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Signaling between Organelles
I'm confused about how organelles communicate with each other. I understand signaling between cells and the whole transcription and translation of DNA process. However, how does a motor protein know the destination of its package? How does a lysosome know when to break down a worn out organelle? How does the cell distribute ATP to the organelles where it's needed (how does it figure out where the ATP is needed?)?

There's no single common mechanism for intracellular communication, and some of the mechanisms (and some parts of some of the mechanisms) are known in much greater detail than other. For each of the processes you mention, we at least know that they proceed via very different mechanisms.
ATP distribution, for example, proceeds mostly by simple diffusion. ATP is a small molecule and is able to diffuse fast enough that it can move from one end of a cell to another in about ~20 ms on average [1].
Our picture of how ATP actually gets taken up by the various organelles is much murkier. For the case of the endoplasmic reticulum (ER), there is evidence that ATP is brought in via an ATP/ADP antiporter [2]. Transporting ATP via an ATP/ADP antiporter would have the effect of keeping the ratio of ATP/ADP stable in both the cytosol and the ER. It is reasonable to assume that similar mechanisms control ATP transport across other organelle membranes, but you'd have to dig into the literature to find out details.
References
1: Diffusion coefficients of ATP and creatine phosphate in isolated muscle: pulsed gradient 31P NMR of small biological samples
2: Transport and transporters in the endoplasmic reticulum

Thanks, but can you tell me more about how motor proteins know where they need to go and lysosomes knowing when an organelle needs to be degraded?


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Plasmid Design and Integration events [Single vs Double cross over]
When linearising a vector by restriction digest within the middle of a homologous region can a single cross over integration event only occur if the plasmid is re-ligated within the cell after transformation? If so, why do some organisms require transformation of a linearised vector rather than plasmid DNA?
An example:
You amplify and clone GeneA into a vector containing an expression cassette. Before transformation, you digest this vector with a restriction enzyme at a site within GeneA to form a linear DNA fragment such as: GeneAStop_ExpressionCassette_StartGeneA.
My understanding is a double cross over event would occur in StartGeneA_ExpressionCassette_GeneAStop and the expression cassette would integrate between the two parts of the gene in the genome.
However, as the gene is cloned directly into the plasmid as one part and then digested to form a linear fragment, the expression_cassette is not in the region between two homologous fragments.
Does this mean a double cross over event cannot occur and a single cross over event would have to occur for the transformed DNA to integrate?
Can this single cross over event happen without relegation of the digested plasmid into circular DNA?
What would happen if you amplified by PCR rather than digested, as it would not be able to religate?

Your post contains many different questions, so I responded to what I considered being the central question. If you were looking for a different answer, please focus your post such that the main question becomes clearer.

Single crossover is not the result of religation in the cell. The double-stranded break (DSB) in the plasmid instead stimulates a homologous recombination event, causing the entire plasmid to integrate into the homologous region in the chromosome. The result is two tandem copies of the homologous region, interspaced by the rest of the plasmid.
The figure below shows (1) a plasmid carrying a wild-type copy of the gene YFG1 (purple) and some selection marker AUXA (blue); and (2) a genome region with the gene yfg1 (pink) that is homologous to YFG1, but carries a mutation (black star). Arrows are shown for orientation.
After introducing a DSB in YFG1, this region will line up with homologous yfg1 region in the genome and integrate as shown. Note how the two tandem copies of YFG1/yfg1 resulting from the integration will both be "chimeras"; i.e., one part originates from the plasmid and the other from the chromosome. Also note how in this specific example, the mutation ends up in the second copy, since the DSB was introduced "upstream" of the mutation.

Figure adapted from (1).
References and further reading

Guthrie & Fink (1991): Guide to Yeast Genetics and Molecular Biology, Part A. pp 285-287. ISBN: 978-0-12-182095-4
Orr-Weaver et al. (1981): Yeast transformation: A model system for the
study of recombination. PMC349037

source: Stack Exchange

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What is (was) this fish carcass found on an eastern Long Island beach?
An acquaintance sent me these photos of fish remains that they found on a beach on the east end of Long Island, NY. The site lies near Gardiners Bay near a channel that is used by trawlers travelling to and from port.
This portion from behind the fish's head is very large compared to what we would normally see. The only real scale I can provide is the fourth photo, a vid capture showing an 11 year old waving their croc above the remains.
I am an avid surf fishing angler with considerable experience in natural history. I am confident it isn't one of the usual suspects such as Striped Bass, Bluefish, or any of the typical bottom fish. I am also confident that it isn't the Montauk Monster.
In the summer we do get some random visitors from further south. Tarpon and Black Drum are occasionally caught in nets near here. There are also cast-offs from the trawlers that go who-knows-where.
So, what is this fish?

Could it be one of the sturgeon or related species (gar etc.) no idea what's in the region personally, but the scales don't look like conventional fish scales to me.

The first picture made me double-take, though I was seeing a bird's wing. The scale-type is known as "ctenoid" (i.e. jagged, comb-like or irregular), which narrows it down a bit to a perciform (perch-like) fish, or something rarer with the same - certainly ray-finned. Beyond that, I've no idea.

@JiminyCricket. Black Drum would fit both conditions. And they get large enough.

@bob1 while Atlantic sturgeon carcasses occasionally show up on the beaches here, this isn't like them from what I can tell.

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ID Request: What is this frog? Eastern Long Island, NY USA mixed hardwood forest
Apologies for the potato quality photos, but can anyone ID this frog?
My son found a few frogs living under a porch at my father's house, which is situated in a mixed hardwood forested area of eastern Long Island, NY. I say "living" because he sees them sitting just at the edge of the low porch every day for a while now.

It is hard to tell exactly from the photos, but given the location and time of year, it is either a juvenile green frog (Rana clamitans) or juvenile bull frog (Rana catesbeiana).

Would a juvenile bull frog be in an upland setting? I know there are bull frogs in the pond about 300m away, but I'd always thought of them staying in the pond.

Yes, they disburse quite far away from their natal ponds as juveniles, often into impermanent water sources, before settling in a permanent waterbody as adults.

Then I think bull frog is likely the answer


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What is this tooth or tusk that was found with several others in a scrimshaw kit from Nantucket?
This was in a scrimshaw kit that was purchased at a yard sale about 20 years ago. Kit was sold by a company on Nantucket, and was old at the time of the yard sale. It is not known if this and the three other similar pieces were original to the kit or were added later on. What animal did this come from?

From the location of purchase, conical shape, color, and size, the tooth is that of a sperm whale (Physeter macrocephalus). Sperm whales have 17-29 teeth in the lower jaw that range 3-8 inches (see Perrin et al., 2009). Their teeth were most often used as scrimshaw, and many can be seen at the Nantucket Whaling Museum.
Just as an FYI, under the Endangered Species Act, it is illegal to buy or sell sperm whale ivory harvested after 1973. So you may want to have the tooth aged.

Thank you. These aren't going to be sold. And based on the age of the kit it seems probable that it predates '73 anyway.


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How can site-directed mutagenesis be used to suppress the production of anti-antibodies?
In a previous post of mine, I asked how to supress the creation of anti-antibodies in vivo. In the answer, it was mentioned that site-directed mutagenesis could be used. Currently, I can't find mcuh on how to do so... How does this work?
Update: As people want to know where this idea is coming from, here is the link to my previous question about it.. look in the answer for more info:
How to inhibit formation of specific antibodies (to antisera)?

Could you link to your previous post for context? Site-directed mutagenesis is nearly impossible to perform in vivo, so I'm wondering what the comment poster was getting at...

You want to do site-directed mutagenesis in unspecified living cells in a living body? How do you want to select the cells which make the auto-antibody? This will never work.

@Chris it was just a comment provided by the answer for my previous question.. I will give you the link

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How do we sneeze? - Part 2
Here is the second part of my question about how we sneeze. How are the sneeze droplets propelled at such a fast speed? I have heard sneeze travels at 100 mph. How is this possible?

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A question involving immunoprecipitation to identify interacting proteins?
Using recombinant Flag-tagged Dcr-2 and His-tagged protein X, pull-down assays were performed to determine whether protein X and Dcr-2 interact directly. The recombinant proteins (either alone or in combination) in binding buffer (150 mM NaCl, 1 mM EDTA, 50 mM Tris pH 7.5, 1% Triton X-100) were pulled-down by Flag antibodies coupled to Sepharose beads. Following extensive washing, the proteins were eluted from the beads with SDS buffer, and duplicate sets of samples were analyzed by SDS PAGE. Samples were also taken of the proteins before they were used in the pull-down assay and these were run on the same gel (input lanes in Figure 2B). One gel was stained with Coomassie blue dye (Figure 2A), and the other was transferred to nitrocellulose for Western Blotting. The membrane was probed with a His-antibody (Figure 2B).

The question asks: Do Dcr‐2 and protein X interact directly?

My reasoning is that they DO interact directly. In Fig 2B: the intense bands on LHS shows that Dcr-2 interacts with protein X-that is bound to anti-His. In Fig 2A: the protein X interacts with the Dcr-2 bound to antibody FLAG. I feel I'm not explaining this very though...Could someone please explain their reasoning? Thank you

If the answer doesn't satisfy you, it would be great to tell me the problem in a comment, so I can possibly improve it. Thanks.

First: You are right with your reasoning that Protein X (X) and Dcr-2 interact directly. Lets go through the blots: In the input you check for the proteins loaded into the setting and stain unspecifically with Coomassie.
This part of the blot shows you no unspecific input, and both proteins of interest present. This also shows that Dcr-2 is much bigger than X which allows an easy identification of band patterns.
In the eluate you will only see proteins which are bound directly in the reaction or which interact with bound proteins. Dcr-2 is Flag-tagged so it will directly bind to the beads and can be eluated from them. This is shown in the coomassie part of the blot. Dcr-2 alone binds and can be eluated, while X alone does not bind and therefore gives no signal. Dcr-2 and X together give two bands, sind Dcr-2 binds to the beads and X is interacting with Dcr-2.
This binding is also shown with the anti-His antibody which only recognizes Protein X. The protein shows up in the input where X is added. It also shows up in the elution lane (where Dcr-2 is also present) showing that X is an interaction partner for Dcr-2.


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What happens during kefir fermentation process?
I’ve found many sources about the positive effects of kefir for the digestive system. However I haven’t found any information about the fermenting process.
What is the exact biology (chemistry?) behind the process of milk becoming kefir?
What do the kefir grains exactly consume from the milk? And what do they defecate?  What happens inside the microbes?

I think this can be answered to some degree with links to some deeper references. In my opinion no need to close it.

The fermentation is relatively complex, as quite a number of different bacterial species and yeast live in the Kefir grains. These are made of of the polysaccheride kefiran which immobilizes the bacteria (in contrast for example to yoghurt). The microbes live symbiotic on this matrix.
According to the references a number of different microorganisms has been found, these include mainly Lactic acid bacteria, followed by yeasts and acetic acid bacteria. The species include: Lactobacillus paracasei, Lactobacillus parabuchneri, Lactobacillus casei, Lactobacillus kefiri, Lactococcus lactis, Acetobacter lovaniensis, Kluyveromyces lactis, Kazachstania aerobia, Saccharomyces cerevisiae and Lachancea meyersii.
In brief the lactobacilli break down lactose to produce lactic acid, while the yeasts make alcohol and carbon dioxide while the acetobacter species make acetic acid. This consumes the lactose and the fat content of the milk making it suitable for lactose intollerant people. It also lowers the pH of the kefir. The exact mixture is hard to identify as this contains strongly on the exact composition of the kefir grains.
If you are interested further, I recommend you have a look into the references, I find both articles relatively good to understand.
References:

Brazilian kefir: structure, microbial communities and chemical
composition.
Microbiological, technological and therapeutic properties of kefir: a
natural probiotic beverage.

Well essentially the added Lactobacillus species ferment lactose and other sugars to lactic acid, thus lowering the pH of the product (they take up lactose use it as an energy source under anaerobic conditions and secrete lactic acid). This gives the kefir and other fermented milk products their sourness. Also the lower pH prevents many other bacteria from growing in the product so this is also serves as a natural preservation method. Further more the low pH can denature some of the protein in the milk/kefir resulting in a more solid form. Many of these Lactobacillus species or their relatives are natural part of our gut flora.


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Explaining natural selection in moth
Industrial melanism is an example of natural selection. Can it be considered as a evolution due to anthropogenic action?

Evolution is a change in allele frequency through time. Alleles underlying moth melanism are changing through time in response to environment change, so indeed moths are evolving.
The environmental change is induced by human activities indeed. But the question of what is the cause of the environmental change causing the selection pressure is totally irrelevant to the question of whether there is such selection pressure.
Artificial selection is in essence the exact same thing than natural selection except that there is a goal (increasing milk production or making smaller dogs for example) that is decided by humans. In the moth example, the environmental changed is caused by human activities, but it has never been a goal for human to put selection pressure on moths to force them to change color. As a consequence, change in color melanism is an evolutionary process that is induced by natural selection, selection toward a new environment.
Evolution is not just the same thing as natural selection. The reason is that other mechanism than natural selection yield to change in allele frequency. One of them is genetic drift. You can have a look to this post to have a better understanding of what genetic drift is.
Hope that helps.

Thanks. I got it. Your post on why genetic drift occurs in small isolated population made it better for me to understand it's occurrence in small population

You're welcome. If I answered your question, you can check the answer. Otherwise, you can point to the elements that are still unclear to you.


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Are Whales More Intelligent Than Humans?
Are Whales smarter than Humans?
Their brain size leads me to think so.

possible duplication of http://skeptics.stackexchange.com/questions/2948/does-brain-mass-have-any-correlation-to-intelligence

related: Is life expectancy linked to intelligence in animals?

I think this is impossible to answer without clearly defining what "smart" means, in some way that is valid across species.  I would bet that whales do poorly on standardized IQ tests for example ;)

I'll say this: If one were presented with both brains and asked which one belonged to a god-like being, seems like 9 out of 10 people would say the one on the left. I find arguments like, "What do we mean by intelligence?" boring. We know: Memory, reasoning ability, etc. If some animals begin to approach human intelligence, why must whales and every other candidate intelligence necessarily squeeze between apes and men?

The "wiring" of the brain is more important than the actual size. If only size would matter that basically humans would be rather unintelligent beings ( many many animals have larger head and brain than us). Intelligence is more related to the complexity of the brain (number and size of different brain components) and the number of connections between neurons. We humans are intelligent because we have high complexity compared to our brain size, our brain has more grooves therefore higher surface than a whale brain. So even though whales are quite smart they're not as smart as us.
EDIT: After getting a few comments I felt I need to clarify my answer, so here it comes: as pointed out by user137 humans have much higher brain-to-body size ration than whales and this is very important. What I was trying to explain (yet failed for the first time it seems), that mere physical size / volume is not that important. The level of development and complexity is that matters the most. Many parts of the human brain is found in lower order animals as shown in the image below:  (taken from http://en.wikipedia.org/wiki/Brain
The surface to volume ratio matters because the higher ratio implies a more complex brain structure. So while whales have a higher surface in absolute value (approx 2-3 times) yet their brain is larger by approx 5-6 times ( lots of comparison data here), thus we have higher surface/volume ratio (i left the ratio part out on my original answer). In the accepted answer on the question linked by Bez it is said that more grey matter in frontal lobe correlates with IQ. Now since grey matter is made of neuron bodies and (fewer)axons, this is quite straightfoward --> more neurons = more connections = higher complexity. But all that comparison was made between humans. So brain size differences between different individuals of the same species may contribute to individual qualities. Comparing mere physical brain sizes of different species is not straightforward because of different brain development levels and brain structure.

I might also be useful to check the wiki pages about brain and brain size
http://en.wikipedia.org/wiki/Brain
http://en.wikipedia.org/wiki/Brain_size

It's useful to think about brain size relative to body size. Whales and elephants have much larger brains than humans, but have even larger bodies to go with them. The large bodies probably cost more "brainpower" because of the extra sensory input and simply having more body to control.

I think being able for fine movement requires far more brain power. Basically all land mammals have the basic senses more or less, so just being big does not imply more sensory input. By this logic tall people would be smarter because bigger body--> more sensory input --> more brainpower.

This section on brain and body size is probably a little clearer than my previous comment. Sperm whales have large brains, about 8kg, but have bodies of about 57,000kg. Humans have brains of about 1.5kg and bodies about 70kg. The brain to body ratio for humans is much larger than it is for whales or elephants. While this does not directly correlate into intelligence, it is at least a useful measurement across species. Trying to apply it within a species ( tall vs short humans ) is not appropriate.

Ahh, okay I misunderstood.

Does our brain have a larger surface- the picture doesn't seem to support this. Further, in your answer you first say size doesn't matter and only complexity does - and then you conclude size does matter because surface matters?

plus the answers in the linked question by @Bez do not support your claims

I left a bunch of reply comments earlier, then decided to edit my answer and delete my comments. I hope this clarifies what I'm trying to say.

In any comparison of intelligence, the most important question is how are we going to define intelligence? The typical inclination is: intelligence is what is required to do the things that we admire as difficult intellectual feats. More generally, intelligence is what it takes to do things that humans do. Making comparisons between species is inherently difficult & limited by our species centered narcissism.
An orca has a brain 5-7 times larger than a human brain. The majority of that brain mass is in the frontal lobes- the part of the brain associated with higher cognitive processes (relatively little is involved with motor processes).
Brains require a lot of energy. Nature doesn't like waste. Whales would not have evolved such huge brains unless they were beneficial (& being used)
Consider the image associated with this link:
How your brain sees your body: Meet the cortical homunculus
https://io9.gizmodo.com/how-your-brain-sees-your-body-meet-the-cortical-homunc-5670064
Much of our brain is devoted to hands.
Whales don't need to use their immense brain power on hands (that they don't possess). Therefore they're using it for something else. I wouldn't be surprised if that something else is more complicated ( perhaps more intelligent) than we can imagine.

Welcome to Biology.SE! While you have an interesting perspective, your answer lacks supporting references for most of the claims you make. Without those references this is indistinguishable from opinion and is unlikely to be well received. ——— Please take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site and then edit your answer accordingly. Thanks!


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"Free space" volume in the nucleus
Take a mammalian cell, say a HeLa cell for concreteness. If a molecule (e.g. a transcription factor) enters the nucleus, what is the effective volume that it can explore/access there by free diffusion? That is, the total volume of the nucleus minus the chromatin, etc.

I'm not sure this is a clear (or answerable) question without more detail — it also would be improved by you telling us: where you've looked for answers, what you do know about the topic, and where exactly you still have questions. ——— One example of a problem with the way you've worded your questions is that chromatin isn't an impenetrable solid, which is why molecules including proteins like transcription factors can directly bind to DNA! ——— It also likely to help if you provided some background about why you care about this number.

No, the question is clear and perfectly answerable: what is the subvolume of the nucleus that a molecule can access by free diffusion? A ref for the total nuclear volume is easy to find (e.g. bionumbers). In Alberts et al., Essential cell biology (5th ed.), question/answer 5-2 estimates that 18% of the nuclear volume are occupied by DNA + histones. That's all so far. Any type of cell would do as a guideline.

Please [edit] your post to include the relevant information from your comment and add complete reference information. Comments are ephemeral and often overlooked and so should only be used to discuss improvements for posts. ——— Some examples of why this question isn't clear: 1) chromatin is not a solid — and the porosity is dynamic; 2) volume will fluctuate depending on what the cell is doing (for instance with cell-cycle state); and 3) even within a single cell the "free volume" is going to vary depending on the molecule that is diffusing.


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Can you freeze an ATP assay sample for later use?
I am going to use adult Drosophila to do an ATP assay (ATP determination kit A22066). The most convenient for me is to freeze the samples and perform the experiment later.
However, the protocol provided by the kit producer keeps saying the assay is extremely sensitive, so I'm not sure if it's okay to keep the homogenized samples under -80°C for a short period of time.

you'll never know for sure unless you run some fresh and run some after freezing - might not be worth the risk

Pure ATP can be stable when stored frozen but I would be worried, perhaps unjustifiably, about storing a homogenized sample. You should try dividing a homogenized sample in half and assaying one half right away and the other half after freezing to see how the signals compare.

Could you elaborate why storing a homogenised sample should be worrying?

@Marzipanherz I would be worried, perhaps not justifiably, about controlling pH and ATPase activity.

I was told that there is no (noteworthy) enzyme activity at -80°C. However, I just took this for granted... Guess it's time to find a reliable source for this :)

@Marzipanherz My supervisor once told me that he was working with a colourimetric substrate that turns from clear to purple during some enzyme-catalyzed reaction. He prepared a stock solution, clear in color, and froze it overnight. The next morning it was purple, presumably due to trace enzyme contamination. There's also the time spent while freezing and thawing it but, again, my concerns may be unfounded.

That's really interesting! Thank you for sharing!

@Marzipanherz Well it's just anecdotal. I found it hard to believe myself.


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Why are some animals so much more intelligent than others?
From what I found many biologists state that animals living in large social groups (elephants, primates, cetaceans etc.) have a tendency for improved cognitive abilities. Yet at the same time there are solitary animals with (suspected) high intelligence such as octopuses and plenty of social animals that fail our cognition tests.
What evolutionary pressures pushed certain animals towards such intelligence when their environments are so different while other animals in a similar environment show no exceptional cognitive skills?

When asking "how does intelligence evolve?", I personally think the first step is to recognize that intelligence is an umbrella term for a whole lot of cognitive abilities which is directly a hint that one ought to expect a whole of selective pressures may affect everyone of these abilities. For example, long winters will select for good spatial memories in lineages that hide food during the bad season. I therefore think the question is quite broad.

I agree that intelligence is a broad term that is hard to measure and sometimes we get too subjective about it.  It is not determined by IQ tests.

I'll admit that intelligence is pretty much impossible to exactly define but still, some animals exhibit superior self-awareness and abstract thinking (passing mirror test, tool usage). This question is more about the different levels of sentience among animals than just capacity for memorizing.

@KoenvdH Minor clarification- Do you mean sentience, sapience, or both?

@HarrisWeinstein Please do correct me if I'm wrong but i thought sapience is considered exclusive to humans?

@KoenvdH Not in definition, and there is evidence that various animals (e.g. dolphins, octopuses, etc.) have cognitive abilities that especially push them towards this. I'll grant that we seem to be ahead of the pack.


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Why do we get scars?
Feeling the hardened tissue of a scar on my head I wondered what the purpose of that scarring is, such skin scars are pretty harmless but from what I understand internal scarring can cause major problems if internal organs get damaged.
An extreme example I vaguely remember is the scarring following nerve damage, the new scar tissue can't transmit signals and so the nerve stops functioning properly.
Why does scarring occur when it seems so detrimental, why don't we rebuild the old tissue?

Scars are fibrous tissue that is left after an injury. The body does its best to fix a body part after an injury and scars are their best attempt at doing so. It would be pleasant to think we could have Wolverine type of healing capacities but we don't and the best we can do are those scars.
The ability to completely regenerate the damaged tissue depends upon the specific tissue. Also, some species are better of than others at regenerating their tissues. Such differences relate to the concept of cellular specialization.
For more information you should have a look at the wikipedia articles

Wikipedia > scars
Wikipedia > Regeneration
Wikipedia > cellular specialization

and the Biology.SE posts

Can a lizard shed a regrown tail again?
Can the regeneration mechanism of lizards be used in humans?

Thanks for the answer! But what exactly makes it so difficult to repair tissue damage for us? An amputated arm or something presents obvious problems but even relatively mild burns tend to cause scarring.

This follow-up question is hard to answer because 1) what you are asking is like asking Why is there not more (or fewer) species?. When asking such thing you should justify why you would expect something else. In other words, asking why is nature as it is? is hard to answer while why is nature not like I would expect for such reasons? is much easier to answer. 2) Because I am an evolutionary geneticists and I know very little about physiology.

I guess I would "expect" that organisms try their utmost to restore original function after damage so scarring seems a somewhat weird phenomenon when viewed this way. Surely there must be some evolutionary advantage?


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Why differentiated cells can't "undifferentiate" (under normal conditions)?
In a process called differentiation, the cells of the developing organism undergo huge changes, which result in cells, functioning "completely" differently. Two cells are considered to be of different types if they are having different sets of template-competent genes, though most of the genes in the human genome are common even in highly differentiated cells. Being able to produce specific proteins from the same genome is achieved by something called open chromatin state of the DNA. What I would like to ask is why can't this specific conformation of the DNA be reversed as this would likely answer the title of this question? I would also like to have some tips on further reading in the topic of DNA conformations and about DNA generally.

I used Gabor Forgacs's and Stuart A. Newman's book called Biological Physics of the Developing Embryo

This "undifferentiation" is actually possible and it is known as induced pluripotent stem cell (iPSC). The first "undifferentiation" cells i.e. iPSCs were mouse fibroblasts created in 2006 by researchers in Shina Yamanaka's lab who got the Nobel prize in 2012 for this work.
You can find further reading on this topic on the according Wikipedia-Page or more scientific details on the according nature.com topic.


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Bioenergetics of bioconversions: is there a surplus of energy?
By bioconversion, I mean a microbial process during which resting cells are used in order to convert a substrate to a desired product, whithout cell growth. For example, in this paper, they used Lactobacillus reuteri to convert glycerol to 3-hydroxypropionaldehyde, while L. reuteri can't grow on glycerol. Basically, during bioconversions, cells produce energy for their metabolism, but do not grow.
The energy thus yielded by cells is supposed to ensure their energetical maintenance cost. I was wondering what happens to cells if the energy gain is superior to maintenance needs? Is there some kind of homeostatic regulation of the ATP/ADP ratio? If not, what could be the consequences of too much ATP?

I am not sure about this pathway that u have mentioned but if u see metabolic regulations of pathways like glycolysis for example or krebs cycle their enzymes are feedback regulated with ATP/ADP ratios.


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Book recommendation on the human muscle system
I would like to learn more about the exact mechanism behind our movements, especially about what happens during intense training when anaerobic state arises.

You can get reviews on those topics. What level of information do you expect?

@WYSIWYG I would like to dig really deep into this topic, so something around university level would be excellent, if that's what you meant by your second sentence, but I'm afraid, I didn't understand it.

You answered my second sentence. I think reviews would be also good.

1. Fundamentals of Anatomy & Physiology by Martini and Campbel Biology are quite useful. 2. Have you seen this one? Muscle: Fundamental Biology and Mechanisms of Disease


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What might this animal be?
I have found two species of this strange looking animal on the Eastern shore of the Adriatic Sea and I was simply unable to recognise them.

As bli said it is Aplysia more specifically Aplysia fasciata ,commonly called Sooty sea hare.
It is an Atlantic species of gastropod mollusc of the family Aplysiidae.

This sea hare occurs in the Western Atlantic from New Jersey to Brazil, and in the Eastern Atlantic including the Mediterranean and the West African coast.

Picture references:

From: ipaq

From: gbif.org

This looks like an Aplysia, or "sea hare", a marine gastropod. Some of them sometimes get stranded and look like fat violet/green/brown blobs, around 10cm diameter. In the water, they swim slowly. I've seen some in Brittany (France) and in Algarve (Portugal).


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How do the homologous chromosomes pair up and position themselves along the center of the cell?
I am not sure... Most textbooks just state "they line up" but I don't know how... Something to do with the cytoskeleton or microtubules? Thanks for any help

Are you asking about meiosis or mitosis?

Welcome to SE.biology! These papers 1, 2 should help you. Don't hesitate to come back with more specific questions if you need to. We are happy to answer them.

If your textbook only says "they line up", then you should get a better textbook.

It is unreasonable to close this as a homework question.

There are many things involved in the pairing of homologue chromosomes.
Before mitosis can occur an important prerequisite must happen: the division of centrosome. This small complex is the principal microtubule-organizing center in the (animal and therefore human) cells. During interphase the microtubules originating from the centrosome, project to the cell perimiter with their + ends (this where they grow). At the beginning of mitosis the duplicated centrosomes separate and migrate to oppsite sites of the nucleus to form the poles of the mitotic spindle. As the nuclear envelope disintegrates the spindle captures the chromosomes at the cetromeres. Since the microtubules are growing from the centrosomes this capture eventually pushes the choromosomes to center. Source: The Molecular Biology of the cell. Fourth Edition. ISBN: 0-8153-3218-1 (hardbound) 0-8153-4072-9 - (pbk).
A searchable online version: http://www.ncbi.nlm.nih.gov/books/NBK21054/
I've found a few good articles with many details:
Current Biology, Volume 12, Issue 17, 3 September 2002, Pages 1473–1483
The Dynamics of Homologous Chromosome Pairing during Male Drosophila Meiosis
Julio Vazquez, Andrew S Belmont, John W Sedat
and
Homologous pairing and chromosome dynamics in meiosis and mitosis
Bruce D. McKee
I took a quick glance at the above mentioned articles, and it seems that homologous chromosomes tend to be close together (paired if you wish) during interphase most of the time.

We need to make a distinction between the pairing of homologous chromosomes that occurs during meiotic prophase--the pairing that is necessary for homologous recombination, and that forms crossovers, or chiasmata--vs. the lining up of mother and daughter chromosomes on the mitotic spindle's metaphase plate after DNA replication (during S-phase of the cell-cycle). So yes, to ensure that each daughter of a dividing mitotic cell gets one pair of every chromosome, a requisite step is to build a mitotic spindle, and so you need to duplicate the centrosome (MTOC) first.

In one of your dividing somatic cells you have 2 copies of chromosome 7, one from your mother, and one from your father. After DNA replication and cell division, each daughter cell will also have 2 copies of chromosome 7, one of each type. The daughter cells never get 2 copies of the father's chr 7 (nor 2 copies of the mother's chr 7). In other words, there is no segregation where the genetic constitution of one daughter cell differs from the other daughter cell, the cells are identical. The two replicated father's chromosomes on the mitotic spindle are not paired along their lengths.

Their centromeres are attached to each other, and to the spindle. More specifically, the two copies of the father's chr 7 may not be anywhere near the two copies of the mother's chr 7. Pairing of chromosomes during interphase is not particularly common. In dipterans, there are some tissues, such as the larval salivary glands, where successive rounds of endoreduplication lead to polyploid cells with giant aligned chromosomes, also called polytene chromosomes, but this is a specialized situation. The gut nuclei of nematodes also endoreduplicate, without forming these lined up daughters.


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How to calculate Oxygen consumption?
I am looking into Glycolysis and TCA cycle.
I have learnt that oxygen is the final electron acceptor.
So, let's say we know the amount of NADH and FADH2 produced under some circumstance related to the Glycolysis and TCA cycle.
How would we calculate the amount of oxygen consumption level?

Assuming that you know the amount of NADH and FADH$_2$ produced by glycolysis and TCA cycle, you can determine the reducing equivalent produced: for each NADH or FADH$_2$ produced, two reducing equivalents are produced. It means that the re-oxidation of NADH and FADH$_2$ will release 2 electrons. Here are the corresponding half-reactions:
$\textrm{NADH} = \textrm{NAD}^+ + \textrm{H}^+ + 2~\textrm{e}^-$
$\textrm{FADH}_2 = \textrm{FAD} + 2~\textrm{H}^+ + 2~\textrm{e}^-$
Knowing the total reducing equivalent produced, divide it by four in order to obtain dioxygen consumption: O$_2$ is reduced into 2 H$_2$O by accepting four electrons. Here is the corresponding half-reaction:
$\textrm{O}_2 + 4~\textrm{e}^- + 4~\textrm{H}^+ =  2~\textrm{H}_2\textrm{O}$
Of course this only applies to aerobic organisms: some microbes are able to use other electron acceptors than O2.

This is of course correct, though I think it might help to just write the reaction: 2 NADH + O2 -> 2 NAD+ + 2 H2O

The half-reaction for oxygen reduction is not balanced, missing 4 H+.


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Are there enzymes for every given reaction?
This is a question that's been bugging me, and I haven't been able to find a definite answer anywhere.
We know there are thousands of enzymes (proteins, let's ignore catalytic RNA for now) that catalyze many different reactions, and they do this because they have the correct shape to fit the substrates.
Theoretically, given some reaction, can an enzyme be created to catalyze that reaction? Or is there some reaction that it's not possible to catalyze with an enzyme? Can any given shape be created out of polypeptide chains? If not, what determines the shapes that it's possible to create?

This will probably be a difficult question to answer definitively without some hand-waving or redefining the question; I can't imagine proving the negative result that no enzyme is possible for a given reaction, except for some cases where the reaction is just thermodynamically impossible outside of incredible conditions (for an extreme example, what about hydrogen fusion: the reaction exists, but the conditions necessary are outside the tolerance of protein-based catalysts).
As @tomd pointed out in a comment, enzymes do not change equilibrium, so enzymes are only possible for reactions that are thermodynamically favorable. However, some enzymes couple reactions that are thermodynamically unfavorable with highly favorable reactions to produce a net thermodynamically favorable reaction, which greatly increases the number of reactions that can theoretically be catalyzed.
As for whether any shape can be created out of polypeptides: given the diversity of amino acids and the structural effects of the tertiary structure of proteins, there is a near limitless array of combinations which exceeds human comprehension, but not a truly mathematically infinite number. There are interesting projects such as this one that seek to harnessed underutilized computing power to iterate all of these possibilities to search for useful drugs and explain the causes of disease.

Are there enzymes for every reaction? The short answer is, "No" - there are reactions that occur within the human biology that do not require enzymes. One example of this is the formation of advanced glycation end products (also known as "AGEs"). These are biological molecules like lipids or proteins that become glycated through exposure to high glucose concentrations, like those observed in diabetes or insulin resistance. The high concentrations of glucose allow non-enzymatic mediated covalent attachment of glucose molecules to the macromolecule. See this review for a more in depth discussion of AGEs as well as other references that discuss them.

The question "Can any given shape be created out of polypeptide chains" is rather tricky, but let's unpack it. A protein has a fold - or topology - that determines its overall shape, but can be considered as a framework on which to hang active residues.
There are 'only' 1,200-1,400 known folds, depending on the classification scheme (CATH, SCOP) which seems quite limited. However, if we take just one of those folds - the TIM barrel - and alter the loops you can get a diverse set of structures. That paper does not discuss enzymatic function, of course.
So for small molecules, it's difficult to see any reason why you can't arrange active sites any way you like. The only theoretical difficulty is that you have to fold proteins before they can be active. It might be possible that some complicated arrangement of active site residues would prevent the whole protein from folding - although that's just speculation.
More complicated might be reactions on macromolecules. For example, there are enzymes that bind to DNA, polysaccharides, and other proteins. These longer molecules are still possible for enzymes to bind to - it generally just requires a long surface. Some of the more complex actions include that performed by topoisomerases or chaperones or whatever vaults do.
By moving from tertiary to quaternary structure, it seems like enzymes can do nearly anything that's chemically possible.


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How can cats' claw grow sharper without replacing the claw?
I cut my cat's claws once a month. The claws always have pointed and sharp tip even though I had cut them last month. I assumed cats cannot change the shape of the claw by growing new keratin at the tip. Also it does not looks like the cat grow a new claw and abandon the old one every once a month or so. How is it possible that the claw grow sharper?

The horn has a specific structure which is different from the round edge that we see on our fingers. It splinters and cracks into flakes, so it is more similar to a flint than a chalk.
The outside of the cone dries out and flakes and is scratched off by the cat, while the inside of the cone is the newer horn that grows towards the apex as a new blade edge.

The image is from this research. If you search "sharp" you will find astonishing vetinary descriptions quoted. Also see page 641 for the conclusion of the research. He sais that it seems to have evolved in the aim of keeping the feline claws sharp.
If someone has the technical ability to rewrite the researcher's descriptions into everyday words, you would be a first.
Vetinary research quote:
The horn-generating living blade epidermis that is
located most centrally on the slanted face of the curved
ledge is continuous with the parietal epidermis (Fig. 9b),
so that the blade epidermal cells generated here lie next
to the parietal epidermal cells. Therefore, the cornifying
parietal epidermal cells are deflected and entrained apically
as the blade horn is pushed apically by the proliferating living
blade epidermis. The direction in which the blade horn is
pushed forward can also be inferred from the arrangement
of the ridges visible on the dermo–epidermal interface of
the parietal horn (Fig. 7). The living blade epidermis that
is located at the outer edge of the face of the curved ledge
is continuous with the living epidermis of the proximal
cone horn (Fig. 9b). These lateralmost blade epidermal
cells, therefore, form a layer that lies directly underneath
the deepest layer of proximal cone horn, so that the
boundary between the blade horn and proximal cone horn
is indistinct. Hence, the layers of horn that are generated
in the dorso-proximal bend of the curved ledge underneath the combined horn layer of the external coronary
and proximal cone horn cover the sides of the apical cone
horn and are designated as part of the blade horn. As
the superficial coronary horn on the dorsal side of the
cornified claw sheath is worn off through normal use, the
superficial layers of the blade horn are exposed and are
shown to hug the sides of the apical cone horn (Fig. 13a).
Remnants of these blade horn layers are discernible near
the very tip of the cornified claw sheath, which consists
mostly of apical cone horn, because the rest of the coronary
horn, including most of the blade horn, has been worn off
(Fig. 13b,c).
The remaining soft-cornified horn segments of the
cornified claw sheath are found in places where the
hard-cornified horn divisions need to be supported and
cushioned.
The soft-cornified terminal horn is a segment of the
third major horn division (i.e. the Hyponychium; see Table 2).
It is generated by the living terminal epidermis, which is
continuous caudally with the parietal living epidermis and
is supported by the dermis that covers the medial, lateral
and palmar sides of the tip of the bony unguicular process
(Figs 3a, 4a,c, 7, 9b, 11a, 12a–j). It supports the apical cone
and crest horn on its dorso-distal side (Figs 3a, 4a,c, 7, 9b,
13b) and the blade horn on its lateral and medial sides
(Figs 4b, 8, 9b–d, 13a,b). By filling the space created by
these converging segments of hard-cornified internal
coronary horn, it is shaped into an elongated, pointed
cone and extends proximally between the blade and
sole horn (Figs 12c,d,f,h,j, 13a,b). Because the terminal
horn is soft-cornified, it can adjust its shape to the
changing conformation of the space it fills in the course of
the deformations of the cornified claw sheath during its
normal use.
The friable soft-cornified sole horn is generated by the
living sole epidermis, which is supported by the dermis
that covers the proximo-palmar side of the bony unguicular
process (Figs 3a, 4, 7, 8, 9b–e, 12c,d, 13a,b). Along its medial
and lateral sides, it is embraced by the terminal and parietal
horn (Figs 1b, 4b, 8, 9c,d, 13a,b). The sole horn, therefore, fills
the space between the paired cutting edges of the cornified
claw sheath. It is worn off through natural wear and tear,
as well as through repeated compression and release, as
the cornified claw sheaths are deformed when they are
subjected to tensile forces during climbing and prey capture.

Differential wear like this is a common sharpening method throughout biology, from beaver teeth to limpet teeth, to beaks and claws.

Feathers and claws come from re-arranged versions of the same cell groups. The researcher wanted to devise a general theory for many animals, to see if the mechanism is the same for beaks also, so he used cat's claws because they are readily available. He states that it is different for beaks. The cat's claw is nearly the same as the human nail, and small differences in arrangement of the keratin producing cells produces striking differences in the resulting claw. The cat has the same fingers as us with keratin producing cells arranged in an arc. It's a difficult document to comprehend.

Genetic codes paralleling claws/beaks/feathers: https://static-content.springer.com/esm/art%3A10.1007%2Fs00709-016-1019-2/MediaObjects/709_2016_1019_MOESM2_ESM.jpg from here: ... https://link.springer.com/article/10.1007/s00709-016-1019-2


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Cells created using differently aligned proteins
I remember reading that scientist were making cells (I assume bacteria), that used differently oriented proteins to create a whole new class of life. Because apparently right and left aligned proteins don't interact in same way, cells made in such manner would behave similarly but couldn't be interacted with differently aligned bacteria/virus.
However I can't find any proof this story was true? I could be wrong about details. Is there a similar mechanism that would allow a whole case of twin (contain DNA, and most molecules that regular cells posses) cells that couldn't interact with existing bacteria?

That seems extremely far fetched to do with current technology... in any case, natural aminoacids are called L-aminoacids and their "mirror counterparts" are the D-aminoacids. Maybe that can help with your search?

I can see an "easy" experiment involving generation of auxotrophic d-amino acids for any given gene. You can now make certain bacterial stop codons code for non-canonical amino acids. Of course for an entire genome...now that would be something.

The problem with this is something called the structure-function relationship. The function of a protein or enzyme is completely dependent on its structure. For example, take a look at this representation of the active site of chymotrypsin:

The side chains of D102, H57, and S195 all need to be in a perfect conformation in order for the enzyme to function properly, with the hydrogen bonds being essential. If any one of those amino acids was in the D-form, the enzyme would lose its activity completely. Having every single amino acid in the D-form wouldn't help either, as the entire protein's structure (and hence its function) would be altered.

This assumes lots of things. There may be instances in which the active site is a bit "loose" to allow for multiple substrates and in which a D-aminoacid would not harm too much. Plus if everything, including the substrate, was D-form I bet there would be a high chance of it working. There are examples of antibiotics becoming more specific or selective when one aminoacid is changed from L to D (e.g. this and this)

@nico - a few D-amino acids here and there may not affect structure/function too much, I agree. But I really can't imagine that a fully D organism could exist. I didn't get into this in my answer, but I doubt that all tRNAs could bind the D isoforms of their respective payloads. Secondary and tertiary structures often depend on H-bonding, and a change in chirality could destroy those bonds, leading to incorrect folding.

I don't see why. If everything in nature was specular, well, it could in theory work very well! I think we simply do not have any proof in favour or against to say more...


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Can inverted microscope also be phase contrast microscope?
I've read somewhere that inverted microscope also allows phase contrast microscopy. Is that true? Do all inverted microscope have this ability? Do they have any other functions?
Many thanks in advance.

Definitely true, an inverted microscope is one where the optics are positioned below the specimen, and the light source above, providing an optimal situation for looking at a live culture. The Phase rings that shift the light come soon after the light source. For phase, the orientation doesn't matter, just the order:
Upright microscope
Orientation:
(top)eye--->objective--->specimen--->phase--->light source
order:
eye-->Phase compatible objective-->specimen-->phase disk-->light source
Inverted microscope
Orientation
(top)light source--->phase--->specimen---->Objective--->eye
order
eye-->phase compatible objective-->specimen-->phase disk-->light source
Not all microscopes have phase no, they are an important and expensive addition to a microscope. Adding phase not only required the phase disk but also a phase compatible objective.

i tried to start a microscopy SE in Area51, no one gave a @#$%


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Is there any difference between Tetanus and Tetany?
Both the tetanus and tetany are related to muscle spasms and the latter is due to lack of calcium but is any collaboration between them regarding Clostridium tetani. also?

Did you do any research on this, and can you share what you found?

@anongoodnurse I want to know if this statement is correct if we say the other way: Tetany is rapid spasm in muscles caused by Clostridium tetani?

Again, did you do any research on this, and can you share what you found?

@anongoodnurse I am asking, not saying !


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If my sunglasses provide "100% UVA/UVB Protection" why can't look directly at the sun?
Is it simply the amount of visible light entering the eye? I'm simply confused as to why experts say that sunglasses do not provide adequate protection when they are advertised as blocking 100% of the sun's harmful rays.

The damage to your eye does not only come from UV exposure, but also from infrared (IR) radiation. Your eye contains a lens that focuses the incoming rays to a narrow point. This point would get very hot if you looked directly into the sun. This is comparable to focussing the sun on a piece of paper with a magnifying glass, it would start to burn. Also, the rods and cones in your retina are only tolerant to a certain exposure of visible light.
Source: https://eclipse.gsfc.nasa.gov/SEhelp/safety2.html

Thanks so much for the source you provided, I had a really hard time finding the information I wanted that gave specifics as to the different dangers of looking at the sun besides "Don't do it." It seems like the main problem is the visible light which is what I suspected, although even in the source it is unclear whether hen they are talking about IR whether it is truly the IR radiation or the near IR radiation (or essentially more visible light) that contributes to the issue. Regardless, thanks for your help!

Visible light too is dangerous to have concentrated into your retina.
When you shine a flashlight at yourself, where does all that  visible light go as it seemingly disappears into your body?
Heat!
It makes your molecules more ever so slightly more.
Also, a lot (but not all) of the uv light is absorbed by your cornea.
Visible light will enter your retina, and focused to a point that is REALLY DANGEROUS. The heat from the light hitting your retina will immediately denature all the proteins inside your retina cells, killing them.
This will happen no matter how much IR or UV you block.


text:
What's the name of this tree?
I photographed this flower on the street in Los Angeles.
It looks like a lilac, but I am not sure.

It is not lilac. which part of earth do you see this? Crepe Mrtyle perhaps - I passed by some.


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May have killed a cutting. Can dead plant cells be revived?
Ok. So, I went to New York City for the first time! My parents picked a hotel, and we had a good trip.
And even cooler, that hotel wasn't very far from a cool cedrus Atlantic a tree.
I got a cutting, but accidentally left in in the car today, and my mom went to work. The new growth has died. The old hardened-off growth still exists, but may or may not be dead.
It's evergreen, and it's not easy to tell.
So, assuming it is dead, and since it will be a long time till my next family trip, how could I bring one of the cells back to life, so I can generate explants?
Obviously this is very hard to do with animal cells, but could it be different with plant cells?
Could I just collect a bunch of dead cells, and pour atp solution on them?
Could I perform a nuclear transfer?
How could this be done?
And most importantly, CAN this be done?

#2. And frankenstein won't work.

Nuclear transfer?


text:
Genotype frequencies and fitness values in haploid population with clonal growth
I found a small problem, and I am not sure at all about my answers. If someone could correct it, that would be awesome.

Consider a heterogeneous population with the following genotype frequencies and fitness values (attention: haploid individuals with clonal growth!) :
ab : $ P_{ab} = 0.8, \quad \lambda_{ab} = 1 $
Ab : $ P_{Ab} = 0.1, \quad \lambda_{Ab} = 1.2 $
aB : $ P_{aB} = 0.1, \quad \lambda_{aB} = 1.1 $

Determine the average fitness of the population
After one generation, what are the new genotype frequencies and the average fitness of the population ?
What are their values in the long-time limit ?
Explain clonal interference in this context.

My answers :

Relative fitnesses values - we take the highest as reference (here: Ab):
$$ \omega_{ab} = \dfrac{1}{1.2} = 0.83   $$
$$ \omega_{Ab} = \dfrac{1.2}{1.2} = 1   $$
$$ \omega_{aB} = \dfrac{1.1}{1.2} = 0.916   $$

Average fitness of the population :
$$ \overline{\omega} = p_{ab}.\omega_{ab} + p_{Ab}.\omega_{Ab} + p_{aB}.\omega_{aB} = 0.8556 $$

$$ p_{ab}(t+1) = \dfrac{p_{ab}(t).\omega_{ab}}{\overline{\omega}} = \dfrac{0.8\times 0.83}{0.8556} = 0.776 $$

same for the others frequencies :
$$ p_{Ab}(t+1) = \dfrac{0.1}{0.8556} = 0.117 $$
$$ p_{aB}(t+1) = \dfrac{0.1 \times 0.916}{0.8556} = 0.107 $$

I know that the fraction of the fitter genotype will grow exponentially compared to the genotype of lower fitness. But how do you demonstrate that ?
I learnt that due to the haploid structure of the population, the two new alleles A and B are in competition under natural selection : this will lead to the loss of one of them in the long term (even if they are both advantageous for the organisme). Then how do I explain that we those data ? Does this mean allele B will disappear ?

Any help would be welcomed :)


text:
Does the genome make sense without knowledge of the ovum?
Much of the literature for laypeople seems to consider (and to spread
the idea) that an animal (or a plant, I guess) is characterised by its
genome. I do not know whether the same goes for more professional
literature. Even on this site, the tag genomes is defined as The
entirety of an organism's hereditary information, which seems to imply
that it contains a description of all that can be be inherited.
It seems to me that attempting to define an animal with the sole
knowledge of its genome (let alone recreate it as envisioned by some people) does not
really make sense, without the complementary knowledge of the cell
structure of the ovum that has to interpret this genome.
This question seems never to be seriously addressed in lay literature.
Is it the case that this decoding machinery evolves much less than the
genome itself? This could be expected, since changing the decoder has
usually more important, global and drastic effects than changing the
genome, which may result in a very localized effect. Hence, changes to
this machinery are less likely to give a viable being.
To refine that question (unless the moderator prefers this to be a
separate question):
Is there any study of the diachronic evolution of that genome decoding machinery in a
given species, or of the synchronic differences between species, which
would probably give a measure of the speed of diachronic evolution of
that machinery?
When two close species cannot mate, is it analysed (for some cases) whether it is due
to difficulties in combining the two genomes, or to the fact that the
ovum of one cannot properly interpret the genome of the other?

Don't forget that the initial cell machinery provided in the ovum is quickly replaced by that of the newly-formed zygote. (e.g. ribosome half-life is about 5 days). Also, and perhaps this analogy does not hold, but kickstarting a bike might be very different from driving down a road, but the engine itself defines the properties of the vehicle, not the way in which the engine was started.

You might want to rephrase the question to ask about the general case of converting genotype to phenotype, because "the ovum" has nothing to do with it -- obviously, since the vast majority of living things do not have ova. Moreover as you suspect you have two unrelated questions here -- genotype to phenotype, and speciation, which have very little to do with each other.

@iayork I cannot well rephrase my question because I am not competent enough
to use most words and concepts with precision. I am rather naive on all this, but
shocked by presentations I found too simplistic. I refer to ovum as the
only way I know to specify the context that initially interprets the
genome - assuming there is such a specific initial phase, which I am
note sure of. Also I first considered the issue for animals. Actually
I wonder whether reproduction can always be separated from cellular
differentiation (same genome, but machinery uses it differently)

The short answer is that there is elaborate machinery needed to convert genetic information into a phenotype; that's nothing to do with the ovum; and it's hardly ignored in biology as it's the topic of intense research.  It's difficult to answer your question any more than that since it seems to rest on so many incorrect assumptions.

@iayork Actually I am not assuming more than what you just said: I meant to
say that genetic information is meaningless without knowledge of the
machinery that will convert it to a phenotype (I did not know to
express it that way). The rest (ovum included) is just my failed
incompetent attempt at expressing it in a more concrete way. My
question is only why most presentations for non specialist are
ignoring that fact. I do expect biologist to deal with it, but is
there a reason this is not explicited for the wider public, to avoid misconceptions. Maybe I
should indeed rephrase.

Nice question! Let's start by talking about different forms of heritability.
What is heritable?
Here is a list of things that can be inherited. Some of them are only ('mainly' would be more correct that 'only') transmitted to the offspring while others can also be transmitted to any individual in the population.
The term epigenetics is used with several meaning. In its narrowest sense it refers only to modifications (typically methylation) on top of the DNA sequence or on top of histones (histones are proteins around which the DNA is wrapped). In its broadest sense, it refers to any element of hererdity that is not caused by the DNA sequence. In the below list, I will avoid using the term epigenetics.
What can be inherited:

DNA (obviously)

Modification of the sequence of DNA

Methylation on DNA

Modification of (typically) methyl group added on nucleobasis

Methylation on histone

Modification of (typically) methyl group added on (typically) the tails of the histones.

Environment (or rather macro-environment)

The term environment can be used with different definitions. Histone modification is generally considered as being the environment of the genome typically. I will however make a (somewhat) arbitrary distinction between this micro-environment and the more intuitive macro-environment
Individuals affect their environment and therefore can shape the environment for their descendents. An obvious example is a beaver dam which last longer the the life of a single beaver. Two key concepts here are niche construction and Ecosystem engineering. You should have a look at the post Does modern theory of evolution include modification of physical environment?

Memetics (See wikipedia > meme)

A meme is any idea or element of culture that can be transmitted. This type of inheritence is particularly important is species that have high cognitive abilites such as humans.

In this kind of discussion, there is often someone who stand up to talk about plasticity, developmental noise and mutational noise to mess things up. I will just consider them as phenotypic trait and will not much attention to them for the moment (even though part of my research is focused on these three concepts).
Consideration of the non-genetic inheritence in the literature
I like that you noticed that "the tag genomes is defined as The
entirety of an organism's hereditary information". Such definitions are common and grounded in an old view of inheritance. As listed above, there are other things than the DNA sequence that is inherited by the offspring. While all biologists know that, it is true that few really acknowledge the existence of these other forms of inheritence in their daily thoughts.
Some authors have argued that these other types of inheritence must not be neglected. Odling-Smee and colleagues wrote a whole book on the subject (Niche Construction: The Neglected Process in Evolution). Some have even argued that we should rename our theory of evolution to the light of the existence of non-genetic inheritence (see Laland et al. 2015). My feeling is the vast majority of biologist recognize the existence of these types of inheritence but do not consider that it is worth a renaming of the theory of evolution (current named modern evolutionary synthesis). Some would not consider this renaming necessary either because they neglect the important of these other forms of inheritence or because they just don't think it is worth renaming our theory even in the recognition of the importance of these other processes.
Viewing the cell as a decoder can be misleading
In your question, you are suggesting to view the cell as a decoder of DNA. IMO, this is misleading. In this discussion, I will exit science and enter in the realm of philosophy (identity).
What is generally considered as the mechanism of decoding DNA is actually part of our geome itself (consider typically the importance of tRNA and rRNA). If uneasy with basic concept of gene expression you might want to have a look at an intro course such as Khan Academy from the section Classical and molecular genetics to the section Gene regulation.
Also, I would argue that all the elements that are being transmitted to the offspring shall be considered as being the offspring. If it turns out (which we actually pretty much know is wrong) that histone modification explains more in the phenotypic variance than genetic variance, it would intuitively be unfair to see histone modification as just being a decoder of the genome. We would rather be tempting to see histone modification as central and the DNA sequence as a side-effect.
Layman literature
You say "This question seems never to be seriously addressed in lay literature". Richard Dawkins book called the extended phenotype, while maybe not directly addressing your question does a good job at playing out with thee concept of environment vs gene separation. You might want to have a look at it.
Note that the laland et al. 2015 cited above is easy to read and would be a good source of information for a layman.

Craig Venter made his first synthetic bacteria by first making a synthetic genome containing all the genes required to run a bacteria (Mycoplasma. mycoides). His team then inserted this synthetic genome into related species of bacteria (Mycoplasma capricolum). The synthetic genome than took over the cell and over time turned the cell from one species to another. http://www.nature.com/news/2010/100520/full/news.2010.253.html
So... just because it does not make sense to your gut, does not make it wrong. Gut feelings are great... it is how we think the world should work. A short hand. But just because we think the world should work one way, does not make it so. The world and biology has many antigut concepts.

I think the reason for the simplification in many contexts is that the machinery that converts genotype to phenotype is ALSO specified in the genome; yes, it is necessary to have that machinery present for cells of all types to function and to create new cells (whether single-cellular or multi-cellular), but this machinery itself is not really inherited; the machinery (proteins and functional RNA) that exists in a founder cell cannot be inherited except in a very unusual and extreme cases.
There can be differences in translational machinery, for example see wikipedia, but precisely because as you write, "changes to this machinery are less likely to give a viable being" - that means that changes to this machinery are most likely to be lethal and therefore do not persist in a population.
Failures of fertility between species are due to simpler factors, and the transcription machinery is highly conserved across many species that are not cross-fertile.


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Why does Sanjay Gupta's brain look so unusual? (brain model shown on CNN) The subdivisions don't look like the lobes I learned in school

above: Screenshot from CNN's May 18, 2023 Feinstein’s office confirms broader health complications, contradicting senator’s denial below: from anatomyinfo.com's Parts of the Brain

Neurosurgeon Dr. Sanjay_Gupta frequently appears on CNN to clarify complicated medical issues for the general public. Today he discussed possible neurological effects of shingles including encephalitis (inflammation of the brain) and differentiated it from meningitis (inflammation of the "protective membranes covering the brain and spinal cord".
He briefly raised a model of a (presumably) human brain to remind us what a brain looks like, but didn't refer to any region specifically.
In school I learned of brain subdivisions as lobes; frontal, parietal, occipital, temporal, cerebellum, etc. but this model has two vertical zig-zag-stripes a bit behind where the boundary of frontal and parietal used to be.
Question: Why does Sanjay Gupta's brain model shown on CNN look so unusual? The subdivisions don't look like the lobes I learned in school.

I don't know exactly what brain model he has, but if you search for "brain model" you'll find lots that have the precentral gyrus and postcentral gyrus colored separately from the frontal and parietal lobes. Here's an example:

The precentral gyrus is at the very posterior end of the frontal lobe, and is the location of primary motor cortex. The postcentral gyrus is right next to it, at the very anterior end of the parietal lobe, and is the location of primary somatosensory cortex.
A couple other things to know are that brains vary a lot between people; it's really a pain in neuroscience because when you do brain imaging and want to compare between people you need to transform everything to a shared space. Also the lobes frontal/parietal/temporal/occipital are only kind of real things. They're roughly delineated by typically deeper sulci, but all the lobes are still closely connected with their neighbors. They are not separate.

I see, are these areas primarily applied to just the cortex? In other words (and pardon my lack of neurology words) are they related to the surface of the brain only, whereas lobes are "bulk" features?

@uhoh Both lobes and these areas relate only to cortex, the "outer" part. Subcortical structures like thalamus are also organized in a way that corresponds to their connectivity to cortex, but not the same.

There are lots of different ways to potentially subdivide the neocortex. Brodmann areas are one example you could read about.

So it seems an answer to my comment might go something like "yes, these areas primarily applied to just the cortex... whereas lobes you studied about in school are 'bulk' features". I'll go off and read some more now. There is so much happening on the cortex it makes me wonder sometimes if the stuff underneath is as much for pure mechanical support of the cortex as it is for actual neurological function. I think I'll ask a new question about that but it will take some time to some basic reading first.

@uhoh No, the lobes are just broader "geographical" features of the cortex, only the cortex. Right below the cortex is mostly "white matter": fiber bundles connecting within cortex and from cortex elsewhere. After that you get into other structures, but all of that is entirely underneath all of the exterior named lobes you're talking about.

Oh, got it, where the connectome manifests itself.


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Why does asbestos cause cancer?
We are probably all familiar with the dangers of asbestos in your rooftop or in various pieces of old equipment as it has been shown that the microscopic asbestos particles reach our lungs and can then potentially cause lung cancer.
Now smoking (for example) can cause cancer because of various carcinogens chemically interacting with DNA, but how can these asbestos particles, specifically prized for being quite unreactive, damage DNA to the point of triggering cancer?

I don't have time to look this up right now, but I think the particles stay in the lung for quite some time and physically damage the cells there - the resulting necessary increased regeneration increases the likelihood of mutations and therefore cancer occurring.

More basic answer; the asbestos crystals have hooks. So the cilia in the lungs have difficulty moving them out with the other dust. This irritates the tissue causing the effects of the first answer. So it is a matter of time and number of asbestos particles that increases the probability of a cancer. Decades ago , the asbestos miners in Africa typically worked for years ( eg 20 years) before getting cancer.

There are basically three hypotheses regarding the pathogenesis of asbestos-induced cancer , which may be summarized as follows:
(1) the "oxidative stress theory" is based on the fact that phagocytic cells that engulf asbestos fibers produce large amounts of free radicals due to their inability to digest the fibers, and epidemiological studies indicating that iron-containing asbestos fibers appear more carcinogenic;
(2) the "chromosome tangling theory" postulates that asbestos fibers damage chromosomes when cells divide; and
(3) the "theory of adsorption of many specific proteins as well as carcinogenic molecules" states that asbestos fibers in vivo concentrate proteins or chemicals including the components of cigarette smoke.
Source

Please add some references to your answer.

@AkramQaasim Feel free to check the edit. Please don't copy paste from the source.

@JM97 sorry for that .but i copied the only question related answer just for shortcut the source . Thanks


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What is this anise smelling plant?
On holiday in southern France and we found this small plant growing out of some rocky soil:

It smells quite strongly like anise but seems to be a different plant?

There are several plants in the family Apiaceae with these kind of thin leaves, and some smell strong and/or are used as herbs in the kitchen. This must be Fennel  Foeniculum vulgare, because you describe it's smell as anise. Dill looks similar, but smells different. Fennel is indigenous to the mediterranean, but planted all over Europe.
It can be quite big, but on poor, rocky soil might remain small.
Picture of fennel from Dutch wikipedia:

Looking at more pictures it does seem very similar, this would be an absolutely tiny fennel plant though


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Dominance/recessivity of new mutations
What is the distribution/probability density function (PDF) of recessivity/dominance of new mutations?

I very welcome any partial answer that does not give the whole PDF but just some information about the expected value or the variance of this distribution.
Here is a related question

Please provide a basic schematic/equation for a possible underlying model to narrow the question down.

I don't really expect insights some theoretical models but from empirical data. I would not refuse some links or answer that predict this PDF from Fisher's or Wrights models of dominance though.

it is not easy to ascertain if a mutation will be dominant or recessive without the knowledge about the concerned gene and its structure-function relationship.

I don't believe you can produce a general function for this. It will depend on the exact gene and organism you are considering.
From a molecular point of view, the vast majority of recessive mutations result from a change producing either a non-functional protein product or a truncated product that is cleaned up by the cell. We can reasonably assume that most modifications significant enough to produce a phenotype will be of this class since there are more mutational sites which can produce a non-functioning product than can produce a product of changed function but the exact ratio of one to the other is not going to be equal across different genes and organisms.
Note as well that the whole notion of recessive and dominant traits is probably an over-simplification and, in fact, there are subtle differences between homozygotes and heterozygotes in many, perhaps most, cases so I'm not sure how useful an estimate would be even if you had one.


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Hill-Roberston effects and effective population size
From this article, first page, middle of the second column:

Even if harmful alleles do not become fixed, they can still reduce the efficacy of selection on neighbouring loci through a process called Hill–Robertson interference. This effect occurs because individuals bearing deleterious mutations are less likely to survive and reproduce, reducing the number of individuals that contribute genetically to the future population. This reduces the effective population size witnessed by a focal locus

I don't understand the link between the Hill-Robertson effects and the effective population size. Why would the effective population size be greater in absence of Hill-Robertson effects? Can you please make this link clear to me?

Here is another question on the same article.

your name changed, I preferred Remi.b because I am not sure how to cite a name with a space!

@hello_there_andy Ha ha you're a funny dude! But thanks for noticing, I didn't change my "display name" on purpose; Mac's auto-filling made it for me! I just wanted to add my "real name". I'm Remi.b again! Thanks for your answer below.

Hopefully this syllogism will answer your question.
Given the following premises:

In the absence of selection, fitness of individuals are at a theoretical maximum.
If a theoretical maximum fitness is achieved then effective population size is maximum.
If there is an allele that confers both increased and decreased fitness you have a genetic conflict (e.g. an allele that turns you green gives you good woodland camouflage but is un-attractive).
If a deleterious allele is linked to a beneficial allele this is similar to having a genetic conflict.

The conclusion follows:
Strong linkage between beneficial alleles and deleterious alleles (Hill Robertson effects, i.e. 3. and 4.) prevents a theoretically maximum fitness to be attained (1.) and thus a reduced effective population size (2.). Which can only be overcome by high levels of recombination and mating (i.e. by separating deleterious and beneficial alleles).

I don't want to repeat the same thing every time you answer my questions (this happened twice I think) but really: As soon as I start reading your answer I realize how obvious was the answer and feel stupid I didn't get it before. Thanks for your help.

No no please don't feel that way!! Funny because I felt the  same way when being taught these things by my research supervisor, Prof. Burt (who's worked closely with "R" as you call him). The only stupid thing to do is lacking bravery to ask the questions.

Who is "R" (as I call him)? Robert Trivers?

ah yes, perhaps it wasn't you who called him that oops :P


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What is the maximum number of babies a human woman can have?
I know you could divide the female fertility period (~40 years, right?) by 9 months which would give something like ~50 kids (with no multiple kids per pregnancy). The limiting factor in this calculation is time but is there a biological upper limit as well?

How do you define the biological limit?
It very much depends on how you define a biological limit. If you prefer, it very much depends on how you define a human! Some women are completely sterile while others are highly fertile and there is genetic predisposition to that.  How much "perfect" should the genotype of an individual be so that it is still considered as a human? There is genetic variance underlying fecundity that is important to consider. For example, in your calculation you took lifespan as a constant but it obviously is not a constant. Fecundity is reduced by all these small mutations segregating in the human populations that reduce the fecundity of any single human. There exist no human that is free from all deleterious alleles. Imagine a giant woman with 10 independent reproductive system! Would she still be a human? That was probably kind of a too extreme thought experiment. Imagine a woman that can have a reproductive lifespan of 100 years. Would it still be a human? The issue behind this question reminds me an old post (now closed, I can't find it anymore) that asked whether a leopard would run faster if it had more legs. Well... one can imagine something running faster than a leopard, but it would not be a leopard anymore. So how many changes from a leopard are we allowed to make to answer the question. So I had to chose a definition of what a "perfect woman" is. Or a definition of a woman that would set this so called biological limit.
The definition I am using to answer this question
In the below answer, I will assume that by biological limit you mean the expected fitness of a female that would live in the same environment than we live in today but would not carry any single of the deleterious locus that are segregating in the human population. In other words I assume that you accept that the "perfect woman", that is a woman that would not carry any single of the deleterious mutations that segregate in the populations will set this biological limit to woman maximal fecundity.
Mutation load Theory
The decrease in the mean fitness of an idealized population where no deleterious mutations would exist compared to the realized mean fitness of a population is called the mutation load. The mutation (in an infinite population) is a function of the genome-wide mutation rate only. Let the genome-wide mutation rate in human be $U=2.2$, the mutation load $L$ in the human population is equal to $L=1-e^{-2.2}=0.89$. The estimates are taken from this video. You may want to have a look to the video in order to have a better understanding of why $L=1-e^{-U}$ and what are the assumptions of these calculations. The main assumptions are 1) infinite population size, 2) multiplicity of fitness effects at different loci and 3) additivity of fitness effect between alleles at the same locus.
So what does mutation load theory predicts?
The above calculation means that segregating deleterious allele reduce the fitness of the average woman by 89%! If we assume that an average woman can have 10 babies (this number is just a random guess) if she wants to, then the maximum biological limit of a "perfect woman" (in a world where there is no more competition than the one in which we are living) is $\frac{10}{1-0.89}≈91$  babies!
According to wikipedia, the world record is 69 and is owned by Mrs. Vassilyev. It is reasuring to see that the observed world record (69) is lower than the the biological limit we just calculated (91). If we were to know the distribution of maximal number of babies per woman (not to be confused with the realized number of babies), we could calculate the probability to have 69 or more babies and compare this probability to the total number of females that has ever lived (or the total number of females that would have never had the idea to have so many babies). Always according to wikipedia, the world record for men would be 867 and is owned by Ismail Ibn Sharif. However, sounds possible to me (but I really have no idea) that some sperm donor may have overshoot this number today.

Did you mean reassuring 69 ?

With many typos and english mistakes I meant It is reasuring to see that the observed world record (69) is lower than the the biological limit we just calculated (91) I edited the answer. Does it make sense? Thanks

Thanks! This is a very interesting approach to the question. Would be interesting to get an estimate of the number of babies for the average woman which would set a more accurate theoretical maximum. Btw isn't the perfect woman a Puerto Rican? Too bad she does not belong to the human genera :) (see PC3). This goes exactly along your thoughts.


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When you blow through your nose while holding it closed to "depop" you ears, why do you sometimes feel it in your eyes?
After your ears have "popped", for example on a flight, I heard you are supposed to hold your nostrils closed and blow through your nose to readjust the pressure to the normal level. Why do you sometimes feel a pop in the corner of your eye when you do this?

The sinuses connect the ear, nose and throat as well as the tear ducts of the eye. The pressure created when holding your nose and blowing is transferred to any area it can get to; in this case, the eyes and ears.


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Can we use the HIV antibody test to detect HIV in newborns?
Adults and elder children can use HIV rapid test to test HIV infection. Can we use the HIV antibody test to detect HIV in newborns too?

It is a prerequisite here on Biology.se to do some research yourself and not only dump in one sentence questions. Additionally your question is rather broad. So please edit your question and add the information you found yourself and ask about what's unclear.

The question itself holds potential, please elaborate to avoid closure.

I found the question fine the way it is. This is how you chase away new members. It's also a prerequisite to assume the question hasn't been answered somewhere else and write an answer here for posterity rather than linking to a uniform resource location that may or may not exist in the future.

The rapid screen usually tests the oral mucosa by swabing the inside of the cheek and checking for the presence of anti-HIV envelope antibodies. Although the precise target of these antibodies seems to be kept propriatary, my guess would be the detection of either p24 antibodies or envelope antibodies that bind the V3 region.
Regardless, the point is they test for the presence of antibodies, which a child does not start making until they are born. See this post for a great explanation
Since a child has mostly maternal antibodies, the presence of anti-HIV antibodies would only mean that the mother has started producing antibodies to HIV (Seroconversion). This means that although the child has been exposed, they may themselves not be infected.
The mucosa, particularly in the oral region has a very low titer of anti-HIV antibodies, so I think this test would probably be best to direct the physician to conduct additional tests that are more indicative of HIV infection like p24 western blot.


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Why do some animals try to imitate other animals?
There is a tendency of some animals (including people!) to be "copy-cats" and try to imitate members of their own, and sometimes other, species.
The most obvious example is a parrot copying human speech. Humans also try to copy the speech of their parents when they are little. "ma-ma, da-da"
The less obvious examples, I'm not even really sure are occurring. Like when a gorilla at the zoo assumes the same posture as a person sitting on just the other side of the glass. Like my cat, who tries to chew on bones similar to the two dogs we have.
I'm sure there are more/better examples I'm not aware of.
What is it that creates this behavior? Is it something that was learned, or is it some natural tendency? Is there such a thing as behaviors that are "encoded in the dna"?

Disagree with "too broad" closing but wouldn't this question be better suited for http://cogsci.stackexchange.com? (i.e. off-topic here).

I think this question is perfectly on topic here. Cognitive Sciences focuses much more on the human aspects.

Mimicry, in biology, phenomenon characterized by the superficial resemblance of two or more organisms that are not closely related taxonomically. This resemblance confers an advantage—such as protection from predation—upon one or both organisms through some form of “information flow” that passes between the organisms and the animate agent of selection.
This link describes different types of animal mimicry

The two step mechanism of mimicry evolution states that,
1) Mutations at genes of major effect first allow a phenotypic leap
  achieving an approximate resemblance to a particular model.
2) Once these mutations have increased in the population, resemblance can be enhanced through the gradual selection of epistatic
  modifiers.

Considering the case of butterflies, the working of two step mechanism evolved through different types of natural selection process. Experiments show that birds associate certain patterns in the butterfly wings to identify the specie and generalize those features, but a small deviation from the exact pattern is neglected. The increased resemblance is advantageous to species having imperfect mimics. So the species which displays/perform imperfect mimics can some how fall under the list of rejection and manages to survive, thereby passing genes to next generation.

"Largesse of the Genome", an idea put forward by J.R.G.Turner states that, it is believed that the modification of a trait can be achieved by so many different genes that some of them will inevitably happen to be linked.Amoung the many possible combinations of the loci, selection could simply sieve out the ones that involve linked genes.
Encyclopedia of Insects by Vincent H. Resh, Ring T. Cardé

Although the exact mechanisms of mimicry is still a questionable area, experiments are giving hopes regarding the two step mechanism and more over natural selection is the predominant factor which makes a mimicry successful.
This link describes insect mimicry and two step mechanism in detail.

References
A Dictionary of Birds
Encyclopedia of Evolution
Rapidly Evolving Genes and Genetic Systems

I think the question is about imitation, not mimicry.

I did have imitation more in mind when I wrote the question, I hadn't really thought about mimicry like stated here.

My intuition would be that this has to do with the neuroscience of social behavior.  Many animals, especially those that live and travel in groups (eg. humans), have a great deal of brain "wiring" dedicated to engaging in social behavior with other members of their group.  This is an advantage from an evolutionary perspective, since it helps with cooperation, exchange of information, establishment of social hierarchy, etc., which confers survival advantages.  In the absence of other members of their group (for example, in captivity), there are documented cases of animals imitating human behavior, which is thought to be a carry-over of the social bonding behaviors they typically engage in.
There was a NYTimes article that mentioned this phenomenon in relation to parrots imitating human speech, which came to mind when I saw your question  (http://www.nytimes.com/2016/01/31/magazine/what-does-a-parrot-know-about-ptsd.html )--not a very scientific source, I know!

This is just an opinionated guess not an answer, and makes little effort to directly answer the question.


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What is the advantage to neurons being asymmetrical?
Does having a central axon and dendrites result in any advantage compared to if the neuron was symmetrical?

Asymmetry to essential to neuronal function, particularly in the peripheral nervous system. This is because the dendrites of a neuron receive synaptic potentials, which are graded and decay with distance. Dendrites are typically short such that a synaptic potential is still above threshold by the time it reaches the axon hillock (sometimes called trigger zone), so that a subsequent action potential can fire. Axons need to be long (some are up to a meter long, in the leg) to transmit signals long distances in the body. To make a neuron symmetrical, one of these qualities would have to be compromised and neuronal function would suffer as a result.
Source: Principles of Neural Science, 5th ed (2012), Kandel et al. Chapters 1-6.


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Query for gene upregulation in cBioPortal
there! Could anyone help me with some biostatistical problems using cBioPortal.
We are looking for cell lines with upregulation of certain genes on cBioPortal. My supervisor is teaching me to use this website because I have no prior experience. She is using EXP >= 0.5 to define upregulation. Although I am of no bioinformatics background, my opinion is that 0.5SD away from the average is not strong enough to define an upregulation. I think it better to use EXP >= 2 or 1.5. I have discussed this with my supervisor but she insists using EXP >= 0.5.
Does anyone have any experience with this issue since I am still not convinced by what I was told. Thanks a lot!

Well, I have worked with expression patterns. Unfortunately there is no clear cut or magical numbers for cutoffs . I agree with you that 0.5 is not stringent. However, to explore data usually one can parse it using lower cutoffs and later on you can rise the bar to see what happens.

Many thanks Andrei! I also asked a friend of mine about this and she has similar opinions with yours. I will do queries with different criteria and compare the results! Thanks a lot!


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Mosquito vs Human: Swapping the roles
Is there a known mosquito-specific lethal (for some relevant species of mosquitos) virus that you could safely (for the humans) put into the blood of living humans? Is it technically possible to engineer humans to produce such a virus?


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Is the innate immune system capable of identifying all foreign antigens?
I've been studying immunology on my own lately and I would like to know if the macrophages and the other components of the innate immune system are capable of identifying all foreign antigens.
As far as I understand the innate immune system is responsible for activating the adaptive immune response that will produce antibodies. So the innate immune system should be able to identify new antigens, antigens that the body has never seen before.
If that's the case, how does it work? Does everything "alive", from virus to bacteria, present the same molecular pattern that is responsible for triggering an innate immune response?
Thanks!

Not essentially. TLRs have evolved to identify some common antigens.

TL;DR the huge block of text:

The innate immune system only recognizes certain antigens, called PAMPs.
The activate immune system usually requires the immune system, but it can get around this in some cases.

You're on the right track.
Pathogen-associated molecular patterns (PAMPs)
Innate immune cells such as macrophages and denritic cells (DCs) only recognize certain pathogen-associated molecular patterns (PAMPs), and this occurs primarily through membrane-bound receptors called Toll-Like Receptors (TLRs). Diversity of PAMPs is extremely limited compared to the extraordinary diversity in recognition by the active immune system. However, they include many molecules and classes of molecules that are essential for certain pathogens, such as flagellin, lipopolysaccharide, and viral double-stranded RNA.
To answer some of your question right away, the immune system can't adapt, but it can recognize antigens that the body hasn't seen before, because the set of antigens it can recognize (the PAMPs) are dictated by the genes associated with Toll-Like Receptors and other "Pattern-Recognition Receptors".
Exception 1: T cell anergy
The major link between the innate and active immune systems that you mentioned is through the presentation of antigens to T helper cells in lymph nodes by DCs: DCs present antigens (digested parts of pathogens) to T helper cells through a process called antigen cross-presentation.
When this happens, the T helper cell is activated through a series of chemical exchanges between the DC and the T helper cell, with two that are important to mention here: 1) the T cell recognizes the antigen–MHC class II complex on the DC (called T cell stimulation), and 2) the T cell receives a signal (called co-stimulation). The first signal only requires cross-presentation and recognition by a T cell. But for the DC to release the co-stimulatory signal, Toll-Like Receptors (TLRs) on its surface need to have recognized a PAMP.
With these interactions (plus some more), the T cell will begin proliferating. However, immunology is very nuanced; you can probably find exceptions to every sentence I just wrote (I see a lot even while writing this). It turns out that a T cell can still be activated even without co-stimulation if its own stimulation is strong enough. This occurs through a process called T cell anergy. Activation of an anergic T cell—that is, one that was activated but did not receive a co-stimulation signal—has to do with the autocrine and paracrine nature of a signal called IL-2, which T cells normally produce only small amounts of but produce much more when fully stimulated.
Exception 2: B cells T-independent activation
But T cells are only half of the active immune system. It turns out that B cell activation follows similar rules, though not through DCs. B cell activation usually occurs with help from activated T helper cells (only one that recognizes the antigen the B cell is specific for). However, B cells can become activated without T cell help in two situations: an antigen binds to the B cell receptor and to a TLR, or 2) the B cell receptors become saturated with highly repetitive epitopes. Situation #2 technically occurs without help of the innate immune system.
So you're mostly correct that the active immune system requires innate immune system help, except that there are these two exceptions. And since immunology has so many exceptions, there are likely to be more.