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Size of Apatosaurus
What are the current and up-to-date estimates of the size of the big sauropod dinosaur Apatosaurus (the biggest species of it) in terms of mass range (weight) and total length? I prefer the answer in metric units.

From the wikipedia page on Apatosaurus:

Most size estimates are based on specimen CM 3018, the type specimen of A. louisae.
  In 1936 this was measured to be 21.8 m (72 ft), by measuring the vertebral column.[5]
Current estimates are similar, finding that the individual was 21–22.8 m (69–75 ft) long and had a mass of 16.4–22.4 t (16.1–22.0 long tons; 18.1–24.7 short tons).[6][7][8]
A 2015 study that estimated the mass of volumetric models of Dreadnoughtus, Apatosaurus, and Giraffatitan estimates CM 3018 at 21.8–38.2 t (21.5–37.6 long tons; 24.0–42.1 short tons), similar in mass to Dreadnoughtus.[9]
Past estimates have put the creature's mass as high as 35.0 t (34.4 long tons; 38.6 short tons).[6]
Some specimens of A. ajax (such as OMNH 1670) represent individuals 11–30% longer, suggesting masses twice that of CM 3018 or 32.7–72.6 t (32.2–71.5 long tons; 36.0–80.0 short tons), potentially rivalling the largest titanosaurs.[10]

"Osteology of Apatosaurus, with special references to specimens in the Carnegie Museum". Memoirs of the Carnegie Museum. 11 (4): 1–136, Gilmore, C.W. (1936).
"A new method to calculate allometric length-mass relationships of dinosaurs". Journal of Vertebrate Paleontology. 21 (1): 51–52, Seebacher, F. (2001).
"Giants and bizarres: body size of some southern South American Cretaceous dinosaurs" Historical Biology. 16 (2–4): 71–83, Mazzetta, G.V.; Christiansen, P.; Farina, R.A. (2004).
"Burly Gaits: Centers of mass, stability, and the trackways of sauropod dinosaurs". Journal of Vertebrate Paleontology. 26 (4): 907–921, Henderson, D.M. (2006).
"Downsizing a giant: re-evaluating Dreadnoughtus body mass". Biology Letters. 11 (6), Bates, K.T.; Falkingham, P.L.; Macaulay, S.; Brassey, C.; Maidment, S.C.R. (2015).
"A giant, skeletally immature individual of Apatosaurus from the Morrison Formation of Oklahoma" 61st Symposium on Vertebrate Palaeontology and Comparative Anatomy - Programme and Abstracts: 40–45, Wedel, M. (2013).

So if I understand correctly, the largest Apatosaurus was about 26-27 meters long and may have weighed 50+ metric tons.


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Do songbirds prefer clean water?
The other day, the water in our backyard birdbath (Eastern US) had become fairly murky. So my wife cleaned it out and replaced it with fresh. Seemingly immediately began an amazing run on the thing. Robins, sparrows, finches , wrens, and catbirds all took their turns splashing and fluttering. At times they even queued up for their shot at a bath.
This got me wondering, are birds affirmatively more attracted to apparently clean water than to more dingy stuff? An easy evolutionary explanation would be that clearer water might be less likely to contain dangerous organisms.
Our experience here hardly counts as a controlled experiment, not least because the water was changed shortly after I had restocked our feeders, so the increase in bathers may simply have resulted from the larger number of birds drawn by the newly available food. But I have never before noticed such bath mania after I have filled the feeders. On the other other hand, it hasn’t rained here in maybe two weeks, so that could be another confounding factor.
But we have had birdbaths in our yard for decades (including the one in question, and in the same location) and we don’t recall ever observing a similar rate of use. Thus my question, which I paraphrase here: does water’s clarity affect its attractiveness to songbirds?
(I’ve done some Googling but turned up nothing.)

clear water might be a factor in this too,i have a garden pond and a little stream where birds can take a bath but they only do so if the water is clear.

Water is used for cement, so murky water won't make the feathers last longer and mantain their static electrical balance.

source: Stack Exchange

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

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Is there a simple way to generate sets of sequences that re-capitulate the topology of pre-defined phylogenetic tree
I would like to generate ensembles of N sequences in such a way that the phylogenetic trees obtained from my ensembles (e.g., by neighbor joining) have the same (or nearly the same) topology as a specified "real" tree obtained from an alignment of N proteins.
My starting point would be an empirically determined amino acid substitution matrix. The matrix would be used to generate a "random" sequence representing the root of my simulated tree. The root sequence would then be evolved, "split", and its products evolved, iteratively until N sequences are generated. Somehow, the topology of the "real" tree would be used to guide the branching process.
This problem arises in determining the significance of correlations between mutations at different sites in a protein (specifically, the "mutual information" measure). One would like to determine the contribution of "pure phylogenetic" correlations to the mutual information for a given alignment of proteins.
The answer to my question seems connected to the "parametric bootstrap procedure" commonly used in phylogeny reconstruction. In fact, the reference below seems to use this procedure to generate the ensembles I describe above. However, their procedure is not explained in detail. This makes me think that there may be a simple answer to my question.
reference :
"Separation of phylogenetic and functional associations in biological sequences by using the parametric bootstrap"
K. R. Wollenberg and W. R. Atchley (2000) PNAS 97, 3288–3291

Yes, what you are looking for seems to be an alignment simulator, which is quite commonly used in phylogenetics. Given a phylogenetic tree and a substitution model, you can use for instance INDELible or DAWG to simulate the extant sequences (N sequences at the tips). These programs can also simulate the indel process (gaps), which means your final sequences won't have, by default, the same length -- but you can change the settings to exclude insertions/deletions.
There is no absolute guarantee that the tree estimated from the simulated sequences will follow the "true" one (used to simulate the sequences), but they should be close enough if:

you don't simulate gaps
the branch lengths are not too short
the sequences are large enough

Thanks Leo. I scanned through the INDELible paper and this seems to be exactly what I was looking for (e.g., calls for an equilibrated root node and a newick tree as input).

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Are the hyphae in mushrooms unicellular or multi-cellular?:
The mycelium is just a collection of hyphae.
Are these hyphae unicellular or multicellular?
If there's any problem in my question please inform me. Thanks!

Welcome to SE Biology. This seems like a homework question and these require that you show you have tried to find an answer yourself.

The haphae of mushroom are multicellular

@Michael_A I got the answer

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Are intestinal and pancreatic lipases different?
For explaining the action pancreatic lipase, my book wrote this equation:-
$$fat\space particles + lipase\rightarrow fatty\space acid + glycerol + lipase$$
But for intestinal lipase, my book has a different equation:-
$$fat\space particles + lipase\rightarrow monoglyceride + fatty\space acid$$
So, did my book make a mistake or are intestinal and pancreatic lipases different?

Does food enter the pancreas? Where do pancreatic enzymes act?

Pancreatic lipase and intestinal lipase are almost same in their functions. In the intestine, the name of the lipase is a triacylglycerol acyl hydrolase it also called colipase dependent lipase or Pancreatic lipase,  Free fatty acids, and 2-monoacylglycerol are the primary products of lipid digestion in the jejunum. and Pancreatic Lipase also produces Free fatty acids and 2- monoacylglycerol.
so we can say that both enzymes are almost same and produce the same products.
Sources Lippincott's Illustrated Reviews Biochemistry 5th edition Chapter 15


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Number of DNA in a chromosome
I wanted to know the number of DNA in a chromosome.
I previously knew that there are 2 DNAs per chromosome, but later I think I saw somewhere that it was trying to imply that the number of DNA is one per chromosome.
Please clarify this

There are two DNA chains per chromosome. There is one unbroken strand of double-stranded DNA per chromosome (except during DNA replication).

There is one or two chromatids per chromosomes (depending upon the stage of the cell cycle) and there are two (anti-parallel) strands of DNA in each chromatid.
As discussed in your previous post, you are using the term DNA incorrectly which makes your questions hard to understand. You should probably just have a look at an intro course to genetics.
If you want to learn through SE posts that I highly recommend you having a look at the posts:

Chromosome and chromatid numbers during cell cycle phases
How is the diploid chromosome number maintained at mitosis?
What are homologous chromosomes?
Interpretation of picture of human chromosomes
What is the relationship between DNA molecules and the chromosomes?

Remi b, could you please suggest edits so that the question renders authentic

What do you mean by authentic. Authentic means "of undisputed origin". Editing it necessarily reduce its authenticity. Do you mean "more clear"? Just adding "molecule" after the term "DNA" would already much improve the question!

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How could a species be engineered to go extinct?
Non-biology background here.
I read this very interesting article: https://www.wired.com/story/crispr-eradicate-invasive-species/
However I am having a hard time wrapping my head around something:
From my basic understanding of natural selection, a gene/trait will spread if it gives the group a relatively higher chance of having children, who will pass on the trait, etc.
However in this example, the trait is infertility! Doesn't it go completely against natural selection? How could this spread??

Not sure about this particular case, but in some cases it involves adding so many of the altered species that non-altered species have trouble finding the necessary food, etc.  In other cases, I've heard that it can involve injecting species which will produce infertile offspring which will do this.

They can't actually cause extinction. I find it irritating that all the news articles are spouting off about that. If I recall correctly, the most recent studies have shown that it can, at the very best, reduce the population by something like 80%.

Short answer
The article in particular that you reference is discussing the possibility of using a mechanism called gene drive. The concept of gene drive breaks the normal "rules" of inheritance and allows a gene to spread much more rapidly than normal in a population.
Longer answer
Gene drive depends on the idea of a selfish gene. There are naturally occurring genes that make copies of themselves to other parts of the genome. Selection pressures can operate at the level of these genes: a gene that can copy itself is going to end up in more offspring than would be expected due to random assortment.
For example, imagine a gene present in one chromosome of one parent. Typically, only half of that parent's offspring will have that gene. However, if the gene is able to copy itself to the parent's other chromosome, now all offspring of that parent will have that gene. The prevalence of the gene just doubled. It's possible that the gene will also confer some negative traits, but as long as those negative traits aren't sufficient to cause a >50% reduction in later reproduction of the offspring, they are going to do just fine and go on and mate, spreading the gene further, potentially to an entire population fairly rapidly.
The new technology CRISPR makes it easier to create synthetic genes that selfishly copy themselves within the genome (note: this is definitely not the only application of CRISPR) and could confer positive traits that are helpful to humans, like mosquitoes resistant to being carriers of malaria, or to introduce deleterious mutations into a population.
As you point out, introducing a mutation that causes sterility and having it spread is still not easy. There are a few clever approaches, though, that can make it possible. Note that the strategy does not to have 100% effectiveness to wipe out a population: once below a certain level, members of the population may have trouble finding mates and face greater predation pressures and the population can collapse.
One technique is to boost the proportion of males. If you can force all the offspring of one male to be male, the proportion of males in the next generation will be higher. Those males-that-only-produce-males don't have any immediate reproductive disadvantage versus normal males. If they survive and mate normally, they will continue to compete with normal males (they may also compete with females for food resources during their lifetimes). Any time a normal male mates, sure, it will create a new generation of some females, but every time a transfected male mates it will effectively double the number of transfected males. Even as the total number of individuals in the species drops, the proportion of transfected males remains high. Eventually there are too few normal males to mate, the number of females drop to unsustainable levels, and the population crashes.
This approach is similar to the technique of releasing sterile males which has been used successfully for population control. The difference is that the gene drive technique raises future generations of the (sort-of) sterile males by itself, which might mean it can be used in population control when it is not possible to lab-raise large numbers of sterile males.
Note that use of these technologies is very controversial. There are concerns that such a gene could accidentally move from one species to another, for example. Future use of the technique will require combined research into safety and efficacy.

References
Burt, A. (2003). Site-specific selfish genes as tools for the control and genetic engineering of natural populations. Proceedings of the Royal Society of London B: Biological Sciences, 270(1518), 921-928.

Thanks. The approach of pushing male offsprings is interesting. Although the article did not mention that so my understanding was really about limiting fertility per se.

The terminology here is a bit confused: all genes are selfish. That, at least, is the fundamental message behind the gene-centric view of evolution (selfless genes are evolutionarily disadvantaged). So talking about CRISPR-generated selfish genes is meaningless.

@KonradRudolph I edited the terminology a bit - I was intending to be readable to a more lay audience understanding of selfish genes, and use the term to highlight places where the gene-centric view of evolution makes different predictions than a more classical organism-centric view, rather than the multitude of cases where they are entirely consistent. Let me know your thoughts.


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In plant cells, is water stored only in the vacuole?
In the turgor of plant cells, is water stored only in the vacuole or can it be stored in the cytoplasm and the other cellular organs too?

One of the properties of "storoge" is that in can be filled or empied when needed. Contents of cytoplasm and all organelles are aqueous solutions so all of them contain quite some water. However, thease solutions need to maintain precise concentration of many solutes in order to facilitate proper enviroment for various biological processes. Therefore, radical changes in amount of water in cytoplasm would be detrimental to life of the cell. Vacuole is not as sensitive and it can expand or shrink and act as a sort of water availibility buffer for the rest of the cell.

The cytoplasm of the cell is 80% water$^1$. All organelles contain water because all enzymatic activities inside the cell require water. However vacuoles are generally said to store water because they generally make up 30% to 80%$^2$ of the plant cell.
Thus the cytoplasm, vacuole and all other organelles contain water and contribute to the cells water potential and turgor pressure.
References:
1.Wikipedia cytoplasm
2.Wikipedia vacuole


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Basic molecular biology of nucleic acids book for a mathematician studying DNA and RNA formally?
I am a mathematician studying DNA and RNA language from the perspective of Formal Language Theory.
Note that I am aware of these posts:

best book for a comprehensive introduction to biology for a computer science graduate interested in undertaking research in bioinformatics
Introductory biology text for an outsider
Material recommendation: molecular biology for mathematicians and computer scientists

I consider my situation more specific, I am specifically dealing with DNA and RNA, so what I need is a basic text that deals with this two structures, rigorous but still accessible.
As an example I quote a paper I am reading:

(...) Inverted repeats are prevalent features of nucleic acids (...)

I would like trustable references for the fact that these features indeed exist, which is fundamental for my work, and maybe a shallow explanation for what they biologically imply, but I do not want to delve into what these features mean (It would be great to understand them from a biological perspective but that is not my priority)


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Why is reducing the amount of detail required to remember the location of an object in one's environment adaptively significant?
In Campbell's Biology Chapter 51, question 36 reads:

Which of the following shows the adaptive significance of cognitive mapping to animals that employ this type of learning?
A) It increases the ability to visually recognize landmarks.
B) Cognitive maps reduce the amount of detail required to remember the location of an object in the animal's environment.
C) Animals can locate essential locations in their environment, such as nests, hazards, and feeding areas.
D) Animals can outmaneuver predators by planning and memorizing getaway routes.
E) Animals can determine their position relative to landmarks by a triangulation process.
Answer: B

I answered by saying that Cognitive Mapping is especially important because animals can locate locations essential to its survival (e.g. nests, hazards, and feeding areas), but the answer was B. Why is that more important?

Hi and welcome. The question you ask here should be self contained. I edited the question; if you don't think it's helpful, please feel free to roll back.


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Are all dead plant cells (that die to do a job), have secondary wall?
Can we say that all plant cells that die to do a job (they are dead now), like the outer cell surface of the root cap, have secondary cell wall?

Not all plant cells perform a function when they die.
But a lot do.
Sclerenchyma is refereed to as:

Sclerenchyma is the tissue which makes the plant hard and stiff...

Mature sclerenchyma is composed of dead cells with extremely thick cell walls (secondary walls).

Plant cell death includes necrosis, apoptosis and autophagy and studying how and why they occur is an active area of plant research.
Some plant cells die because they are not provided enough energy. Plants garner energy via the sun and biochemical process known as photosynthesis.
When the days start to become shorter there is less sunlight and parts of some plants die.
E.g. Leaves die.

I add an answer since Andrew's answer "Do all plant cells that die do it while fullfiling a function" and the question asks wheater all plants cells that die to fulfill a function have a secondary wall.
Hyper-virulence response is a plant defence mechanism from pathogenes similar to "scortched earth" strategy. The plant kills all cells near the infection to prevent the proliferation of the pathogen.
If you consider this as a "job" than no, not all cells that fall in the line of duty have secondary walls
Root cap cells are parenchyma cells that undergo programed cell death.
By definition parenchyma cells do not have a secondary wall


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What is this soil digging insect?
It is in Texas(Month: May). Are these flying ants?termites? or Cicada Killers?

Certainly not cicada killers--those have yellow stripes on them, are considerably larger, and also have a very different shape of abdomen. Here's a good pic of one of those: https://bugguide.net/node/view/1721236/bgimage.
They certainly look to have a hymenopteran "waist" so that means they aren't termites, they are some kind of winged ant. Possibly carpenter ants due to the large size (for ants) and the reddish-brown color (like this one https://bugguide.net/node/view/1056576/bgimage).


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Animal body size determination for abundance
Does an animal being small or large determine its abundance?

Welcome to Biology.SE! There is an expectation that question-askers show that they have done preliminary research prior to posting. There appear to be many good and free-to-read papers addressing your question, found by a simple Google Scholar search.  See -- Relationships between body size and abundance in ecology (PDF)

closely related https://biology.stackexchange.com/questions/24482/how-big-should-the-human-population-be-as-predicted-by-body-mass/24495#24495

I'm sympathetic to @Dirigible that this seems like the kind of thing that should be easy to research, but I was surprised to see that there's not an answer to this already on SE.Biology. So very quickly:
Yes, there is what is known as an "allometry" relationship between body size and abundance in which the two tend to be inversely related.
Here is one meta-analysis that attempts to describe the relationship across food webs. Here is a review article that may be easier to read describing the law in somewhat more general terms. Here is a figure from the review with plots showing the relationships in different kinds of organisms from different studies:

In some cases people talk about the population density in some area rather than overall abundance, as density is easier to estimate and can be thought of as a local measure of abundance. From the review you can see that there are some equations that people have derived to describe the relationship:

For large compilations of population densities, the relationship between the average mass of a species (Msp) and its average density (Ncomp) is generally well fit by a power function ($r^2 > 80\%$), with an exponent near 0.75 so that $N_{comp} = cM^{\frac{-3}{4}}$, where c is a constant (also known as Damuth’s Rule)...


text:
What species mimics two others?
Richard Dawkins in 'the selfish gene':

But there are species of mimic that do something very strange. Some individuals of the species mimic one nasty species; other individuals mimic another. ... One butterfly may mimic species A while his brother mimics species B.

What is an example of such a species, along with the two species its members mimic?

How about Mimic Octopus? they mimic sea snake, lionfish, and others.
https://en.wikipedia.org/wiki/Mimic_octopus

Thanks Polypipe wrangler.  Dawkins seems to have something else in mind:  One allele in the gene pool that makes the butterfly look one way, another allele (for the same gene or gene complex) that makes the butterfly look another way.  Not a shape-shifter!  I'd like to know a specific butterfly species like that.


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What are the effects of sleep deprivation?
Having recently pulled an "all-nighter" while trying to fix a fatal bug in our release code, I started thinking of any health risks that I might have.
What are the adverse effects of staying up for staying up for 42 hours, considering I took no caffeine or other stimulants, as well as no depressants such as alcohol?
Upon googling I found a lack of facts, what would be good is a list of effects and rough times that they start happening.  And any significant problems I would face, but moreover I would like to know what causes them?  Unfortunately I only studied Biology until GCSE (UK - SAT/TAKS Alternative) and might need some simplified explanations or links to help understand more complex tasks.
I'm not even sure if this question is grammatically correct, and my brain power has slowly dwindled, should I be worried?  I have read this and understand it to a vague extend.

Something that I know is that it affects memory negatively. If you search google scholar then you'll get a lot of articles on sleep deprivation experiments.

I've never heard of google scholar before.  Thanks for pointing me in that direction!  It seems a cool google sub-site.  Also thanks for the information on more sleep deprivation experiments.

Personally, I notice that most cognitive effects of sleep deprivation become very strong during times in which I would be habitually asleep, and minimal when I would awake normally. Arousal also seems to minimize perception of sleepiness, while being idle/bored makes it worse. You don't seem to have experienced this, your symptoms just get worse and worse.

You seemed to have answered your own question with your edit.

I noticed it worst when I was actually having a shower Superbest - Not sure if it was the heat that made be drowsy or what.  I guess I did Eastman, however why this is caused was not answered, and whether there are any lasting effects.

I recommend watching this youtube video by Hank Green (SciShow): https://www.youtube.com/watch/?v=pwNMvUXTgDY

24 Hour Mark
The consequences of sleep deprivation at 24 hours is comparable to the cognitive impairment of someone with a blood-alcohol content of 0.10 percent, according to a 2010 study in the International Journal of Occupational Medicine and Environmental Health.
36 Hours
Now your health begins to be at risk. High levels of inflammatory markers are in the bloodstream, said Cralle, which can eventually lead to cardiovascular disease and high blood pressure. Additionally, hormones are affected — your emotions can be all over the place.
48 Hours
After two days of no sleep, the body begins compensating by shutting down for microsleeps, episodes that last from half a second to half a minute and are usually followed by a period of disorientation. “The person experiencing a microsleep falls asleep regardless of the activity they are engaged in,” she said. Microsleeps are similar to blackouts, and a person experiencing them is not consciously aware that they're occurring.
72 Hours
Expect significant deficits in concentration, motivation, perception, and other higher mental processes after many sleepless hours, Cralle said. “Even simple conversations can be a chore,” noted Kelley. This is when the mind is ripe for hallucinations. Kelley recalled a time he was on guard duty and repeatedly saw someone standing with a rifle in the woods, ready to sneak into camp. Upon closer inspection, he determined he was actually looking at a branch and shadows.
Sleep: Why We Need It and What Happens Without It - SciShow from Humza Zaidi's comment
.

According to healthysleep.med.harvard.edu:
Sleep and Disease Risk
The price of insufficient sleep may be poor health. Study after study has revealed that people who sleep poorly are at greater risk for a number of diseases and health problems. And now the search is on to discover why this might be. more
Sleep, Performance, and Public Safety
Lack of sleep exacts a toll on perception and judgment. In the workplace, its effects can be seen in reduced efficiency and productivity, errors, and accidents. Sometimes the effects can even be deadly, as in the case of drowsy driving fatalities. more

Little more specific citation/reference will be better.

Edited :) @Dexter


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Is there a bacterium that became a virus?

Is it possible for a virus to be a descendant of a bacterium that was not through horizontal gene transfer?

How I think this could happen:
Suppose a species of bacteria lives in an environment where it gets all the resources it needs to reproduce (and let's assume that there will be no major changes in the environment).  That is, if it loses a gene that synthesizes some substance (or regulates some process), it will not be at an evolutionary disadvantage.  Because it can achieve this from the environment.  Even depending on the gene, it can even be an evolutionary advantage, as it can become more efficient when it comes to reproducing.  And I have seen that an experiment was carried out related to this question, it was shown that viruses can lose some genes in an environment where it can naturally find the protein that is associated with those genes.  Thus, there is a chance that this species will become so simple, that it will end up becoming a virus.

The fundamental difficulty with this theory is the bacterium would somehow have to learn to make multiple proteins to encapsulate and deliver the genetic material.  This is a classic chicken-or-the-egg problem for evolution: to iterate and to evolve the mechanism, the mechanism must exist.  This is an open problem for evolution, so I don't want to nix your theory on this aspect alone.  But -- you must realize this idea requires knowledge far outside what we understand well about evolution.  Is it possible? No one knows.  Is it plausible? Yes, but very difficult

Mitochondria and chloroplasts are descended from endosymbiotic prokaryotes that can no longer reproduce outside a eukaryotic host, and in billions of years they've not simplified anywhere near that much. As with @BAMF4bacon's point, this is a non-fatal but significant difficulty.

Could you be a lot more realistic, Raphael?
Your bacterium does get all the resources to reproduce, with no changes in the environment. If it loses (an important) gene it can achieve (this?) from the environment? That could be an evolutionary advantage; it could become more efficient at reproducing?
Then, how did the experiment you saw switch from bacteria to anything about viruses?
Perhaps viruses can lose genes when they find proteins in the environment and how does that change bacteria into viruses?
Is your thesis simply that “there is a chance” or what?

This virology site has a post about a 2017 paper about membrane-vesicled plasmids that act in ways that are theorized to be precursors to how viruses work:

It is likely that the plasmid-containing membrane vesicles are precursors of what we know today as virus particles. It is thought that viruses originated from selfish genetic elements such as plasmids and transposons when these nucleic acids acquired structural proteins (pictured; image credit). Phylogenetic analyses of the structural proteins of many enveloped and naked viruses reveal that they likely originated from cell proteins on multiple occasions (link to paper).
The membrane-encased Archaeal plasmid seems well on its way to becoming a virus, pending acquisition of viral structural proteins.

Though plasmids are not viruses and are not bacteria, bacteria are hosts for plasmids, and plasmids add indirectly to the genetic constitution of bacteria. Expression of plasmid genes can help bacteria survive hostile or extreme environments, and they reproduce along with bacterial chromosomes. Via the Wikipedia link:

Unlike viruses, which encase their genetic material in a protective protein coat called a capsid, plasmids are "naked" DNA and do not encode genes necessary to encase the genetic material for transfer to a new host; however, some classes of plasmids encode the conjugative "sex" pilus necessary for their own transfer.

There are giant viruses that some people think could be degenerate bacteria.
https://en.wikipedia.org/wiki/Mimivirus

Mimivirus shows many characteristics which place it at the boundary
  between living and non-living. It is as large as several bacterial
  species, such as Rickettsia conorii and Tropheryma whipplei, possesses
  a genomic size comparable to that of several bacteria, including those
  above, and codes for products previously not thought to be encoded by
  viruses (including a kind of collagen[20]). In addition, mimivirus has
  genes coding for nucleotide and amino acid synthesis, which even some
  small obligate intracellular bacteria lack. They do, however, lack any
  genes for ribosomal proteins, making mimivirus dependent on a host
  cell for protein translation and energy metabolism.

It is plausible that organisms like this started as cells and dispensed with various things they did not need in their parasitic lifestyle, resulting in something that fits the definition of virus.  Other parasitic bacteria (like those mentioned in the article) lost other unnecessary components but retained such that they still fit the definition of a cell.

Can you reference your claim that "some people think (Mimivirus) could be degenerate bacteria"? Preferably someone with the relevant expertise? The Wikipedia page does not include this point of speculation and it seems likely to be false.

The giant viruses like minivirus may be degenerate free-living organisms, possibly a bacterium but more likely an archeon or eukaryote (based on number of homologous genes).  One paper you might reference is Abrahão [2014] doi: 10.1186/1743-422X-11-120

@BryanKrause - saying it seems likely to be false means you did not check at all past reading wikipedia, and I suspect you are able.   But if not, here is the link to the first hit for mimivirus on google:  https://www.nature.com/articles/nrmicro.2016.197. Here is text from that link: Furthermore, there is disagreement as to whether the large genomes of giant viruses are a result of smaller viruses acquiring genes or of a genome with cellular ancestry adapting to escape the cell nucleus2,9,10,11,12,13.

@Willk It's up to you to provide a complete answer, not up to me to research the entire question for you. It's also not acceptable (and I think of it as academically dishonest) to cite a source for a claim that doesn't make that claim - it makes it look like you have support that you don't have. So far you've only cited Wikipedia which does not make that claim. Please edit proper citations into your answer for claims you are making rather than having them in comments as comments are ephemeral.

@BryanKrause I agree he should cite a source, but do you care to cite a source for your claim that his claim is "likely to be false"? I've tried preliminary research and can't really find much to back up either point... more like a lot of "it's a weird, huge, virus with a ton of gene sequences we're confused about, and some similarities to cells > other viruses... but really we have no clue" - 100% just fishing for good reading because I found this interesting ;) (but it should improve the answer)

@TCooper The Wikipedia page includes statements like "its lineage is very old and could have emerged prior to cellular organisms" and "It has been suggested that Mimivirus and similar kinds are remnants of a "fourth domain" of life, and that other giant virus may represent other ancient domains" as well as being part of https://en.wikipedia.org/wiki/Nucleocytoviricota which are genetically related, so if one of them is derived from a bacterium than they all are. My statement about "likely to be false" was mostly based on OP's own source ranging from saying nothing to contradicting it

I get very skeptical when I see people using citations as support for claims they make when those very citations don't provide any support.

Re "it's up to you": I'm pretty sure that collaboration is more constructive, and answers can be edited by others.(BryanKrause's points are fair, and that "up to me" means "as a moderator", but the tone of this conversation seems to have derailed...)


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Alternative hypothesis for learning in brain beyond the hebbian rule
I was reading on wikipedia that there are exceptions to the hebbian rule, and I was curious about the possibilities of other hypotheses of how learning occur in the brain. So I would like to know:

are there alternative (or complementary) hypotheses to the hebbian rule?

this may be a better fit for the neuroscience stack.

There is Karl Friston's free energy principle.


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How are human rotaviruses generally transmitted?
I know rotaviruses are double stranded RNA viruses and i am wondering if the human transmission is similar to the modes of veterinary transmission.

Faecal-oral transmission. Ref from https://en.wikipedia.org/wiki/Rotavirus

Ah, that makes sense. Thank you.


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Is the 6th rib attached to 7th rib, and 7th rib to 8th?
I'm just confused between a lot of pics that draw the thoracic cage in their way. what are these white things that I've shown?
or why the 7th rib is attached to the 8th?

Those are just a part of the costal cartilage, which is only found at the anterior ends of the ribs, providing medial extension. This connects the ribs to the sternum and is made of hyaline cartilage. Here is a clearer diagram of the cartilage part:

Ribs 8–12 are called false ribs (vertebrochondral ribs- attached to vertebra and cartilage). The costal cartilages from these ribs do not attach directly to the sternum, but are all attached to the cartilage of the 7th rib. For ribs 8–10, the costal cartilages are attached to the cartilage of the next higher rib. So, in a way, you are right in saying that the 8th and 7th ribs are attached.
The 6th and 7th ribs, though, are not attached. There are just cartelagenous bridges present in between them. The first seven are called vertebrosternal ribs. (attached to vertebra and sternum)

Sources:

https://opentextbc.ca/anatomyandphysiology/chapter/7-4-the-thoracic-cage/

https://en.wikipedia.org/wiki/Rib

https://www.pulsus.com/scholarly-articles/cartilaginous-bridges-between-the-adjacent-costal-cartilages--a-case-report.html

thanks man really thank you


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mitochondria has more activity or the numbers of them are more?
If a cell is needing energy more than the other cells, does it mean that it has more mitochondria or the activity of them is more?

This question would seem to be related, although the accepted answer there does not provide supporting references. As part of your own attempt to answer this question, you might consult a cell biology text and look at images of cells with different oxidative metabolic activity to see whether the number of mitochondria varies.

You might also want to look into condensed and orthodox states of mitochondria. When ATP requirements are high mitochondria will change their state from orthodox to condensed. Condensed state is considered to be the active state.


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How can RNAse degrade any RNA?
Every RNA has an unique sequence. Since RNAse is an enzyme and substrates react to its active site in a lock-key mechanism, how is RNAse able to degrade any kind of RNA?

smart question; Note that indeed there are different kinds of RNAses - including those that do not lock on the sequence but rather a different part of the RNA (such as its ends) - and RNAses that lock to the RNA through cofactors such as the RISC complex (which are targeted to certain RNAs by another set of special, sequence-specific RNAs)...

Welcome to SE Biology. If you read the Help on "How do I ask a good question" you will see that we expect you to “Search, and research” before asking. You do argue your case — although you haven’t asked yourself what the fallacy is in your argument, but you don’t show any evidence of having searched for the answer. Try to do this another time.

Enzymes vary in substrate specificity
This is covered in most textbooks of biochemistry, but you can find explanations on the web, e.g. here. As far as ribonucleases are concerned, there can be high specificity (e.g. recognition of a RNA with a specific base sequence), lower specificity (3′- or 5′-exonucleases — act from these respective ends) or specificity limited to the particular bond to be broken (e.g. pancreatic ribonuclease digests any RNA phosphodiester bond — but not DNA). (There is also specificity of strandedness—  between double- and single-stranded RNA.)
What determines this varying specificity?
Evidently, the substrate specificity is determined by the extent of the structure of the substrate that the enzyme has to recognize — i.e. bind to like a ‘lock and key’, refered to in the question. This requires familiarity with the chemistry of the substrate, in this case RNA:

In the diagram above (modified from Berg et al.) the phosphodiester bond which must be cleaved is highlighted. We can deduce from this diagram that in order to be specific for RNA — but no more — a ribonuclease needs to be able to recognize the ribose 2′OH (i.e. distinguish it from 2′-deoxyribose) as well as recognizing the phosphodiester bond. There is no need to recognize the bases.
The mechanism of action of bovine pancreatic ribonuclease
The mechanism of pancreatic RNase was established in the 1960s, long before any RNase that recognized particular sequences, although it has been refined subsequently. A diagram from the paper by Roberts et al. (1969) is shown below.

The diagram does show a ‘pocket’ for one of the bases adjacent to the phosphodiester bond, but this need only be generally hydrophobic, able to accomodate any of the four bases.
To study the interaction of the bases with RNAase one has to obtain crystal structures of RNAase complexed to pseudo-substrates or inhibitors (the true substrate hydrolyses, of course). The literature here is complex, and I am unable to provide a convenient review of the topic. It does appear that the binding of RNA is stabilized by the interaction of particular bases with the protein, but the key point is that any such interactions are not a requisite for the binding of the substrate. As a starting point to the literature I suggest the Protopedia page on RNase A, and a paper by Birdsall and McPherson.


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How many strands of Myosin Head is in a Myosin filament?
I am doing a research about sacromere in striated muscles, I read a paper (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3963759/
) and it states the follow:
"Rotational symmetry is defined by the number of strands present. Actin filament has two strands and hence has a 2-fold (C2) rotational symmetry; myosin filament has three strands and hence has a 3-fold (C3) rotational symmetry. Helical symmetry is defined by the integral number of sub-units contained in a given number of turns in a single strand. So for example actin filament strands have a 13/6 helix, i.e. thirteen subunits in six turns of a strand, whereas myosin strands have a 9/1 helix, i.e. nine subunits in one turn of its strand."
Now what does it mean by "myosin filament has three strands and hence has a 3-fold (C3) rotational symmetry" ?
How many strands of myosin heads is in myosin filament? I saw visualizations in different papers showing different numbers.


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Bug species identification
Found this bug in my bed. Don't think it's a bed bug. Pretty small but fat and round and had deep reddish coloring.

That's a bed bug who drunk blood.

Are you sure? I checked my entire mattress and couldn't find any other bugs.

No. That's definitely not a bed bug. See this post for detailed image/description of bed bugs. Among other obvious clues, bed bugs do not have long antennae like the insect in the OP's picture.

@Torqk Please provide information regarding your location and the size of the insect. Without that information, it will be difficult to provide an accurate ID. Thank you.

That is not a bed bug. The picture is rather poor, which makes an ID difficult, but I think it might be the beetle Ptinus fur (spider beetle), or another species from the same genus. This species is found all over the world, and often indoors (they can e.g. feed on dry foods).
Reasons for this suggestion is the body shape (incl relatively hidden head), color ("reddish"),long legs with thick femurs, long hind legs, and long antenna. The long legs together with the long antenna (the antenna can look similar to a fourth set of legs), as well as the hidden head (so the body look two-segmented) is what makes it look somewhat like a spider .

(picture from bugguide.net)

(from weedimages.com)


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What kinds of animals does insular dwarfism affect and how large does an island need to be to escape it?
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I've been wondering about insular dwarfism, and would like to know if it only affects certain animals (Since some animals grow larger upon colonizing an island, often due to the absence of predators.) Do only big animals get smaller, and if so, how big is "big"? Are there any taxonomic groups that are more or less prone to insular dwarfism?
The second thing that I'd like to know is the minimum size of an island without insular dwarfism could be. Also, I'm not sure if resources, biodiversity or climate affects it too (Considering Bergman's rule, the increased competition in jungles, etc.) This may sound like a lot of questions, but the main components of an answer I'd like are shown in the title - who and where.

There are no general rules. We have just observed repetitively that organisms living on small pieces of lands tend to be particularly large (insular gigantism) or particularly small (insular dwarfism) compared to the main land counterparts.
There are several possible reasons for these changes and those reasons vary among species. Dwarfism is most definitely not always a consequence and there is no hard coded minimal island size for such change to happen or not happen.


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What animal classes has also "Like Humans" XY Chromosomes for Males and XX for Females?
Are other mammals. birds, reptiles, or even insects same to humans in that the male organisms have XY Chromoson at the end and female XX?
Thanks for the ansver

https://en.m.wikipedia.org/wiki/XY_sex-determination_system

specifically from that Wikipedia link: " humans, most other mammals, some insects (Drosophila), some snakes, some fish (guppies), and some plants (Ginkgo) tree"

Does this answer your question? Do males of all sexual species have Y chromosomes?

In mammals, Y chromosome determines the sex. SRY gene present on Y chromosome is responsible for sex determination. And, in absence of this gene results in female sex. Non-human mammals use several genes on the Y chromosome.
Platypus and Drosophila also uses XY sex determination system, but in different way. Like in platypus, combination of genes present on XY chromosome are used to determine sex characteristics. And in drosophila, two X chromosome gives female characteristics, and Y chromosome determines maleness.
Reference:
https://en.wikipedia.org/wiki/XY_sex-determination_system


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Are there any proteins assembled from non-adjacent parts of the genome?
Many proteins are assembled from multiple exons with the introns between adjacent exons being spliced out. But are there any proteins that have unrelated to them exons in the middle of their sequence?
I think the equivalent question would be: are there any protein-coding genes (in any species) that are broken in two or more parts by another protein-coding gene(s)?

Not directly related to the question as you have asked it, but do consider https://en.wikipedia.org/wiki/Protein_quaternary_structure as well.

I think that you are talking about trans-splicing. This does indeed happen. It is fairly common in protist organisms, though in humans it is quite rare. For more information about how this process works, including mechanisms in vertebrate organisms, see this paper.
Here is one model from that last paper for how it works:

Yes, this is what I was thinking about. Thank you!


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How rapidly do human mitochondrial ribosomes turn over?
How rapidly do human mitochondrial ribosomes turn over?
The inside of the mitochondrion is a highly oxidizing environment that can damage RNA and DNA. How long do mitochondrial ribosomes last before needing to be replaced?


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To what extent is prion aggregation responsible for Alzheimer's disease?
I was intrigued by a description of prions as a factor regarding 'Mad Cow Disease', the epizootic threatening the cattle stock of the United Kingdom and France predominantly.
Understandably, the prion, a misfolded protein causes neurodegenerative damage through inducing an aggregation of prions into a complex capable of converting functional proteins. Disregarding Creutzfeldt-Jacob disease, thus far believed to be a Dementia characterised by the accumulation of prions, I simply seek clarification as to whether the onset of Alzheimer's disease should have a direct correlation with an aggregate of misfolded proteins.
Nota Bene
Although the hypothesis regarding the accumulation of amyloid-derived diffusible ligands, toxic oligomers, may be associated with the prion causing Bovine Spongiform Encephalitis, if any further clarity regarding the direct correlation between these two events in humans would be appreciated.

"I simply seek clarification as to whether the onset of Alzheimer's disease should have a direct correlation with an aggregate of misfolded proteins." This is easily googled (in other words, provide your actual research, not just a question.) "What causes Alzheimer's on a cellular level" should give you all the information you need, or "Alzheimers and prions".

@xusr - I disagree; most basic questions which show no attempt on the part of the OP at finding an answer are not excellent. But you know what opinions are like... everybody has one. (BTW, I never said the cause of Alzheimer's was/is known. The OP asked if folded proteins were the cause of Alzheimer's. I think that's easily googled. And while I'm at it, why don't you post an answer?)

To What extend is prion aggregation responsible for Alzheimers's disease?
Until recently, there was no 'hard evidence' implicating an infectious, self-propagating protein or prion (proteinaceous infectious particle) in Alzheimer's disease, or any convincing evidence that  a prion-like mechanism  is involved in this disease.
However, I quote from a recent review (Alzheimer’s and Parkinson’s diseases:  The prion concept in relation to assembled A$\beta$, tau, and alpha-synuclein) by a leading researcher in the Alzheimer's field:

Transcellular propagation of protein pathogens, reminiscent of the spread of viruses, represents an unprecedented concept of disease. It is now known to extend beyond CJD [Creutzfeldt-Jakob disease], to include AD [Alzheimer's disease]  and PD [Parkinson's disease], which are the most common neurodegenerative diseases.

Pruisner,
 who
 received a Nobel prize
 for his work on prions ('a new biological principle of infection'), was one of the first to suggest that neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease, like Creutzfeldt-Jakob disease (CJD), may be due to a prion, or to a prion-like mechanism. He points out that over 80% of these diseases are sporadic, late-onset, and involve proteins present since birth (see
 A Unifying Role for Prions in Neurodegenerative Diseases
 ).
However, there  is one caveat.  The prion causing CJD, scrapie and kuri may be transmitted from one individual to another, and there is no evidence that Alzheimer's disease or Parkinson's disease may be so transmitted or  are in any way infectious.
What is Alzheimer's disease?
Alzheimer's disease is a neurodegenerative disease, and a disease of ageing, that causes severe dementia worsening over time. It affects 10% of those over 65 years of age, and 50% of those aged over 85  years. There is no known cause, and no known cure.  It is the leading cause of dementia, ahead of Parkinson's disease.  Most cases of AD are sporadic, but a small percentage have a genetic origin (familial AD).
The disease was first described (On certain peculiar diseases of old age)  by Alois Alzheimer in 1906. After histochemical analysis, Alzheimer described  two characteristic abnormalities in the postmortem brain of a 51-year old woman :  the (extracellular) neuritic plaques and the (intracellular) neurofibrillary tangles.
There is a very nice picture of both neuritic plaques and neurofibrillary tangles in Fig 1(A) of Goedert (2005).  For a great summary of the history of AD and references to the above summary, see  A Century of Alzheimer's Disease (2006) by Goedert & Spillantini.
What are the neuritic plaques?
Neuritic plaques are extracellular structures primarily composed of  a small peptide of (usually) either 40 or 42  amino acids known as  the amyloid-$\beta$ ($\beta$A), where the '$\beta$' refers to their tendency to form beta sheets.
This small peptide arises by proteolysis of a much larger protein of unknown function, the amyloid precursor protein (APP). The APP is a trans-membrane protein with  a single membrane-spanning segment, where the N-terminus (28 amino acids) is extracellular. Two proteases are responsible for generating $\beta$A :   $\beta$-secretase and $\gamma$-secretase
Peptide bond cleavage by   $\gamma$-secretase  occurs within the membrane-spanning region of APP and components of this proteolytic complex (the presenilins) are 'major players' in the Alzheimer's story.
It is thought that A$\beta$ is a 'normal' brain peptide, that is it does not arise from 'aberrant' proteolysis, but its function is unknown (Goedert & Spillantini, 2006).
Finally, mutations in the APP gene are known to cause familial AD, but account for only a minority of cases. (Goedert & Spillantini, 2006).
So, the structure of the neuritic plaques is known. They consist of a small peptide of unknown function derived from a much larger trans-membrane protein of unknown function.
And the neurofibrillary tangles?
Under the electron microscope, neurofibrillary tangles have a ribbon-like appearance called paired helical filaments.  It is now known that these structures are composed of a single protein, microtubule-associated protein Tau, or Tau protein  in an aggregated and hyper-phosphorylated state. There is  a very nice picture (electron micrograph) of a paired helical filament in  Fig 1(B) of Goedert (2005)
What is Tau Protein?
Tau is a 'normal' brain protein characterized by Kirschner and colleagues (see here and here)  as a microbutule-binding protein, long before its role in Alzheimer's disease was realized.
In humans, it consists of six isoforms generated by differential mRNA splicing of the transcript from a single gene, and 'imperfect repeats' within the amino-acid sequence are thought to be responsible for microtubule binding.
Mutations in the Tau gene are not known to cause Alzheimer's disease, but are responsible for very rare neurogenerative diseases (taupathies ) such as frontotemporal dementia  (FTD) (Goedert, 2005)
In the 'native' state Tau is phosphorylated, and is considered an intrinsically unstructured protein, (there is no crystal structure available), and it is now accepted that  'hyper-phosphorylated' Tau is the major structural component of the paired helical filament of Alzheimer's disease.
I simply seek clarification as to whether the onset of Alzheimer's disease could have a direct correlation with an aggregate of misfolded proteins
This is where things get interesting.  There is no doubt that aggregated proteins are involved in AD. The case of Tau and $\beta$A attest to that, and the paired helical filament could be considered a misfolded state.  Can either of these proteins act  as a prion and transmit the misfolded state?  That is, can Alzheimer's disease be considered a prion disease, where a 'rogue' form of a protein transmits its 'rogueness' to 'normal' proteins?
In the case  of Tau, it has been shown that extracellular Tau aggregates can "transmit a misfolded state from  the outside to the inside of a cell, similar to prions" by inducing fibrillization  of intracellular Tau .  In addition, aggregated intracellular  Tau can transfer to other cells. (Propagation of Tau Misfolding from the Outside to the Inside  of a Cell)
Testing of the hypothesis that prions or a prion-like mechanism is the cause of AD is a very active field and much more detail and discussion will be found in Goedert (2005).
What are the other 'players' in the Azheimer's story?
There are many 'players' in the modern understanding of AD.  Two further important ones are the presenilins and  apolipoprotein E  (APOE).
What are the presenilins?
Presenilins are part of the $\gamma$-secretase complex, a protease that cleaves trans-membrane proteins including APP. Mutations in the presenilin-1 gene are the  most common cause of familial AD; presenilin-2 mutations also known to cause AD. (See  Goedert & Spillantini, 2006).
And apolipoprotien E4?
A risk factor for sporadic AD is inheritance of the  ${\epsilon}_4$ allele of apolipoprotein E (APOE), a protein of fat metabolism,  but the molecular basis for this is a complete mystery.   (Goedert & Spillantini, 2006, Goedert, 2005). Inheriting a single copy of the APO-$\epsilon_4$ gene more than doubles the  likelihood of developing AD; inheriting two copies increases the risk by 12-fold (see Smith, Dana, 2018)
In what looks like a major advance, gene editing has been used to convert a  APO-$\epsilon_4$  phenotype to one resembling 'normal'  APO-$\epsilon_3$.  For a great recent article, see Scientists Fix Genetic Risk Factor for Alzheimer’s Disease in Human Brain Cells by  Dana Smith (2018).


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biological difference between 9 month and 7 month pregnanted humans
it possible baby born when 7 month of pregnancy, and possible when 9 month pregnancy.
what happen in additional 2 month?
what their difference. do they have different something.

The child is still developing, just as the child will continue to develop after it is born. Is there something in particular you have in mind? I don't know much about fetal development, so it may just be me, but it doesn't seem quite clear what answer you're looking for.


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What do the initial cell divisions look like in bird embryogenesis?
The germ disc in a bird (a disc because its a chordate) is a mystery to me. The ovum (yolk) is a huge mass of nutrients. It then gets impregnated. Then, what? What does the initial cell divisions look like (they can't be symmetrical since yolk is clearly pushed to one end of the whole thing. )

I'm pretty certain the ovum isn't the yolk. Ova are way smaller than that. Human embryos also have a yolk sac, and it develops during early embryonic development. According to wikipedia, in birds it's a specialized structure made in the mother's body and is part of the ovum in very small animals like some fishes or invertebrates, not birds.

I'm just interested in what is true. I've kept hearing the meme that the yolk in birds is a single cell, and it looks plausible but always sounded a bit weird. The human yolk sac isn't homologous with birds yolk sac, at all. It develops from the germ disc long after fertilization during the formation of the gut tube. Overall phylotypical stages in embryogenesis are hard to master because there is so much variation, one thing that looks identical is achieved by a completely different procedure, is common.

The yolk of birds may well be a single cell, but it doesn't mean that cell is the ovum. (actually I read down the wikipedia page, and it has a section on chicken eggs that explicitly says the claim you're describing is false "in strict sense". I know I know, wikipedia, there's a reason this is a comment and not an answer, but the citations might be useful). I didn't know the human yolk sac wasn't homologous to other yolk structures, thanks for that!

Overall, how the embryo gets to different stages differs a lot while the stages look the same. It's pretty confusing until you get that the processes aren't homologous. The mammal yolk sac is a part of the gut tube, it forms as the initial germ disc (that exists to conform to notochord organizational axis) bends into a cylinder.

Looking at this diagram and this one from this page, it looks like a small portion of the edge of the yolk develop a "cleavage furrow" which then develops into a multi-celled "blastodisc" or "blastoderm" that becomes a more differentiated embryo.

@Hypnosifl still a bit of a mystery. Since the unit those processes deal with are cells, if the yolk to begin is a single cell, the ovum, assuming the initial cell divisions are normal mitosis, doubling number of cells, is it originally undergoing an asymmetrical division where one cell takes the entire yolk and the other forms at one pole, and, does that other pole cell then continue from there to form the germ disc and all that?

This page also says that "The hen's egg consists of just a tiny patch of cytoplasm resting on the surface of a large ball of yolk" and that the initial cells during cell division have a plasma membrane on top and sides but not on the bottom, where "the bottom of the cell [meaning the cytoplasm I guess] is in direct contact with the yolk". Calls this "meroblastic cleavage", might google that term to find out more.

@Hypnosifl You should write that as an answer. I think using the contrast with frog development (where the yolk is more... 'intracellular') is probably also quite informative.

@Hypnosifl that sounds a bit contradictory, if the tiny patch of cytoplasm is continuous with the yolk, isn't it a single cell. Or do two cells partially fuse in the ovary?

@BryanKrause Do you know if the yolk is the same cell as the ovum and a single cell?

@IanMalcolm It is not controversial that there is one and only one cell present before post-fertilization devisions (which occur before the full egg is developed). What is a bit unclear is what you call a "single cell" after that in the early stages of development. I'm not an avian development (or any development) expert and people tend to pick up chickens as model organisms after the first day or so after many many cell divisions (frogs are much nicer models for the first few divisions), so the earliest steps of avian development are often left out of textbooks.

What I call a "single cell" is what you call "not controversial that there is only one cell present". No need to misrepresent my statements. @Oosaka thought the ovum and yolk were different cells (easy to think since the yolk is huge), I've heard that they're a single cell, although it is a bit counter-intuitive, but there are other examples of huge single celled structures. Main question is how that huge single cell does the initial cell divisions.

@IanMalcolm You can call that a single cell, but there is a lot of non-cellular material in a living organism as well. The majority of the yolk is kind of...in between. Hence the potential for controversy. "There is one cell" is not the same as "This is all one cell". Hypnosifl gave the answer already to "how that huge single cell does the initial cell divisions", though in a comment that should be an answer.

You call it "not controversial that there is only one cell present". If the material of the yolk is intracellular, is it not misrepresentative to point out that living organisms can have non-cellular (extra-cellular) material?

That's just it...it's kind of intracellular, kind of not. There isn't a lipid bilayer there from what I can tell, but it's also definitely segregated from the cytoplasm part of the ovum. It's also all material that originated in other cells.

@Bryan Krause - If you want to give an answer that repeats the points (or specific links) I mentioned in my comments go for it, I just found this much by googling and don't really feel I know enough to comment on the issue Ian Malcolm is interested in about whether the yolk itself would be considered a giant cell or more like "cell + giant blob of nutrients attached", I suppose this would depend on what definition of "cell" is most commonly used by biologists.

@Hypnosifl Alright, I'll take a stab at it later.

The point here is mostly that the yolk is often said to be a huge single cell. If its just material deposited by cells lining the follicles, then, it's clearly not a cell but extracellular, and the ovum is just enclosed in it. Grau and Wilson said so here, they also mention that most people believe the yolk is a cell. https://link.springer.com/article/10.1007/BF02146023

This is covered well in almost any text that talks of early embryonic development in birds. Basically, the cleavage divisions look roughly symmetrical if you look end-on from the animal pole. But, as mentioned in the question, the process is quite asymmetrical in profile, with the blastoderm being at one end and the huge yolk occupying the other.
The yolk later gets invested by a layer of cells (the splanchnopleure) to form the yolk sac while the blastoderm forms the embryo proper.
You could see this page for more details. (Not just this page, this site in general is an excellent resource for learning embryology.)

The question is based on the false belief that the ovum contains the yolk as a single cell. This is a belief that is very common, and often spread in the literature. Grau and Wilson said in 1963 in Avian Oogenesis and Yolk Deposition: The yolk of the hen's egg is often given as an example of a huge cell containing a food supply for the developing chick embryo. Current views hold that oocytes grow by removing nutrients from the blood and the follicle cells which surround them. Thus yolk deposition is thought of as primarily an intracellular phenomenon. We believe that this viewpoint is inadequate, and wish to propose the following alternative hypothesis.
Of course, if the yolk is not inside the ovum, then there is no mystery to the early cell divisions.

Hi, it's me, the person telling you the bird yolk isn't the ovum! I told you wikipedia confirmed, and I let it at that initially because it was just a comment, I didn't feel the need to do deep research, but I saw the question continued to spark debate so I actually went to look at wikipedia's sources. And from what I was able to read of "Atlas of chick development", a 2005 book, I'm thinking... the wikipedia page was maybe wrong and you were right all along? But also, the book is detailed enough (and chapters free to read on google books) that it might answer your questions regardless.

https://books.google.fr/books?id=JAjGAgAAQBAJ&pg=PA1&hl=fr&source=gbs_toc_r&cad=4#v=onepage&q&f=false

The yolk is both part of the oocyte and yet separate from the cytosol of the cell including the nucleus, mitochondria, and all the other normal cellular stuff. Grau and Wilson are merely arguing (without much evidence) that the oocyte doesn't play much of an active role in growing itself.

@Oosaka You were probably right, I always thought the claim that the yolk was a single cell seemed wrong. But it seems like a very common myth, myths are good at capturing attention so it took me a while to get that the yolk is extracellular and secreted by cells surrounding follicle lumen. That's what Grau and Wilson said, seem as credible as anyone else, and it fits with my own reasoning.

Bryan Krause opinion differs from Grau and Wilson. I think they seem credible, if anyone has strong evidence or indisputable evidence that they are wrong, feel free to present it in comment. If anyone has better answer, feel free to produce a separate answer.

To be supportive of differing opinions, here is the credentials of the author I cite, so that anyone may discredit his claim: Charles Richard Grau, Professor of Avian Sciences, Emeritus. https://senate.universityofcalifornia.edu/_files/inmemoriam/html/CharlesRichardGrau.htm
His claim supports Oosaka's initial comment, thanks for all comments and for making me understand what I wondered about. Everyone contributed to my understanding. It was also what my intuition was, but for some reason I trusted the popular myth. Shame on me.

@IanMalcolm Grau's credentials are great but that book being from 1963 less so; it's why I pointed out "Atlas of Chick development" being from 2005. I don't know if the sources actually disagree though, I would have to see what both say.

false. scientific theory does not disprove itself as a factor of time. most current scientific theory that still holds as fundaments much older than 1963, lots of good work from around that time as well. your initial comment was beneficial. anyone who has strong evidence Grau and Wilson were wrong may publish an answer.

@IanMalcolm Grau and Wilson are not claiming to prove anything, and they show no data. They're just publishing a hypothesis to motivate research. Their paper has only been cited a couple of times and none of those citations provide evidence for their hypothesis. The quote is from what is effectively a "letter to the editor" rather than a scientific paper.

Feel free to produce an answer that is the most accurate you can conceive of. That yolk is extracellular (see my answer, or your own comment, "a lot of non-cellular material in a living organism as well") resolves issue in initial cell divisions. If superior answer is provided, not a problem.

@IanMalcolm Um... scientific theories that are correct do not disprove themselves as a matter of time, no, but not all scientific theories are correct, if they were science would be finished. Plenty of old scientific papers still hold up, but when they do then the more recent review/consensus documents agree with them. "More recent sources are more likely to be more accurate" is a completely correct rule of thumb for figuring out what science says about a question.

@Oosaka I don't think you and I disagree. Anyone with an open mind understands that "if they were science would be finished", the problem is status quo bias, so many people lack an open mind. "scientism" is the belief that the present social agreement of what the world is, is somehow the perfect world view and the scientific process end state. This forum is not very open minded, so I see no benefit to you and me "debating", debate is just a fallacy based on instincts monkeys have to fight over territory, with ideas irrelevant but our monkey brains do not get that.

I'd be open to chatting over some other medium, but in this forum, I just wanted to sort out what I wondered about. Peace.


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In what "space" does egg mature in Kiwi?
This huge egg here, is it sort of tethered to the ovary, filling up the coelomic cavity, and then exiting out of the infundibulum, or, where is it in the bird exactly? What "space" does it occupy?

I can't find the original source for your image, but it is likely an artist's rendition of an X-ray image, or is very edited.  Here is a real X-ray of a kiwi with its egg: https://www.audubon.org/news/why-kiwis-egg-so-big

In birds, eggs mature post-fertilization in the magnum and "shell gland", sometimes called a uterus.
I can't find anything to suggest a kiwi is any different, despite their large egg size. An exception is that kiwi have two functional ovaries (yet the join in one functional oviduct and the rest of the reproductive system is only present once) (Ballard & Cheek, 2016). Given this source mentions this specific difference, it seems unlikely they would have omitted any other important differences.
This course page may be useful for bird reproductive anatomy more generally: http://people.eku.edu/ritchisong/avianreproduction.html
Ballard, B., & Cheek, R. (Eds.). (2016). Exotic animal medicine for the veterinary technician. John Wiley & Sons.


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Why do we see colours when we close our eyes and press our hands against them?
Whenever we close our eyes and press our hands against them we either see some colours or sometimes some weird patterns(similar to hypnotic patterns).
What is the cause of this phenomenon?
Also, is this the right place to ask this question? Does this question have more to do with biology than physics?

Does this answer your question? What do you see when your eyes are closed?

Yes, this is a biological phenomenon, not a physical one, because the phenomenon depends on a cellular response. Pressing your eyeballs (mechanically stimulating them) causes you to see phosphenes.

What is the cause of this phenomenon?

The increased pressure in the eye causes activation and inhibition of cells in your retina (retinal ganglion cells). These cells are intermediates between the light-sensitive sensory neurons and the brain which interprets information into an image.
Quoting a well known study from 1989:

Eyeball deformation [pressing] in total darkness led to an activation of the
  on-center ganglion cells, while the off-center ganglion cells were
  inhibited. The latency and strength of this activation or inhibition
  varied considerably between different neurons, but were fairly
  constant in the same neuron when the eyeball indentation was repeated
  after a pause of 1-3 min. The latency and strength of neuronal
  activation or inhibition seemed to be dependent mainly upon the neuron
  location relative to the point of eyeball indentation. Some on-center
  neurons also exhibited a short activation at "deformation off". [...] We assume that the activation of on-center and inhibition of off-center ganglion cells by eyeball deformation are caused by retinal stretching, which also leads to horizontal cell stretch. Stretching the horizontal cell membrane probably generates an increase in membrane sodium conductivity and a depolarization of the membrane potential [neuron firing]. This depolarization of the horizontal cell membrane potential is transmitted either directly or indirectly (via receptor synapses) from the horizontal to the bipolar cells.

This is a phenomenon at the retina (periphery), i.e. not in the brain region associated with vision processing (occipital lobe). You can achieve the same visual effect by vigorously sneezing or blowing your nose, stimulating the same cells electrically (by injecting current with electrodes) or magnetically (with coils that generates a local magnetic flux, whereby currents are locally induced). It is also possible to duplicate the effect by stimulating only the visual cortex, but it is likely due to the fact you are simply approximately replicating the retinal firing patterns coming to the brain via the visual nerve.

I recommend to use the biology.SE search bar at the top with the term 'phosphene'; there are some archived answers on the topic already.


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Why are so many species reproducing late this year?
Hope this question is OK for this site, couldn't see where else to ask it.
We've spent a few days out in the countryside recently, and have been very surprised at how many species appear to have very young offspring so late in the season. I was always under the impression that the vast majority of animals and fish produced young in the spring (March/April).
For example, we saw tadpoles, fluffy (ie obviously very young) coots and weeny minnows. I would have expected that all of these would have been born/laid a good 3 or 4 months ago, and so would be more mature by now.
Caveat: We didn't do a scientific study, this is just a strong impression we got from days out in north west England.

It's hard to say without more information, but one substantial possibility is that you are mistaken that species are reproducing late - that's a problem with anecdotal rather than scientific data!
Additionally, species you mention like the common coot can attempt multiple broods where the season is long enough. Wikipedia specifically mentions Britain:

Eurasian coots normally only have a single brood each year but in some areas such as Britain they will sometimes attempt a second brood

The same could be true for species of frogs/toads and fish, so without knowing specific species it can't be known whether these are species reproducing again or species reproducing late.

OK, thanks for the reply. All makes sense.


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What is the smallest oligocelluar organism?
What is the smallest oligocelluar organism?
How many cells does it have?
EDIT
The question is motivated by this comment@Philosophy.SE
EDIT as recommended in comments
I'm looking for an example of an organism made of very few (the fewer, the better) sister cells (obtained by mitosis or aggregation) that are morphologically and functionally different. I would accept examples of species that exist in different "conformation" (unicellular and multicellular).

I thing the answer depends on what you will accept to consider as multicellular. If you use a very broad and open definition, than the answer will probably be "2 cells".

@Remi.b do you know an example with 2 cells? But in fact I  thought about organisms where different cells serve different tasks...

No I don't have an example right now. As someone already voted to close, I would suggest you to re-edit your question and make sure we understand what you ask for. For example, you might say that you're looking for an example of an organism made of very few (the fewer, the better) sister cells (obtained by mitosis) that are morphologically and functionally different. You can also say that you would accept examples of species that exist in different "conformation" (unicellular and multicellular). I think/hope this would be a valid question.

I can only support Remi's comment. The question is pretty broad at the moment.

@Remi.b thanks for your suggestions. I hope you don't mind that I borrowed from your comment...

@Chris better now...?

Seems much better to me! +1

From my point of view definitely.

Volvox is a genus of chlorophyte that has been used in several studies as model organism for understanding the transition from unicellular to colonial or multicellular (I don't mean that multicellular and colonial mean the same thing!). If I am not mistaken, the species of this clade present quite a good transition from unicellularity to multicellularity. Some species create a bottlneck while reproducing, while others don't for example. One might investigate a bit the clade in order to answer draks …'s question.

This might interest you (I haven't read it though!)

The classic example, though I am sure there are others that are smaller, is the slime mold Dictyostelium discoideum:

It can have up to 100,000 cells and exists as both single cells and as a multicellular organism (emphasis mine):

Dictyostelium amoebae grow as separate, independent cells but interact to form multicellular structures when challenged by adverse conditions such as starvation. Up to 100,000 cells signal each other by releasing the chemoattractant cAMP and aggregate together by chemotaxis to form a mound that is surrounded by an extracellular matrix. This mechanism for generating a multicellular organism differs radically from the early steps of metazoan embryogenesis. However, subsequent processes depend on cell-cell communication in both Dictyostelium and metazoans. Many of the underlying molecular and cellular processes appear to have arisen in primitive precursor cells and to have remained fundamentally unchanged throughout evolution. Basic processes of development such as differential cell sorting, pattern formation, stimulus-induced gene expression, and cell-type regulation are common to Dictyostelium and metazoans.

100.000 is quite a lot, C. elegans has 956 cells which would surely classify into the smallest. Some of the algae mentioned above can have even lower cell numbers.

@Chris well yes but dicty cell counts go from 1 to 100.000 while the worm is always at 956. The interesting part is that dicty exists as a single celled organism as well.

Slime molds are faszinating. And as we see, this question is not easy to answer :-)

@draks... thanks for the accept but there are probably more extreme examples.

true. It was the "independent cells but interact to form multicellular structures when challenged" that I was looking for. And acceptance is revertible :-)

nice example @terdon

@terdon I personally see no point: C. elegans doesn't always have 956 cells, zygote is a single cell. I don't think "Dictyostelium" is the right answer given the current wording of the question.

@har-wradim hello and welcome to the site. There is no such thing as "the correct answer" on the stackexchange network, the OP chooses to accept whichever answer suits them and that answer is, by definition, the "best". It may be wrong or incomplete but if the OP feels it answers their question then that's that. As for dicty, the cool thing is that it exists and can live as both a single cell and as a multicellular aggregate. The worm cannot and the zygote is an "unfinished" animal, they are completely different.

Quite late for a welcome, but you are right.

Actually, a clever point. I would also mention syncitial organisms, which are formally multicellular, but have no cell boundaries between cellular "loci".

@har-wradim yes please post an answer...

@draks I think har-wradim is talking about Plasma molds.

Not sure, whether it fits in your requirement (since it was not clear for me with the terdon's answer), but I'd also mention plasmodia and other cases of species with syncytial organization: they have multiple nuclei, sometimes have even macroscopic sizes, but formally there is only one cell boundary within their body.
(If we broaden this definition, we may also include all kinds of protists with multiple nuclei: from diplomonads (which have two equal nuclei) and ciliates (most of which have two functionally differentiated nuclei) to Pelomyxa or giant foraminiferans with huge numbers of nuclei.)
Some examples:

Myxosporidia, once thought to be a group of protists and now believed to be highly aberrant metazoans - are parasites of fish (first generation) and some invertebrates (second generation), which form highly differentiated plasmodial bodies in their hosts.
Orthonectids, a group of "lower metazoans", have a biphasic life-cycle with sexual generation represented by oligocellular free-living males and females, which produce zygotes developing into parasitic plasmodia.
Myxogastrid slime molds are famous in having plasmodial fruit bodies: they are relatives of Dictyostelium and have a similar life-cycle with mono-nuclear amoebae, which conjugate and produce the plasmodium. So, these are still formally "unicellular" even as fruit bodies.
Some algae have plasmodial organization with the most famous case of Caulerpa, species of which "are unusual because they consist of only one cell with many nuclei, making them among the biggest single cells in the world.".
Cannot recall right now the name of the group (can someone help?), but there are amoebae, which are "normally" unicellular, but able to aggregate on rich food resources to form trophic plasmodium.
Lots of other cases.