but a detriment for more energy demanding animals. Stability is the other concern, sucrose is a lot more stable than glucose, animals are burning through glucose as fast as they can release it from storage so it doesn't matter how stable it is, whereas plants keep it around for longer and move it slower so it has a chance to breaks down on the way which would be a problem. Sucrose is more chemically stable than glucose and slightly more favorable osmotically (takes less water to dissolve the same energy value of sucrose than glucose) Both of these reasons make it more beneficial for plants to convert the sugars to sucrose, (if starch was water soluble they would likely only convert it to that.) They do this right at the end of photosynthesis then break it down just as it is being used in respiration so the energy investiture is minimal, while for animals they would be spending energy to break it down (digestion), then energy to put it back together, then energy to break it down again for respiration, its two extra steps for no benefit.
Just as a extra you can see why animals would evolve to break it down for absorption since as has been mentioned glucose is easier to absorb, whereas plants don't have to worry about extracting it from anything.

Short answer: Because sucrose is a pain.
Sucrose = glucose + fructose bound together. Obviously, a larger molecule has the disadvantage of inherent decreased cell membrane permeability except if you're using transporter constructs.
Glucose metabolism largely comes standard across human cells. Meanwhile, sucrose must first be split into glucose and fructose, then the fructose must largely be metabolized in the liver (https://en.wikipedia.org/wiki/Fructose#Fructose_metabolism).


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What are the response frequencies of sensory neurons?
Both visual and auditory stimuli are sent to the brain via ganglion cells (retinal resp. spiral). Both are the first cells along their resp. pathways that produce action potentials.
My question concerns typical frequencies of action potentials sent along the axons of the visual vs. auditory ganglion cells as a reaction to a "typical stimulus", i.e. a medium long, medium strong signal of some fixed frequency (e.g. light: red, sound: 440Hz) against a white resp. silent background.
Are these frequencies of comparable range, or does one type of ganglion cell (retinal vs. spiral) fire with a significantly higher or lower rate than the other?
(The question would not make sense, if the physical frequencies of light and sound - which trigger the receptor cells - would be coded by frequencies of action potentials. But I assume that this is not the case, is it?)

The auditory brainstem shows "phase-locking" typically up to 1-3Khz at most; 3000Hz is an incredibly high firing rate for a single neuron, but this phase-locking is achieved not by individual cells firing in-phase with an auditory stimulus, but rather with a population of cells that tend to fire in-phase, such that if you average across the population you get a phase-locked population volley.
In some cases, in some animals, this phase locking can even get to the higher frequencies (see here for example).
However, this phase locking seems primarily important for sound localization via interaural time differences. Frequency itself is encoded by which population of hair cells is activated, according to the properties of the basilar membrane. Firing rates of individual spiral ganglion cells are only faster than 100 Hz at very high stimulus intensities.
Similar to the spiral ganglion cells, retinal ganglion cells primary encode intensity information in their firing rates.
However, in both cases, it's important to recognize how crucial adaptation is in sensory systems. RGCs in particular fire primarily to transients, so it is typical to use light flashes, drifting gratings, or other dynamic stimuli. The response to a "medium long, medium strong signal of some fixed (wavelength)" is going to be brief, followed by silence, not a constant response like you imply.

You write "phase-locking" in quotation marks, as if you were not quite sure what it means, resp. you don't want to commit to a specific definition. Can you give me a source where phase-locking is explained in detail which I can rely on?

The quotes were not to indicate I don't know what it means, but to indicate it is a specific term rather than a descriptive one. https://www.google.com/search?q=phase+locking+in+the+auditory+system gives many sources.

Please don't feel offended, I know that you know what you are talking about. Alas, your hint how to google doesn't help me a lot (short-termed). There's too much to go through (and too specific: "auditory system"). Do you have a more general and concise reference?

I don't have a specific reference in my pocket, which is why I am suggesting you look at some relevant search terms and try to find the answer on your own.

Just for the record: I already gained some knowledge about "phase-locking" (its meaning, its origins, its contexts, its mechanisms,..) but am still missing an overarching overview.


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How many nucleic acids is there in "one molecule of DNA"?
I am confused...  People usually say that "DNA" is made of two strands deoxyribonucleic acid bound together. Nonetheless, the acronym "DNA" means "deoxyribonucleic acid".
So by logic, a molecule of "DNA" should be only made of one strand of deoxyribonucleic acid, and not two! Right?
This is really confusing...

DNA as we think of it is double stranded in its native (normal) state, so when we say "a molecule of DNA" we mean the standard, double stranded helix found in our cells. DNA is unstable as a single stranded molecule, so when saying "one molecule of DNA" it refers to the double stranded helix that DNA forms as this is the most common stable form. :)

Ok... So  "one molecule of DNA" is made of two deoxyribonucleic acids, right? Even though "DNA" is an acronym for deoxyribonucleic acid, the number of deoxyribonucleic acids that makes up "one molecule of DNA" is not specified when saying the word "DNA". Am I correct on that?

Yes. "One molecule of DNA" encompasses 2 strands in a double helix shape.

You are thinking about a nucleotide (A, C, G, or T). Nucleotides are molecules, and are the building blocks of DNA. DNA is synthesized from existing copies (not de novo), so there is always one strand, from which nucleotides are added to in a 3'-5' direction.

Uh no that's not what he was thinking about...


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Which information can be extracted from time course RNA-Seq Data?
So I am very new to the area of biology so I am sorry if this is a stupid question.
I have RNA-Seq data carried out over a span of 100 days and I have gene expression data in the following format. Each expression value is the mean of
3 replicates.
           Day 1         Day 10     Day50     Day 100
Gene 1      12             42         35       12
Gene 2      50             53         23       100
.           .              .          .        .
.           .              .          .        .
.           .              .          .        .

so on, the above data is just something I came up with, but can you tell me what information I can extract from this type of data ? Such as differential gene expression. Thank you very much

Note that there is also a bioinformatics.stackexchange.com site.

It can be complicated because RNA-seq data is looking at gene expression, in the form of mRNA. But there are thousands of housekeeping genes that are expressed constantly, as long as an organism is alive. So the real interesting genes in a time course are those that are differentially expressed. So gene 1, in your example is not that interesting. Gene 2 however shoes a 4-fold increase between day 50 and day 100. Still, that is not that huge. You need computer programs to sort all this out. But what you want is to be able to associate a huge change in mRNA (gene expression) that can be distinguished from background.

Hello Karl, thanks for your answer, I need to mention that each expression value I have is the mean rpkm value of 3 replicates. So the change in expression is not due biological noise. Yes, I was thinking of using R to perhaps classify the genes by the time points during which they have maximum expression.

Even though there are replicates that doesn't mean you've eliminated noise -- just reduced one of the many different sources of noise. You should have data for housekeeping genes that you can use to normalize gene numbers against; see for example this question and answer

I have never seen people extracting data from data, maybe you meant which type of information you might want to extract and the answer is "genes differentially expressed". You should check whether your data are normalized or not if they are you can use popular R package like DEseq2 or Limma to detect genes differentially expressed. In case your data have not normalized these tools have the proper way to normalize your matrix.
Here is the link of limma:
https://www.bioconductor.org/packages/devel/bioc/vignettes/limma/inst/doc/usersguide.pdf
at page 46 you have an example of how to handle with time-course analysis

Yes, that is exactly what I mean, I want to know what information I can extract. But since each data point is the mean of 3 replicates is it possible to find the differentially expressed genes? Thanks for the lead on DESeq and Limma !!

Yes, of course, you can, it would have been better if you have all the replicates for each sample, but you have to do with what you have unless people in the lab can give you the raw data. Please check the new answer. I have pointed you to which page you have to go to perform the analysis.

if this reply answered your question, mark the question as answered. Best


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What are null cells?
My histology textbook says the following:

The pluripotential hemopoietic stemm cell (which resembles a lymphocyte) is a member of the null cell population of lymphocytes.

It then goes on to add:
There are three types of lymphocytes:

T cells
B cells
Null cells:

Pluripotential hemopoietic stem cells
Natural Killer cells

However, this is the only text I find that classifies Pluripotential hemopoietic stem cells as null cells.
My question is: what are null cells? (and is this textbook accurate)
Thank you,
jsx

When quoting, can you please make sure to quote exactly what is being said? It is part of academic ethics to not misquote (but typos happen, don't worry about it). I doubt your textbook says stemm cell and by this small typo of yours , it makes me wonder whether (which resembles a lymphocyte) was added by you or was in the original quotation. You also want to cite which textbook it is (and eventually add a link to it). Are the bullets a direct quote as well? If yes, you should start the lines with > to highlight that it is a quote.

This seems like either a very basic, very old, or very misleading textbook. The obvious meaning of "null cell" here is one that lacks both B cell receptors and T cell receptors. Such "null cells" would cover vastly more territory than the two sets mentioned, which is why I question the accuracy of the book.

Did you have a look at wikipedia > null cell?

@iayork I understand that that is the definition of a null cell. I'm using Gartner's 'Colour Atlas and Text of Histology'. So, null cells are simply cells that lack the receptors that T and B cells possess, and as such include the natural killer cells, killer cells, PHSCs and other cells too?

@jxs As far as I know it's obsolete terminology. It probably included all those, but just by accident, just as "horseless carriage" would include a Tesla and a Ferrari as well as a Model T.

@iayork That was my impression. Thanks for clarifying!

This is easily found with a simple google search. "What are null cells"  https://en.wikipedia.org/wiki/Null_cell

@akaDrHouse as the term is virtually obsolete (and was previously used to refer to what we now call natural killer cells and killer cells), I was simply confused as to whether PHSCs truly belong to this classification. The text is misleading in that the pluripotential stem cell which gives rise to all the blood cells is then found again as a subtype of a subgroup it itself generated. I wouldn't come to ask a question before a google search.

Null cells are a "slang term" for cells of the lymphocyte progeny that are not APC (antigen presenting cells) and lack T and B cell receptors - therefore they are the natural killer (NK) cells.


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How many generations between the first lifeform and humans?
I expect very large error bars, but what's the number of generations between the very first lifeform (that can be described as evolving in generations) and humans? Is it closer to a quadrillion or a trillion?
A related answer estimates that there were around 300,000 generations between us and the chimp/human common ancestor.

The generations that preceded multicellular life will so vastly dominate the answer that the last 500,000,000 years don't even matter. So life is 3.5 billion years old, and for most of this time, life was prokaryotic, dividing every 20 minutes or so. Thats 26,000 generations per year. Multiply that by 3.5 billion and you get 9 trillion generations. That is likely an overestimate, based on optimal growing conditions of bacterial in exponential growth. But it is unlikely to be orders of magnitude off.

eukaryotes have been around for ~2.7 billion years so this should be taken with a large margin of error. Also we don't know how fast the earliest life reproduced, but it is probably accurate within one or two orders of magnitude.

I agree. It is difficult to know how fast the division time was. My original estimate came from my experience with bacteria in exponential growth in optimal media. I am going to edit my answer.

prokaryotes often make clones, so their generations are of a different kind.

We cannot be sure that the earliest life forms had well defined generations. It must have taken eons to learn replicating regularly. It is not even given that the life emerged just once and that we descend directly from the earliest organisms.

There may have been some failed first attempts. The optimized codon table is evidence of this. But all life on Earth today is evolved from a single common ancestor. There is no doubt about that. The evidence comes from conserved molecules like rRNA, tRNAs and the codon table.

Yan Wong and Richard Dawkins estimate the number of generations between modern humans and common ancestors of clades going back to the first life form in the book The Ancestor's Tale. Each chapter begins with such an estimation, for each clade as you descend down ("back in time") to the last common ancestors of each consequent clade. However, even they woefully give up after a while. There's just no way to estimate it beyond a certain point, past the metazoan clade, because it just doesn't make sense to speculate without basis anymore. Any attempted error margins will very necessarily be huge.

I would also mention that we switch definition of 'generations' at some point to even attempt to answer this question. For humans, a parent is 1 generation back. For cells, it is a division into daughter cells whereby there is no parent, only two "sister" cells that come from an originating cell ("mother cell", though this is a misleading term given the prior context). I too disagree with the estimation of a 20 minute division time, I don't think that's close to the reality of it. At least, it's a projection based on best-possible time for extant microbes, which is a stretch.

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


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Does the given pedigree show a Y-linked dominant trait?

I think that since every generation has males affected only, the trait must be Y-linked. Also, since every generation expresses the trait, I think it should be dominant. However, the answer key says that the answer is autosomal dominant. Could someone please clarify this and give a tip on how to recognise the difference?

Unfair question. With that short pedigree, it's hard to distinguish Y-linked from autosomal. And given that none of the females is affected I would have also opted for Y-linked dominant.

You're right that this could just as well be Y-linked dominant (althought that is pretty rare due to the small size of the chromosome).
The only reason pointing more towards autosomal dominant is the mention of "extra fingers and toes". Most cases of polydactyly are inherited in an autosomal dominant way.
Does seem like an unfair question, though, since (at least in theory) there's more than one possible answer.

(more likely to be X-linked recessive than Y-linked dominant, though)
Why is that? What about the fact that none of the females are affected?

Y-linked is very rare in general, just because there are so few genes on the Y chromosome. - X-linked recessive, on the other hand, is fairly common (hemophilia, anyone?) and also only affects males (because females have two X chromosomes, therefore one mutant copy doesn't affect them)

"more likely to be X-linked recessive than Y-linked dominant, though". This is not correct: the father doesn't pass the X chromosome to the son. For this to be the case, all mothers should be heterozigous, and some daughters would be affected.

ooops, yes, you're right - thanks for pointing it out; I'll edit my answer.

Ok so this is how I solve a pedigree:

This clearly shows that the disease is autosomal dominant. But there is one problem.
An autosomal dominant pedigree has the following features:
1. Appears in both sexes with equal frequency.
2. Both sexes transmit the trait to the offspring.
3. Doesn’t skip generations.
4. When one parent (heterozygous) is affected, and the other parent is unaffected, there is a 50% chance of the offspring getting affected. (You can refer to the cross I’ve drawn below your picture)
The pedigree in the question satisfies all 3 points except the last one. If there are 6 offsprings, at least 2 of them should be affected (if not 3), but there is only one, and that too a male.
Since only the male is affected in all generations, you’re right in thinking it’s Y linked. In my opinion, it can be Y linked dominant, since that’s very rare. And your question specifies that the trait is rare. It could DEFINITELY be autosomal dominant, had there been more affected offsprings in the third generation.


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Is ivy (genus Hedera) a shrub or an herb?
It seems like the difference between a bush (shurb) and an herb is that a bush has a woody stem.
What does that make ivy (genus Hedera)? I know that ivy can get a pretty hard stem, does that count as woody? Is there something between a bush and an herb?

Woody plants are usually either trees, shrubs, or lianas. Ivies are lianas, they can have 40 years of woody growth rings and bark. The categories are flexible. It's an arbitrary division for convenience, it isn't that clear cut. Bamboos for example, are a woody grass.
https://weedwise.conservationdistrict.org/weeds/english-ivy#foobox-1/7/Untitled-4-copy.jpg
Does that count as a woody plant? yes it's a woody liana.

Wow, that is one impressive ivy stem. - Thanks for the info, it does seem like liana would be the category to place ivy in.

Cheers, villager. It's happened often that I chop through an ivy and that it takes a few minutes with a saw and I think "I can't believe how tough these darned ivies are!!!" they are so tough. it's so woody it's surprising, you'd think it was another vascular flesh than a tree... ivy is like a real tree inside.


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Why are "itch signals" transmitted so slowly from the skin to the human brain?
In the second half of the BBC radio (and podcast) program Cats and Itch;
Discovery, The Curious Cases of Rutherford and Fry Episode 2 of 5 the phenomenon and origin of the "itch" and related sensations are discussed, with input from several specialists, including "Neuroscientist Prof Francis McGlone from Liverpool John Moores University and dermatologist Dr Brian Kim from the Center for the Study of Itch at Washington University. Yes, that is a real place."
Here is an unofficial transcription of a small segment starting at about 17:30:

Until quite recently, the same nerve fibers were thought to transport feelings of both pain and itch, from the skin to the brain. In 1997, a ground-breaking discovery revealed that itch has its own separate nerves responsible for that oh-so-familliar itchy-scratchy sensation. Now, if you accidentally lean on your “hot”, the sensation will travel through your fast pain fibers at 80 miles per hour; you can almost-instantly pull your hand away.
By contrast though, itchy signals crawl towards your brain at a sluggish 2 miles per hour, so once you’ve been bitten, it takes a while for the itching to begin.

Those quoted speeds equate to about 130 m/s and only 3.2 m/s, respectively.
What causes the "itch" fibers to transmit signals to the brain so slowly? Is there thought to be some evolutionary benefit to such slow conduction, considering that the speed of most signals from skin to brain are transmitted so much faster?

@uhoh - I am flattered! Great question btw +1

@AliceD I've orphaned your comment through clean-up, but indeed this site has great moderation; a key ingredient for a successful SE site.

Cleaning up is great. Thanks for your words. Mods often get virtually yelled at. Some appreciation to balance the scales is warmly welcomed.

What causes the "itch" fibers to transmit signals to the brain so slowly? Is there thought to be some evolutionary benefit to such slow conduction, considering that the speed of most signals from skin to brain are transmitted so much faster?

The interview most likely refers to the findings of Schmelz et al., J. Neuroscience, 1997: Specific C-receptors for itch in human skin
In essence they found tested the sensitivity of unmyelinated nerve fibers (note: myelination also increases transmission speed) towards distinct stimuli. They found that some of those fibers would selectively respond to stimuli which would be perceived as itching (such as histamines). They find that:

This slow conduction velocities attributable to small axon diameters ...

Note that since they don't need to, they also don't speculate on the physiological reason, why itching should be processed by slower fibers (and some potential explanations will be recognized quite well by readers of their article).
Please also note that the original claim, from 1997, however has been softened with the years, and there appears no strict separation been stimuli like "hot", and itching, in terms of distinct fibers and transmission speeds; e.g.: Davidson et Giesler, Trends in Neuroscience, 2011: The multiple pathways for itch and their interaction with pain

Great! Thanks for the references, I'll give them a read.

OK I've looked at these references. While I can't quite say I've read them thoroughly because I don't have the background to take it all in, I've learned more about the diversity of nerve fibers, and also that in contrast to what I'd thought before, some nerve fibers do not require a myelin sheath. Thanks for your help!

From a biologist background, one consideration: a distinction between itching and other sorts of pain would be that itching usually signals to our body that we have some prolonged inflammation or stimulation, whereas our reaction to strong heat or cold should be immediate. To avoid us having to sense itching all the time (which would be uncomfortable and distracting), it would seem likely that small or temporary signals must be filtered out. By having a slow transmission this may be achievable as spreading out a signal over time can ensure that only strong and prolonged signals are registered.


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Is a single polynucleotide necessarily and always a nucleic acid?
I am confused. I know that a DNA molecule is made of two polynucleotides.
But does each polynucleotide represent one nucleic acid? If so, a DNA molecule is made of two nucleic acids, right?
Or do the two polynucleotides (that form a molecule of DNA) make up only one nucleic acid? If so, a DNA molecule is only made of one nucleic acid, right?

What do you mean by "two polynucleotides"? I would say "two polynucleotide strands" - start with a nucleotide, connect some of them together and you have a nucleic acid (strand), join two of those and you get double-stranded DNA. Is this not covered in wikipedia pages like : https://en.wikipedia.org/wiki/Nucleic_acid ?

Well, each strand of a DNA molecule makes up one polynucleotide... Right?

I would just say it "is" a polynucleotide, but yes - double stranded DNA is two polynucleotide strands wrapped into a helix.

See that's the problem... You're talking about "polynucleotide strands". But how many polynucleotides is there in one strand of DNA: a) one b) many?

One. A polynucleotide is made of multiple nucleotides - it is a strand.

Oh ok. So, there are two types of nucleic acids: 1) DNA --> which is double-stranded, so it's made of only two polynucleotides 2) RNA --> which is single-stranded so it's made of only one polynucleotide. So if we get back to my original question "Is a single polynucleotide necessarily and always a nucleic acid?" --> the answer is no, for DNA is a nucleic acid and it is made of two polynucleotides. Am I right?

Yes, that's right.

Hallelujah! I finally understand! Thanks a lot, man!!

Mark: No, you don't. See my comment to your answer.

Possible duplicate of Is a DNA molecule a single strand of polynucleotide or two of them linked together?

I would advise you to focus on ideas in molecular biology rather than questions of nomenclature, which betray a chemical attitude to the topic. Counting strands is not where the action is, but if you do so at least get it right.

There are two types of nucleic acids: 1) DNA --> which is double-stranded, so it's made of only two polynucleotides 2) RNA --> which is single-stranded so it's made of only one polynucleotide. So if we get back to my original question "Is a single polynucleotide necessarily and always a nucleic acid?" --> the answer is no, for DNA is a nucleic acid and it is made of two polynucleotides.

Wrong. Some viruses have single-stranded DNA (ssDNA). One polynucleotide = one DNA molecule (always). Two polynucleotides = two DNA molecules (always). (Note: two strands of DNA are two molecules; two strands in double-stranded DNA are still two molecules, because there is no covalent bond between them.

...and some RNA viruses are double-stranded. As I commented previously, I suggest you stop counting the strands in nucleic acids and study their biology.

Your question arrangement is wrong, DNA is made up of 2 polynucleotide strand indeed. And these polynucleotides are the polymers of nucleotides, where nucleotides consist of deoxyribose sugar in case of DNA and ribose sugar in case of RNA+nitrogenous base+phosphate. Yes it is always a nucleic acid.


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What is the opposite of a mutation (the regular state)?
What is the term, if there is one, to describe the natural state of a gene? The one single word to describe it, just like mutation is the one single word do describe a deviation from that state.

If you had written "what's the opposite of mutant", I'd have an answer for you. However, mutation and mutant are not synonyms.

If you brought this up and mentioned clearly that the two are not synonymous, what is it for Mutant? I'm asking for general knowledge.

I just added an answer and edited your title. Feel free to roll it back.

A mutation can be both the act of changing the genetic material (the process) or the changed genetic material itself (the result of the process). You're using the second meaning. See What is the definition of a mutation? for more info.
That being said, the opposite of a mutant allele is a wild type allele.
According to Pierce in his book "Genetics: A Conceptual Approach" (2012):

The normal allele for a character is called the wild type because it is the allele most often found in the wild. (emphasis mine)

The same way, the opposite of a mutant phenotype is a wild type phenotype.
Besides that, you can sometimes find "wild" alone, without "type": wild allele, wild phenotype etc...

Source: Pierce, B. (2012). Genetics. New York, NY: W.H. Freeman.

This is correct +1. In response to your comments above, note that many people use the term "mutation" for "mutant allele" which is a little confusing. Just type "carry the mutation" in Google Scholar to find examples. You might also want to have a look at What is the definition of a mutation?

Yes, very confusing I'd say... And that annoys me. Anyway, OP just rolled back my edit, so I clarified the issue in my answer.

@Remi.b thanks for your edit, the linked answer is very didactic.


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Is there enough vitamin B12 in lakes, rivers and ponds, for humans not to need to take supplements?
Vegans will often say that having an animal-free diet is best for our health and is actually the diet that humans should be eating to function optimally. To which meat eaters will raise the issue of B12, and how (they believe) it is only to be found in animal products [thus vouching for an evolutionary need to eat meat and eggs). These days, with all our water being treated to remove pathogens, it is obviously best to take b12 supplements, but the question remains: do vegans have a point? Is there actually enough b12 in water for humans to not develop an insufficiency?

I was not aware that drinking water was a source of B12 at all! It might be clearer to start with that information, and then ask whether the source is sufficient.

Even if it was the case that B-12 could be absorbed from water-borne microorganisms, 1) Wouldn't it depend on the particular body of water you drink from, e.g. a stagnant pond vs a spring-fed mountain stream? 2) Before water treatment, weren't water-born microorganisms a major source of diseases such as cholera?

@jamesqf It would certainly depend on the source I think. Obviously, stagnant water with more algae, particularly in lakes would contain more B12 than a mountain spring.  I was concerned about cholera, but cholera and many other such diseases are the results of non-nomadic living. City environments, where waste is allowed to build up, cause widespread epidemics. My question is in terms of human history, before the advent of agriculture and settler communities.

Of course there is no evidence for the superiority of the vegan diet claim to begin with, so there is that, and there are plenty of vegan foods fortified with B12, even some from non-animal sources.
No, there is not enough B12 in treated water nor well water for a human. There can be enough B12 in untreated river/lake water because it contains high levels of fecal matter or algae which is high in B12 (b12 is manufactured by anaerobes).  Of course these are the things you want removed from your drinking water so reducing B12 is inevitable. Also can contain enough being the key phrase it depends on the water source, cleaner river contain less.
Evolutionarily speaking humans eat animals for the same reason every omnivore and many herbivores (deer, ect) do, because we can, it is generally a superior nutritional substrate which is more than enough for evolution to favor it.
source 1
Source 2
source 3

Could you elaborate on your definition of 'superior'? I said vegan diets were healthier not 'superior'. @John

which there is no evidence for. And by superior substrate I mean easier to digest, more calories, more vitamins, an animals contains everything you need since it is basically made of the same stuff.

No evidence? https://www.youtube.com/watch?v=30gEiweaAVQ

@Samuel   Vegetarian not the same as vegan diet, it is a pretty important distinction.

The video compares research from 3 primary groups, meat eaters, vegetarians, and vegans, on most points.

It is also a video put out by one individual trying to sell something, an actual source would be important. It is basically one long string of cherry picked data and conclusions out of context. Sourcing requires more than just flashing the headline of a paper for a few seconds. Gregor is a known for exagerated and unfounded claims and the video has been debunked before, https://sciencebasedmedicine.org/death-as-a-foodborne-illness-curable-by-veganism/. Worse many of his claims are outright lies counter to the papers included actual conclusions, the video is pure propaganda.

Fermented food is a safer and higher b12 option for a vegan, it can have a lot higher content of yeasts and bacteria than safe water, and it can be controlled.
Most vegan foods (not protein rich) can safely ferment until 50% to 99%(sry for the humor) of their expiration date, living plant matter in any carb/plant mix will generally kick off a good fermentation. some foods like salad couscous are full of yeast and become unappetizing and gluey with yeast a long time before they become unhealthy to eat.
It would be difficult to design a pond/lake which has high content of bacteria and archea and chlorella to be optimal for humans, whilst also being safe for children. Rivers should have mats of algea that filter the water, however they are so variable, it's pot luck if a river has an excess of nitrogen or a silty bacterial nuisance, A river can be jam packed with nitrogen detritus, and after a storm/ in the wrong place it's not reliable.
In winter the lake can become less productive biologically, too high in nitrogen, and if it's biologically rich it will be subject to wild seasonal variability.
Blooms of animals, daphnia, cyclops can occur, eating whatever is making the vitamin b12, and any unseen bacteria can bloom, which benefit from warmth and that will thrive noxiously in the gut.
A snail doesn't even have a lot more neurons than a tardigrade, and definitely a lot less neurons than small insects and acarians that you accidentally consume from plants.
You can reprimand me for the lack of references, it will give be a subject of study, however it's too broad a topic to reference and research right now, unless you think i've made an overstatement.


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How many polynucleotides are there in one molecule of DNA?
I always thought that a molecule of DNA was made of two polynucleotides each making up one strand of the molecule... Is that right?

One polynucleotide: one molecule of DNA. One DNA "strand": one polynucleotide: one molecule of DNA. Two DNA "strands": two polynucleotides: two molecules of DNA.

No, you're wrong. One molecule of DNA is made of two polynucleotides. You should have a look at this: https://biology.stackexchange.com/questions/66343/is-a-dna-molecule-a-single-strand-of-polynucleotide-or-two-of-them-linked-togeth .

Look, i have been working with computational models of DNA molecules since 2009. i look at and analyze structure, dynamics, and energy of DNA molecules daily. i have given you the right answer. What you do with it is up to you.

@MartinKlvana Being more assertive, stating i have given you the right answer or making an argument from authority by appealing to your experience is not how you convince anyone of anything. On the other hand, Mark pointed to a post offering evidence of authors clearly defining a molecule of DNA as being made of two strands. If you disagree with this terminology and think that most authors use the term differently , please respectfully suggest your own answer at the linked post.

@Mark This post seems to contradict your claim would be better than No, you're wrong. Martinklvana would probably had reacted differently if your opposition was made in less absolute terms. Note that when dealing with questions of terminology, it is better not go into absolute certainty as different authors may use the same word differently.

The term molecule was coined by chemists to describe small entities in which the atoms are joined by covalent bonds. When one is talking about large biological entities involving non-covalent bonds (proteins, nucleic acids) the strict definition often conflicts with the way one conceptualizes these entities, and this has led to common usage that may strictly be regarded as incorrect. However the definition of a molecule is of no real concern to molecular biologists and few people care that the situation is ambiguous.
Definition of Molecule (Wikipedia)

A molecule is an electrically neutral group of two or more atoms held together by chemical bonds

By this definition double-stranded DNA consists of two molecules, and haemoglobin consists of four molecules (or perhaps eight, if one regards the haem as a separate molecule).
Use of Molecule to refer to multistrand Nucleic Acids and Proteins
Because we are often concerned with the functions of a double-stranded nucleic acid or a multi-subunit protein in its entirety, one finds them referred to as molecules by quite reputable sources. For example:
Encyclopedia Britannica

Each hemoglobin molecule is made up of four heme groups surrounding a globin group, forming a tetrahedral structure.

Protein Data Bank: Molecule of the Month

DNA is arguably one of the most beautiful molecules in living cells. Its graceful helix is pleasing to the eye. DNA is also one of the most familiar molecules, the central icon of molecular biology, easily recognized by everyone.

Conclusion
It would be better to spend one’s energies on more important and intellectually interesting topics concerning nucleic acids and proteins then whether only their individual strands or subunits are truly molecules.

In general, it is right since with the term DNA you commonly refer to the double-stranded DNA. However, you need to be aware that DNA may exist in different forms.
Single-stranded DNA (ssDNA), for example, is composed of only one strand of DNA, so one chain of nucleotides or one polynucleotide molecule.
Double-stranded DNA (dsDNA) is the common form of DNA found in cells and it is composed of two polynucleotide molecules.
Triple-stranded DNA (tsDNA ?) also exist, which of course, is composed of 3 polynucleotide molecules.

There are four ways to answer a question (Anguttara Nikaya); a counter-question is one of them.
When water changes its state from gas to liquid to ice does the number of water molecules in the system increase, decrease, or remain the same?
The answer is: The number of water molecules in the system remains the same. (Note: The three states of water differ by spatial arrangement of water molecules and by the number of "hydrogen bonds" between the molecules.)
Now, let's replace "water" with "deoxyribonucleic acid" (DNA) . . .
When DNA changes its state from dissociated to associated does the number of DNA molecules in the system increase, decrease, or remain the same?
The answer is: The number of DNA molecules in the system remains the same. (Note: The two states of DNA differ by spatial arrangement of DNA molecules and by the number of "hydrogen bonds" between the molecules---cf. water.)
The "water" analogy goes even further: The process of dissociation of DNA molecules is called "melting."

i melt DNA (computationally) for a living. Seriously. No kidding.

As you are working as a chemist (physical biochemist or whatever) you are correct. In a chemical sense the single covalently bonded chain is a molecule. However, it occurs to me that there may be a practical as well as psychological explanation for people thinking of dsDNA or multi-subunit proteins as molecules. This is the osmotic affect of these molecules. I am ashamed to admit not being certain of this, but if osmotic pressure is related to molarity, then don't these multi-chain species act as molecules? (This would indicate the equation needs restating rather than the definition.)


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What is this bug I found at my house?
I found it on my door. I live in Southeast Texas. What is it?

Can you include more information in the question itself (not as a comment). For example, the size, how fast it moved (if at all) time of day, time of year...

It looks like an insect larva, maybe a dipteran. The white tree-like structures on its side could be its trachea (respiratory system).