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Total dark deprivation at day-neutral plants
First of all, I am not a biologist.

Almost for a week, a question has come to my mind:
"Is it harmful ceaselessly exposing a plant to light?"
(I mean with natural & artificial light with proper spectrum)
I have been searching for a week, and I stumble upon many weird and wonderful things, and by them, I have become able to consider this topic more deeply, and refine my original question. However I have still not found the answer.
I am already familiar with these topics:

Light-dependent reactions
Light-independent reactions
Calvin cycle
Photoperiodism
Phytochrome
Cryptochrome
Long-day, Short-day, Day-neutral plants
Grow light

So my main question:
Does ceaseless light exposure with proper spectrum adversely affect a day-neutral plant?
As a layman I have started to fumble towards light-independent reactions, but I have not found strong claim. I have learnt that there are processes which taking place during dark phase, but are these reactions impossible in presence of light?
But probably there are other factors.

My resources were: Google, Wikipedia, (a tons of) academic paper, many article from Botanical Gazette, many blog & webpages about botany & greenhouses etc.

I cannot say anything about the general case, or specifically for day-neutral plants. However, Sforza et al. (2012) have studied the effects of light conditions on algae (used for biofuel production), and their results indicate several problems with continuous light. In continuous light conditions they find lower chlorophyll contents and higher carotenoid concentrations in cells, which leads to lower photosynthetic efficiency.

This figure shows chlorophyll contents (black) and chlorophyll/carotenoid ratio (red) under different conditions, with the two treatments to the left representing continuous light. (graph from Plos One)

Results show that Nannochloropsis can efficiently exploit even very intense light, provided that dark cycles occur to allow for re-oxidation of the electron transporters of the photosynthetic apparatus. If alternation of light and dark is not optimal, algae undergo radiation damage and photosynthetic productivity is greatly reduced.

However, they also experiment with pulsed light, which in some cases lead to even lower rates of photosynthesis:

However, similar experiments, at different frequencies, also showed that alternating dark and light may be detrimental, as demonstrated by the growth inhibition observed in the 1200-1 and −5 Hz curves. These cells showed a decrease in Fv/Fm values similar to that observed under constant strong light, indicating that the inhibition of growth was due to photoinhibition.

They also find that light pulses can be very short, and still allow for the photosystem to reset:

The optimal duration of light pulses was found to be around 10 ms, which is consistent with the suggested PSII turnover rate in whole cells [4], [46]. Accordingly, after photon absorption by the photosystem, 1–15 ms are needed to reset the system, before it is ready to receive another photon [22]. If the illumination is this short, most photons are exploited for photosynthesis and do not lead to the formation of ROS which then causes photoinhibition. These results indicate that even strong light does not cause damage if it only lasts a short time. Conversely, longer exposure allows the generation of ROS and damage and, in this case, the abrupt changes in illumination undergone by the cells are as harmful to the photosynthetic apparatus as constant high light.

Different species of plants can have mechanisms to handle light stress in different ways, so the effects on different species and types of plants are likely to differ. However, their results should generalize to some extent/for some plant species.
You may also find this paper by Li et al. (2013) interesting.

Astonishing!!!
That is way more what I expected as answer.

@osiixy Glad you found it useful. I also want to compliment you on a nice first question, with a good background.

Your answer was an amazing start point.
One of the most important keywords was light stress, which gave me a huge momentum (as it turned out it is very basic concept - but as not to be biologist I did not even think to seek that way).

About dark processes:
I find a paper which mentioned that spirulina for example needed long dark stages because the protein synthesis taking place in this phase.

@osiixy Goes to show that the proper key words can be a large part of finding useful information, especially if you are new to a field. Also, feel free to post an answer to your question if you find good information during your studies - to post complete or partial answers to your own questions is encouraged at StackExchange sites.


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Does the necessary Carbon Dioxide need to be in the atmosphere for mammals?
In the answers to this question, we've learnt that carbon dioxide is necessary for mammalian life, but is it necessary in the atmosphere/to breathe it in?
Or does the act of respiration give a human (or other animal) enough carbon dioxide to fulfill all of the functions that carbon dioxide is needed for?
Or, phrased another way, if you put an animal in a carbon-dioxide-free atmosphere, and continually removed the carbon-dioxide that they generate upon respiration/exhalation, would they get enough carbon dioxide to fulfill these requirements:

fatty acid biosynthesis (FAS)
mammalian/bacterial biotin-dependent carboxylation reactions.
blood pH regulation

possible duplicate of Is there any use of CO₂ in human body?

I think the core of the question is very different from the suggested duplicate. The duplicate is on what CO2 is used for, this question is on how much CO2 is sufficient to fulfill it's roles.

No it isn't necessary to breathe in CO2 from the atmosphere. For the buffer system your brain detects the amount of CO2 (H+ which is an indicator of excess or too little CO2) and adjusts your breathing automatically to compensate so that your blood's pH stays normal. No outside CO2 is needed. Your kidneys also play a similar role but the lungs are what provide a rapid response.

I know this seems intuitive, but can you add sources that support this answer? There are plenty of examples of short term non-CO2 breathing (nitrox, heliox, pure oxygen, etc.) but what about long-term?

The body is producing an excess of CO2 at all times. In fact, we need to keep venting it out just to keep alive. Furthermore, there is always expelled CO2 in our lungs, and since they never get fully empty, we always breathe air with some of our CO2. Therefore, although an answer with an experiment would be slightly better, this answer is well funded enough in basic biology.

No, mammals need not take in CO2 from atmosphere. The body's homeostatic function will maintain its composition by checking the amount of CO2 released out by lungs. So certainly animals would survive if put in a CO2 free atmosphere.

So, fatty acid synthesis (for example) occurs using carbon dioxide created within the body?  Also, got a cite?

@Hari:It would be nice if you add some references to substantiate your claim.:)

It is unneccessary for a mammal to breath in CO2, though our bodies are able to expel unneeded gasses easily. However, if there were no CO2 in the atmosphere, animals would all die, as no oxygen could be produced by plants. In other words, we don't need to breath in CO2, but we need it to be plentiful.

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Birth control hormones in the water? Or not?
This prior question talks about natural estrogen (TL;DR: Months to years):
How quickly do estrogens break down in the environment?
Ref:
http://dx.doi.org/10.1038/485441a
A lot of media has said, "birth control hormones in the water!!!!"
Ethinyl estradiol (EE2), is a synthetic hormone
eg: www.livescience.com/20532-birth-control-water-pollution.html
Conversely, a birth control advocacy group, says, "Naw, it's a very small part of the total estrogen load in the environment."
eg: www.arhp.org/publications-and-resources/contraception-journal/august-2011
(can't post more than two links) :P
What I recall reading was that one of the types of birth control hormones got processed by the human body, looked like it was changed (in the urine, etc), and so they were fine with it not causing an issue - but when it got into the environment, it rapidly got changed back into the (estrogen?) it was originally - and thus caused problems.
I'd like a nice summary of what's thought to be going on, preferably from a more neutral source.

Have you tried checking the Environmental Protection Agency's site? It you are talking about the United States, that is likely a chemical that they keep track of and have data on. There is also a distinction between what is in the drinking supply and what is being released into the environment through treated waste water. One would be a concern to humans and one would be a concern to wildlife (fish, birds, etc). I think the issue is that the molecule is excreted but the current methods of treating waste water do not break down the hormone and it is released into waterways.

Hormones are powerful signaling molecules that affect gene expression, and do not just control pregnancy. Many tumors are estrogen or testosterone positive, so there is a legitimate concern of what these molecules could do to the ecosystem of waterways.

On a related (but possibly tangential note), also check out the USGS NAWQA. I don't think it covers birth control, but does look at other pollutants.

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Enzyme kinetics: recommended literature to grasp the concepts better
I have had a few biochemistry courses, but I still feel confused and a bit scared each time they try to explain and apply enzyme kinetics or even chemometrics in different situation during class. On our last lecture we had kinetics regarding:

Pingpong reactions (with two substrates A, B):
$V_0 = \dfrac{K_{cat}[E]* [A][B]}{K_m^B [A] * [B] * [A][B]} $

General reactions (with two substrates A, B):
$V_0 = \dfrac{K_{cat}[E]* [A][B]}{K_m^B [A] * K_s^A * [B] * [A][B]} $

And we also had something about analyzing the "principle component" in multivariate data, from enzyme kinetic measurements (as effect of e.g. pH of temperature).
I really don't understand this, or how I would apply this - or analyze my data if I have two substrates.
Question: In general, is there a good web site which goes beyond the normal Michaelis menten analysis, or a very good book which explains both the basic and more complex scenarios regarding analysis/application of enzyme kinetics for biochemists?

Is there a textbook for your course? If so, which one? At the undergraduate level, Voet & Voet is the most comprehensive for my money (and that is a lot of money).  However, for detailed discussion of kinetic mechanisms, like Dan Koshland's ping-pong model, you probably need a book focusing exclusively on enzyme kinetics (not a general textbook)

there is no textbook, just the teacher drawing on the board. Its okay to memorize exactly what they say, and then just paste it in on an exam.. but i would really like to understand this. Thank you for your suggestions!

I always used the book "Enzyme Structure and Mechanism" by Alan Fersht. (Structure and Mechanism in Protein Science: A Guide to Enzyme Catalysis and Protein Folding is the latest version, published in 1998.) Both in some courses I did and when working on (complex) enzymatic mechanisms. It's a classic (so a bit old maybe), but it covers all the basics and includes most of the common complex mechanisms like ping-pong. I don't know if it will teach you how to analyze multivariate data, so maybe you need something else for that.

Yes, thank you for mentioning this one. It is excellent, and it is a classic. I have an older version somewhere but I could not remember the name.


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How fast the human eye can [temporarily] change its color?
I know that human eye can change its color during lifetime because of disease or medication (similar question on Biology.SE). And I know that it may change depending on the lighting.
But I saw several times as the eyes of man with the bright eyes changed color  (blue/gray/green) without changing environment. Is it possible to temporarily change eye color due to the change of emotional state (as a consequence of the effect of hormones or something else) in just a few of minutes? If so, what are the processes behind this?
Or it just optical/psychological illusion for the observer?

It is just optical illusion of observer. Eye color cannot change by effect of hormone (somebody correct me if I'm wrong) and not at all in a few minutes.

In a few minutes? Hardly possible - it will take some time for the pigment cells in the eye to produce and distribute the pigment.

@another'Homosapien',  thanks for your comment.

Keep in mind blue eyes contain no blue pigment, it is purely a refractory effect.


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About modern dating techniques
In a comment to this question, it was said that

Radiocarbon dating won't work. For a start the tree needs to be dead, which since you're not using the rings I'm assuming it isn't. Also the atomic testing in the 20th century completely messed up the level of C14 in the atmosphere, so radiocarbon dating can't be used for anything that didn't die 70 years ago or more.

I did not know this. So, what kind of dating techniques biologists use today? :-)

The question involved dating a live tree. Radiocarbon dating does not work on live organisms, as they are assumed to be still in equilibrium with the environment. It measures the time after death of the organism.

In order to date the age of a tree, you have three solutions :
If you can cut the tree then you can simply count the number of rings. Note that for very old trees the central rings will have rotted and you will only have a lower bound on its age.
If some parts of the tree are dead, you can use radiocarbon dating to estimate the time of death with a relatively bad precision (the error is about 100 years which can be a lot for a tree)
You can estimate its growth rate (either using the width of the rings, or by doing multiple measurements for several years), and deduce the age from its size.


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When should I use cryofixation and chemical fixation?
We know that the technique used in TEM sample preparation involves multiple steps, one of the most important of them is fixation.
Fixation can be of two types:

Cryofixation, that suggests that the specimen are subjected to freezing temperature to perserve the cell's living material before we observe them.

Chemical fixation involves the use of certain chemicals, such as formalin, glutaraldehyde, etc. for almost same purpose.

The question is when it is mandatory to use one of them only? Such as, cryofixation or chemical one? At some instances, have the researchers ever need to use both of the techniques at the same time?

Cryofixation usually preserves the organelles inside the cells better, but is more work and usually results in TEM images that are lower contrast. Chemical fixation is easier and gives good contrast, but is more likely to destroy details in delicate samples. Chemical fixation will usually be used unless it is found or expected to not work well for a particular sample. It is possible to mix the methods, for example by including glutaraldehyde in freeze substitution solutions. Here is an article that describes everything you asked about in more detail, if you can access it: A comparison of cryo- versus chemical fixation in the soil green algae Jaagiella

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Can the natural loss of memory be modeled with a continuous function?
Disclaimer: I have little to no background in biology, so this question is based on anecdotal evidence. I've tried to spell out all of my suppositions, but please let me know if I'm making any leaps I'm not explaining.
Some Context/My biology assumptions
There are some things I can recall very clearly and quickly, other things that are maybe a little fuzzy and take me a second to remember and others still that will feel "on the tip of my tongue" for minutes before I can recall them. And then there are things that I don't remember at all or that I know I knew but can't recall.
To me it seems there's a range of how "clear" or easy a memory is to recall. This clarity and "recallability" seem to decrease over time (assuming I don't use the memory) and it seems there's some minimum clarity/"recallability" that is required for me to recall a memory. Can the clarity and "recallability" of my memories be modeled with a continuous function? And if so...
A (maybe false) Conclusion
According to the Intermediate Value Theorem,

if a continuous function, f, with an interval, [a, b], as its domain, takes values f(a) and f(b) at each end of the interval, then it also takes any value between f(a) and f(b) at some point within the interval."

So if we can model the clarity and "recallability" as continuous functions, and I can perfectly quickly recall a memory at one point and not recall it at all at another, then there should exist times with every flavor in between.
If this is true, would it be true to say that there existed a moment when my clarity/"recallibility" of a memory was high enough for me to recall it should I have chosen to and there is another moment when it wasn't (where these moments are some small distance apart)? Or is my understanding of memory incomplete to where this is all horribly wrong?
To put it in other words, how small can the time be between when you are able to recall something and when you no longer can? And following my logic, could this time be seconds or moments?


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Cleaning Masterclave
When i finish operation. My masterclave has smell, I think has media moulecular bind into the surface and microbial can live in. My labs don't have SOP to clean it. I promote use detergent but wonder it'll bad effect in the suface. Do you know how I can clean masterclave effective?

This's my masterclave

Have you contacted the manufacturer?

Sorry, my mistake. I don't think it. I will contact manufacturer.


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Parietal and Visceral epithelia
If you google visceral and parietal you get: The parietal layers of the membranes line the walls of the body cavity (pariet- refers to a cavity wall). The visceral layer of the membrane covers the organs (the viscera).
but
the first image that pops up is this :

I don't understand how the inner layer is covering and the outer is lining ?

Yes, the parietal pleura is on the wall of the thorax. That picture isn't great.  Each lung has its own pleural cavity, ie its own visceral+parietal.  Another important thing is the folding over.  Imagine the parietal pleura running along the inside of the ribcage...when it gets to the middle of the chest (the mediastinum), it folds over, or "turns the corner", and is now the visceral pleural running along the surface of the lungs.  The pericardium functions similarly, and so does the peritoneum/mesentery.  Here's another diagram that could help:


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What does completing the course of antibiotics accomplish?
This article from the WHO states:

If you stop treatment early, there is a risk the antibiotics won’t have killed all the bacteria that made you sick and that it will mutate and become resistant. This will not happen to everyone – the problem is that we don’t know who can safely stop treatment early.
By taking the full course prescribed by your doctor, even if you start to feel better earlier, you increase the chances of killing all of the bacteria and reduce the risk of resistance.

A clarification: When the WHO says “[bacteria] will mutate and become resistant,” they are implying that using antibiotics will create a selective pressure for bacteria with antibiotic resistance, arising most likely through mutations, correct? Bacteria don’t mutate into antibiotic resistant strains in direct response to a drug; rather, antibiotic resistance is a phenomenon of natural selection. I’ve seen so many articles about antibiotic resistance worded this way and I feel it’s simply wrong.
Presuming I am correct about my first point, here’s my true question: Say you’re prescribed a course of antibiotics. It kills the bacteria that are not resistant to the drug and leaves those that have developed resistance behind. What does it matter if you finish the whole course? Taking more of the drug is not going to affect the resistant strain. The only rationale I can think of is that it would kill off any residual non-resistant bacteria and prevent them from gaining resistance (via conjugation) from the resistant kind. However, is this the only mechanism whereby completing the course prevents the rise of antibiotic resistance? How effective is this at all at preventing the rise of antibiotic resistance in the bacterial population in general (i.e. beyond the host)?

Good points. Yes, it is worded misleadingly. Resistant bacteria are selected for in the presence of antibiotic. when you stop an antibiotic, levels are still present for a while and it may select for more weakly resistant bacteria (that can survive at low levels of the antibiotic - very common.) Stopping your antibiotic early mainly means you've left a lot of bacteria behind (that colonized part of your body) and reinfection is possible, requiring yet another course of antibiotics. It's the "yet another course" that confers the increased possibility of selection of a resistant strain.

"it will mutate" could also be read where "it" is the population of bacteria and not the individual bacterium.

As anongoodnurse has mentioned in the comments, an incomplete course can allow weakly resistant stains to expand their population. As you mentioned, the antibiotic does not cause the bacteria to mutate but it kills all strains that do not carry the mutation that provides the resistance. This mutation arises randomly (in certain cases it can be acquired by other mechanisms such as lateral gene transfer).
Many antibiotics may not kill the resistant strains but may still impose some burden on their growth. Now, with a complete course you would have eradicated a lot of strains and only a few resistant strains would be left. The probability of extinction/eradication depends on how many individuals are present in a population. When you do a complete course, then the chances of extinction of the resistant strains due to random birth-death process (and attack by the immune system) would be high because of their low numbers. However, with an incomplete course these bacteria would quickly expand their population once the antibiotic is gone. Now, with the next round of antibiotic treatment you would have more number of resistant cells to kill. As again pointed out by anongoodnurse, this will lead to further selection of resistant strains.
There are additional factors:

Microbial community (colony) is more than just a bunch of cells. They can protect each other.
There are some cells called persisters which are not really genetically resistant strains but tolerate the drug because of adaptive phenotypes. Again, the microbial community plays some role here.

Furthermore, resistance comes in many strengths. A weakly resistant strain is less likely to die from an incomplete course of antibiotics. But a weakly resistant strain is many more times likely to become a strongly resistant strain...

@Aron "a weakly resistant strain is many more times likely to become a strongly resistant strain” Why is that so?

@lightweaver Imagine one strain randomly mutates an enzyme that breaks down the antibiotic. But it's a very weakly binding enzyme. Then imagine how much it would take to optimise the enzyme.

@Aron Could you give an example? Maybe it’s the lack of experience but I’m not quite imagining it.

@lightweaver An enzyme that can break down the antibiotic could requires thousands of mutations. But it might only be good enough to break down half the antibiotic in your blood. So if you take a full course, the bacteria that makes it still dies. However, if it survives a half course...all its rivals are dead. It multiplies, and all the bacteria has a weak immunity. All of them mutates...maybe 10 or so mutations. But out of the trillions of bacteria ONE hits the jack pot, and evolves the 10 mutations required for FULL strong immunity. Congrats, you just killed man kind.

You also have bacteria that go through dormant phases, they are not resistant they just are not active so they are unaffected , following the full course will catch these guys when they wake up. Otherwise you are just instantly reinfected when they become active again. TB is notorious for this.

@John those cells are called persisters (fancy term)


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How do proteins perform their function
I have asked a question on physics stackexchange, but was redirected here. I copy the entire question word for word. The original is here.

Let's, for example, take a ribosome. It is an enzyme that is in turn just a molecule that must follow the laws of physics.
Correct me if I'm wrong, but it can be looked upon as a molecular machine made up of several pieces. What exactly makes those pieces work together?
Why does the ribosome bind to a strand of RNA? Is it just the shape and electric charge or is it something more? Once the ribosome is bound to a piece of RNA, how does it move?
In a way, I'm looking for the "ghost in the machine". I'm interested in molecules in general, not just ribosomes. What is it that, on a level of single atoms, makes molecules "alive" - move, assemble a protein, etc. ?

PS. I'm having trouble phrasing my question, so if anything is not clear, please leave a comment and I will address it.

Edit 1: This is most definitely a physics question. I'm looking at the scale of several atoms.
Let me give a hypothetical example:
Imagine a strand of carbons. Also imagine that there exists a molecule that can move along this strand. How would it do it? What forces would move it along this strand? Is it electromagnetism? Would gravity be involved to a significant degree? What effect would shape have?
Does this make the question clearer?

Looking at the scale of atoms will not help understanding a molecular machine made of thousands of them.

@Chris How should I try to understand molecular machinery? What topics, books, resources should I look for?

I agree with Chris, a lot of how enzymes process things is related to their structure and the charge or lack of charge in the active site.  You also have to consider that ATP is used to catalyze many reactions, meaning you have to take a more macro look.  I'd start with Biophysics.

@Nathan do you have a suggestion for a resource to start? Maybe a textbook?

http://www.amazon.com/Molecular-Modeling-Simulation-Interdisciplinary-Mathematics/dp/038795404X/ref=sr_1_1?ie=UTF8&qid=1452024349&sr=8-1&keywords=038795404X

@Chris Looking at the scale of atoms will not help understanding a molecular machine made of thousands of them. It does help, it's just really, really difficult.

@tel I'd say its like looking at a screw in a robot that puts doors on cars and trying to understand how the robot puts doors on cars.  In the reference of what a particular screw does in light of the whole, you may gain something.  But in just looking at the screw you can't understand the bigger picture.  And that's a decent analogy since the atoms will make up the amino acids, most of which (in a high number of proteins anyways) are structural and have little function in the actuation of the protein.

@tel I would say it's lloking at the atoms of a car when you want to know how it works. From the viewpoint you can only see very small parts of the machine and this will not help you with overall understanding.

@Chris Your analogy is off by about 8 orders of magnitude in terms of the relative scale. Rather, it's like looking at all of the hundreds of gears, shafts, pistons, etc that make up a car's drivetrain in order to fully understand how it works. You don't just look at each of those parts in isolation, rather you try to characterize the network of their interactions.

@Nathan Yes, the level of detail can be overwhelming, but modern science is capable of productively dealing with much of that detail. Remember that one of the ultimate goals of this type of work has always been to produce and control our own custom-made proteins. It's fiddly work. The lesson of the last 40 years of progress in this field is that the details matter, often in surprising and significant ways.

@tel So is the functioning Ribosome an extremely complex machinery. I would start by reading a standard biochemistry book, which usually has a good overview and then start going more specific.

This question is waaaay too broad, but I'll give some short and simplified answers to the hypothetical you asked at the end. First, let's reformulate your example a little bit:
How does the ribosome move along a strand of RNA?

How would it do it?

By hydrolyzing GTP and somehow coupling the free energy associated with that reaction to forward motion. Keep in mind that both ribosome and RNA are constantly undergoing random-walk Brownian motion (ie jiggling), so it's more a matter of biasing the ribosome's motion in a particular direction than it is of moving the ribosome in the first place.

What forces would move it along this strand?

The current understanding of molecular biophysics, which is by no means complete, says that the primary driver of this sort of protein activity is electrostatic forces.

Is it electromagnetism?

There are no electric currents, per se, so magnetism does not play a role.

Would gravity be involved to a significant degree?

At these scales gravity does not have a significant effect.

What effect would shape have?

Shape has an enormous effect. One of the fundamental axioms of molecular biophysics is that function follows form. The 3D configuration of those electrostatic forces I mentioned is determined in turn by the 3D configuration of the involved macromolecules.

If you want to know (a lot) more about this specific question, and if you have access to journals, check out this review: How Should We Think About the Ribosome?

You write "By hydrolyzing GTP and somehow coupling the free energy". When you say somehow, do you mean to say that it is very complex process or that humanity does not know?


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Find Mutations Frequencies by Cancer Type
Is there somewhere that has mutation frequencies by cancer type? So if I were looking at CML, AML, or even more generally at something like leukemia. Is there some database that would contain mutation frequencies? So that I could find that in leukemia 50% of cancers contained a T100G mutation.
I have looked through COSMIC but haven't had much luck.

What exactly are you looking for? There is a paper which looked at the mutation frequencies of different cancers, I can look it up in my database if you want.

@Chris If that much info is in a paper that would certainly work. I figure this sort of thing would be in a hosted database though.

Try http://dcc.icgc.org

There is one paper called "Mutational heterogeneity in cancer and the search for new cancer-associated genes" from the "The cancer genome atlas" which should be interesting for you. This project aims to map the mutations occurring in different cancers, one of the results is this figure (from reference 1):

The project itself has numerous data on the different cancers available on the project website, which can be found in reference 2.
References:

Mutational heterogeneity in cancer and the search for new
cancer-associated genes
The cancer genome atlas project website

Thanks I actually remember this paper, I have it in my ref manager as well. I'll go back and look at it and check those sites to see if I can find what I need.


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Variance of frequency in expanding populations
I'm trying to understand the variance in frequency of some strain after some time as passed in a growing population. The idea is to then plug this in kolmorov foward equations and get the classic results (probability of fixation, time to fixations, mean fitness).
However, I got a weird result.
I started with the model definde here
$N(t) = N(0)W^{t}$
and from the answers I got that the variance of $N(t)$ would be
$\text{Var}[N(t)] = N(0) W^t(W^t-1)$
Now, the frequency of strain $N_{m}$ is
$f_{m}(t) = \dfrac{N_{m}(t)}{N_{m}(t) + N_{b}(t)}$
assuming only two sub populations. From there I need only the variance of $f_{m}(t)$ and this and this helped me build a formula. However, the variance of the frequency is not $0$ when $f_{m}(0) = 1 $ and it has units much larger than 1...
My question is, have I done something wrong?

You suddenly talk about two strains while it was no present in the beginning of your model. Can you please link the existence of these two strains to the beginning of your model. Where is your calculation of the variance of this frequency which you state is wrong?

Indeed I had made a mistaken when calculating the variance. As the formula is very large, I will just point to the fact that using the references I gave it is possible to get the variance of the frequency.


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How do carbon 13:12 ratios confirm the biological origin of oldest microfossils?
I was reading this article about how Schopf and Valley’s findings in 2017 confirmed that the 3.5 billion–year-old microfossils found in the Apex chert of Western Australia are indeed remnants of living organisms, as opposed to abiotic geological structures. The most detailed part of the article’s explanation is:

Using SIMS, Valley’s team was able to tease apart the carbon-12 from the carbon-13 within each fossil and measure the ratio of the two compared to a known carbon isotope standard and a fossil-less section of the rock in which they were found.
“The differences in carbon isotope ratios correlate with their shapes,” Valley says. “If they’re not biological there is no reason for such a correlation. Their C-13-to-C-12 ratios are characteristic of biology and metabolic function.”

Can someone explain this in more detail? In particular, why should this ratio be different in biological carbon samples, compared to abiotic carbon samples?

Via: https://en.wikipedia.org/wiki/Carbon-13#Uses_in_science

Due to differential uptake in plants as well as marine carbonates of 13C, it is possible to use these isotopic signatures in earth science. Biological processes preferentially take up the lower mass isotope through kinetic fractionation.

Via: https://en.wikipedia.org/wiki/Kinetic_fractionation

All organisms preferentially use lighter isotopic species, because "energy costs" are lower, resulting in a significant fractionation between the substrate (heavier) and the biologically mediated product (lighter). As an example, photosynthesis preferentially takes up the light isotope of carbon 12C during assimilation of an atmospheric CO2 molecule. This kinetic isotope fractionation explains why plant material (and thus fossil fuels, which are derived from plants) is typically depleted in 13C by 25 per mil (2.5 per cent) relative to most inorganic carbon on Earth.

The second Wikipedia article points out that kinetic fractionation also occurs in at least some known non-biological processes. So why is this being used as evidence of life?

Non-biological processes referred to in the Wiki article appear to discuss oxygen and hydrogen, not carbon. However, I have not read the paper you're referencing. My guess would be that selective uptake of lighter carbon isotopes is evidence of carbon-based life, and that there are other indicators to corroborate that conclusion.


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Are all cells organisms?
As the title says, are all cells organisms? Why or why not?
As I understand, not every cell is an organism because some of them -those which aren't organism- require the rest of the organism to live. But arguing with someone about that, he says that, for that matter, every cell needs of others to live in some way or another, or that they can be kept alive and sometimes reproduce in a petri dish, without the need of the organism. So every cell, he says, even those which constitute larger organisms are organisms in themselves. I tell him that saying every cell is an organism is awkward, that would imply that every multi-cellular organism is really a colony, rather than an organism.
Is this only a philosophical question or can we say for sure, for example, that an epidermal stem cell or a lymphocyte are not organisms?

I would say that some cells are considered organisms (e.g. bacteria) but others not. For example, a skin cell wouldn't be considered an organism because it can live by itself, it needs to be part of something bigger.

MattDMo's argument is that a single cell from within a human, if extracted from the body is not perfectly self sustaining. Would it not apply then to a human extracted from our own environment? The middle of space? We could not survive there. So are we not organisms? I myself couldn't find food or water in space that's for sure. Put me in an all you can eat buffet restaurant however, and I assure you I will not starve. Like I said, not much of an answer, but certainly food for thought.

What is the point of this semantic debate?

Related: http://biology.stackexchange.com/questions/7053/can-you-consider-a-human-as-alive-or-is-it-the-cells-on-the-body-that-are-alive/7054#7054

This semantic nonsense (or as @Superbest more politely puts it debate) was posted two years ago  and I'm the only one that has voted to close.?Come on put it out of its misery and let's focus on "practical problems in biology that people actually face".

Your friend is incorrect. From Wikipedia:

The word organism may broadly be defined as an assembly of molecules functioning as a more or less stable whole that exhibits the properties of life.

(Viruses are specifically excluded, as they depend on a host cell to fulfill all the functions of life.)
While cells extracted from a multicellular organism like a plant or a person may be able to be cultured in vitro for a time, they cannot survive independently - they require the intervention of humans (or very well-trained monkeys) to obtain nutrients and oxygen, and process/remove waste. A unicellular organism like a bacterium, for example, can handle these functions on its own - it can either synthesize or find a source for its own nutrients, and can reproduce on its own to create more organisms.
The key difference is being self-sustaining. An organism needs to be able to feed itself, take care of its waste, reproduce a full version of itself, respond to stimuli, etc. (see the "properties of life" link above). A single cell from a multicellular organism cannot do all that without assistance (kind of like a virus, actually), while a true unicellular organism can.

MattDMo's argument is that a single cell from within a human, if extracted from the body is not perfectly self sustaining. Would it not apply then to a human extracted from our own environment? The middle of space? We could not survive there. So are we not organisms? I myself couldn't find food or water in space that's for sure. Put me in an all you can eat buffet restaurant however, and I assure you I will not starve. Like I said, not much of an answer, but certainly food for thought.

What do you make of this answer.  If it is correct and your answer is correct, it would seem to mean that cells are alive, but they aren't organisms.  But then that would contradict your premise for organism-ness (IE organisms have to be alive).  So this sole-upvoted answer would have to be wrong, or your is wrong?     One thing to note:  a human is no more self-sustaining outside it's environment than a cell is.  So maybe this answer does not stand up to scrutiny, even though at first I agreed with it!

@GreenAsJade This answer is saying that certain cells are alive and not organisms.  The criteria specified in this answer are "stable" and "alive"; those cells meet the second criteria but not the first.  Based on your comment, you appear to be assuming all cells have the same capabilities - but they do not.

@R.Hull this entire thing is really a semantic argument in the truest sense of the phrase, as we are arguing about the meaning of a term that ultimately matters very little to the organisms/cells involved. Yes, your space-extraction argument is true to an extent, but I am assuming that the extracted cells are put into a hospitable environment where they can find food, etc. A sulfur-dependent chemosynthetic bacterium from a deep ocean vent won't survive if you just put it in plain tap water, just like a plant won't survive in complete darkness.

@GreenAsJade Izkata pretty much got it right. Just because something is alive doesn't mean it's an organism, and one could argue that terminally-differentiated keratinocytes (corneocytes) in the skin are not truly "alive" because they can no longer reproduce. Even many types of lymphocytes, to take the OP's example, cannot reproduce at all, or cannot reproduce alone, in the absence of signals sent from other cells (for example, follicular B cells in the spleen require antigen, Tfh cells, and follicular dendritic cells to send the signals to divide and differentiate into plasma cells).

@Izkata thanks for your contribution, you pretty much got what I was trying to say :)

Many large organisms cannot survive without the help of other non-species organisms. For example ~ the ant species "Formica subintegra" cannot survive because they are physiologically unable to forage for and nurse their colony. They must raid other ant colonies to take slave care-givers.
While reading everyone's thoughts & deliberating, I've decided to reject the idea of "life" entirely.
At one stage, life needed to be created from non-life and this process would require the original arrangement of "non living" molecules to have the "properties of life" in order to create life to begin with.
Ex: chemical evolution in lipids.
Let us evaluate a lipid molecule's "properties of life"
(drawing definitions from wikipedia)
Homestasis: Lipids must maintain a molecular balance to be categorized as a lipid, their current state. Like us, this process of seeking balance is largely beyond their "free will" (or conscious awareness). Should either we or they become overcharged with electrons our current state would burn to ash and all functionality as a whole is lost.
Organization: "being structurally composed of one or more cells – the basic units of life"
How is it possible, that cells are established as life and then used to define what life is? I reject this circular thought.
Metabolism: "transformation of energy by converting chemicals and energy into cellular components (anabolism) and decomposing organic matter (catabolism). Living things require energy to maintain internal organization (homeostasis) and to produce the other phenomena associated with life."
Living things require a balance of energy, to be specific. Lipids may not transform energy but they have clear agency that effects 'other' molecules (being polarized) which does include asserting their agency upon the energy within those molecules, we also know they form structures and can create isolated environments for further chemical evolution. Indeed this is a tricky question, but life is a poorly defined concept, queue this forum. <3
Growth, response to stimuli, adaptation, I feel, are answered above. That or I am getting lazy, this took longer than I thought to articulate. I'll stop here and await new thoughts. Thank you for the platform, you're my kind of people, merely by asking this question, regardless of the answer.

I am 8 years too late. But I would say he is right.
With regards to your intuition, I ask: if we can accept that a living cell can emerge from the interactions of matter, why should we not equally accept that our bodies and our cognition emerges from the interaction of living cells?
Take a look at this video of brain cells:
Brain cells in a culture dish trying to form connections with each other
Brain cells have no "clue" about their role in the body/brain, yet when you look at the video, you see that they, like single cell organisms, have some form of agency.
We, the human beings, seem to be an emergent phenomenon based on a higher order of complexity. In other words, through the nature of the cells and their way of "living" they bring forth something that cannot be explained by the sum of the cells. These cells do not have to care about your body. They merely do what they are supposed to do. Just like any other cell, they found some niche. Alongside, however, this behavior gives rise to a self organizing behavior that creates us human beings.
From this persepctive, yes, they are a collborating colony and our body is merely their environment that sustains them.


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What made *silphium* difficult to domesticate?
I tried this question at Worldbuilding SE, and was told that perhaps this place would give me a better chance at an answer. So, leaving aside the worldbuilding aspects of the issue, I am interested in the now-extinct plant called silphium, which was widely used as a contraceptive in the Classic world, and was overharvested into extinction at the beggining of the Middle Age, being apparently non-domesticable.
So, why exactly was it non-domesticable? Was it actually non-domesticable, or its domestication, like that of strawberries, just depended on some techonolgical innovation that was not available at the time it become extinct? If it was really impossible to domesticate, what measures could be taken, in a pre-industrial society, barring it not being used as contraceptive, to at least protect it from extinction?
More generally, what factors lead a plant to being non-domesticable?

Welcome to Biology.SE. From wiki: we cannot even accurately identify the plant we cannot know for certain whether it is extinct. and The cause of silphium's supposed extinction is not entirely known. Because we know nothing about this plant (but the name people gave it in the middle age), it impossible to make much speculation. I am voting to close for this reason.

The factors that make anything hard to domesticate rely largely on factors that make it difficult to artificially select domestic traits. Perhaps it was long-lived or germinated infrequently, or needed a different kind of space or environment than the people at the time were giving it, or had some other unseen condition that civilization at the time wasn't able to rescue. For example, it's hard to domesticate elephants because they only birth every 5 years and sexually mature after about 15 years. By the time you select for a trait, you may very well have died many times over!

Have you found any reliable sources for this plant's existance? The wikipedia page seems to be from that era when wikipedia wasn't exactly trustworthy... Note that there are many extant species going by the name of "Silphium" [wiki ; article].


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Are spinal nerves myelinated and unmyelinated at the same time?
I was trying to answer this question when I remembered that the somatic axon is myelinated, while both sympathetic and parasympathetic preganglionic axons are also myelinated. Are they only myelinated or are they both myelinated and unmyelinated? Thanks
Edit:
This is a question from an old lecture quiz (previous year) and unfortunately I do not have the answers for the questions. The wording of the question was

Spinal Nerves are
a.) myelinated
b.) unmyelinated
c.) answers a and b
d) none of the above"

Welcome to Stack Exchange Biology! If you have any questions, please visit https://biology.stackexchange.com/help.   Perhaps I am missing something, but can you clarify what you are seeing that makes you think some of these nerves are unmyelinated?

I was answering a quiz on a lecture slideshow which was from a previous year course, which unfortunately lacks answers. The question was, 'Spinal Nerves are a)myelinated b)unmyelinated c) a and b d) none of the above."

I added those details in an edit to the question. Hopefully no one treats it as a homework question since that is not what it is intended as.

Spinal nerves are mixed nerves containing afferent and efferent neurons of various types. Anatomically, they protrude from the spinal column bilaterally at each vertebral level. They contain both myelinated fibers (e.g., A fibers) and unmyelinated fibers (e.g., C fibers).
The answer is (c): both myelinated and unmyelinated.
Please note that spinal nerves are NOT located in the spinal cord, despite the fact that neurons in each spinal nerve will either originate or terminate there. A spinal nerve is a peripheral structure. It starts at the point where the dorsal and ventral root converge (See April's Clinical Anatomy, Ch. 1). If you have the opportunity to observe back surgery or dissect a human cadaver, you can see and touch a spinal nerve. They are cable like structures containing bundles of many many many axons, but no neuron in its entirety. A nerve is not a neuron. This is a common misconception.
Just to add, the details here may seem like trivia, but they are not. Similar questions (and questions that require you to understand the distinction between a nerve and a neuron) are often asked on US medical licensing exams. This is because they are relevant to understanding and interpreting neurological symptoms and physical exam findings.

Yes, there is grey and white matter in the spinal chord and the parasympathetic nervous system, so they are both myelinated and unmyelinated:

Here is an image of parasympathetic nerves:

Primary afferent fibers of the dorsal roots are either myelinated or unmyelinated. In the rat, cat, and monkey, thin unmyelinated and thick myelinated fibers are located in the lateral and medial parts of the dorsal roots, respectively, in the dorsal root entry zone (Light and Perl, 1979a).

Nothing is false in this answer, but it doesn't answer the question. Spinal nerves are not in the spinal cord, they are the nerves leaving the spinal cord. The presence of gray or white matter in the spinal cord is not relevant to the question.

thanks. He said: are they both myelinated and unmyelinated? I see what you mean. I updated the information.

I think you have a misunderstanding about what a nerve is. The boundaries of a nerve (e.g., a spinal nerve), a gross structure, are not the same as the boundaries of the neurons, a microscopic structure. A spinal nerve, at any level you measure it, will have fibers of different conduction velocity. Some of these (e.g. A fibers) are fast
and heavily myelinated. Some of them (C fibers) are slow and unmyelinated. The gray matter in the spinal cord doesn't have anything to do with the question, which is about a spinal nerve, a PNS structure, not the spinal cord (a CNS structure).

Grey matter mostly isn't myelinated. Grey matter is distinguished from white matter in that it contains numerous cell bodies and relatively few myelinated axons. What are you talking about? you are overcomplicating it. The inside of the spine, the spinal roots, and the parasympathetic system all contain myelinated and unmyelinated nerves. By nerves I meant nerve cells. Where did I say that nerves are assemblages of nerves?

Gray matter is not present in any nerve. Gray matter is a central structure that has nothing to do with the question. Nerves are not cells, they are bundles of fibers (a part of many many cells, but no neuron in its entirety).  You can see an individual nerve, and distinguish it from surrounding structures (vessels, muscle, ganglia). You cannot see a neuron, or, as some may call it a "nerve cell". This is not over complicating it, but it is something that many students and neuroscientists who focus on cell biology miss.

It may be helpful to read the wikipedia entry for nerve

The type of fat in myelin makes it look white. The presence of white and grey matter demonstrates that it does. it is relevant. It answers an element of the question:  Are they both myelinated and unmyelinated? Grey and white matter are an obvious visual indicator of the presence of myelin. let's avoid turning your good initial criticism into a baseless confusion over detail.

Let us continue this discussion in chat.


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Photosystem I and the ETC
In the light reactions of photosynthesis, Photosystem I receives electrons from the ETC after Photosystem II sends them to the ETC. Then, when Photosystem I receives light, the electron becomes excited and passes the electron back to the ETC. This leads me to my question: In the following question, are both $B$ and $E$ correct?

Which of the following are directly associated with photosystem I?
$A)$ harvesting of light energy by ATP
$B)$ receiving electrons from the thylakoid membrane electron transport chain
$C)$ generation of molecular oxygen
$D)$ extraction of hydrogen electrons from the splitting of water
$E)$ passing electrons to the thylakoid membrane electron transport chain

What research have you done before asking it here?

@another'Homosapien' Looked online and in two biology textbooks

What answer is it, according to you, and why/why not?

@another'Homosapien' Please read my question first before commenting. Thanks.

You are correct as any college level Biology text should comfirm. Was this a "choose one answer only test"?

Yes; the answer was supposed be only $B$ but I thought that $E$ was also correct so I asked here

@suomynonA please read my full comment first before replying; I asked why too. This question is likely to be closed as homework unless you specifically ask why it should (not) be the answer you're saying.

@another'Homosapien' And that's why I wrote that little paragraph before writing the question.

It appears the author of the question is trying to use "thylakoid electron transport chain" in an overly specific way. The chain from which PS I receives electrons has far more components and is different from the shorter chain to which PS I passes its electrons. But according to my copy of Biology, Campbell & Reece 7th edition, both are called "electron transport chains" and both reside in, or on, the thylakoid membrane. Perhaps the "directly" in the question refers to the fact that PS I's electron is first captured by a "primary receptor" before being passed to ferredixon, the first member of the chain to which PS I passes electrons. But, again according to Campbell, this primary acceptor is considered part of the photosystem.
I used to teach this stuff. I'd toss out the question.


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when you are to non-culturally detect the presence of E. coli in the soil from a cow pasture?

You are to non-culturally detect the presence of E. coli in the soil from a cow pasture. You do this by extracting the total DNA from a sample of the soil and PCR amplifying with E. coli-specific primers that bind to a gene only found in E. coli that amplify a region of the DNA 167 bp long. Propose a postive sample that could be tested alongside your experimental sample.
A. Known Shigella DNA
B. Water
C. Number of Injections
D. Muscle DNA
E. Known E. coli DNA

I think the answer is (E) Known E. coli DNA. That would be the positive control in this context. For a positive control, you need something that you would know the response for. E. coli specific primers would amplify the known E. coli DNA. Water is obviously wrong. I could be wrong. Am I missing something?

To the homework close voter: this user has made an attempt to answer, so has fulfilled the requirements of the homework policy.

Yes, you're correct. The question is asking for a positive sample that would be amplified by E. coli specific primers. Known E. coli DNA would do the trick.

@user50592 you're welcome. If you'd like to mark this as the answer, click the gray checkmark next to it. I would also recommend you take the [tour] and visit [help] to learn about this stack exchange site.


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What are these bladder snail parasites?
I collected some bladder snails several months ago. While checking them out one day, I noticed that they were now infested with worm-like ectoparasites.
Appearance and behavior
Here's a picture of a snail with a bunch of the worms hanging off of it's head, where they tend to congregate. I've also circled one of the worms crawling along the glass.

I sampled some of the worms and took a look at them under a microscope. Here's a video ("Video 1" below) I recorded of one of them crawling around. They have some notable characteristics.
First, they appear to have some sort of sucker mouth.

Second, they have some interesting "legs" tipped with hairs (?) at the ends of their tails. Here's a short video ("Video 2" below) of a worm writhing around that shows them off a little better than pictures do. They appear to be in pairs of two.

Animated clips from the linked videos:

 Video 1 (left) and Video 2 (right)
The length of the worms ranges from 1-5 mm (edit: they get larger; see below).
Update: After keeping infected snails for a while longer, I believe that these worms only parasitize bladder snails when the worms are young (within the aforementioned size range). Larger, adult worms appear to be free-living and growing up to 1-1.5cm, and will actually crawl away when snails disturb them. Here is a picture of an adult specimen (along with some smaller ones), no microscope required:

Here's a much better picture of the hair-like legs, of which this adult specimen has numerous pairs:

Lastly, here's a very interesting detail: These worms are highly specialized, and do not seem to affect ramshorn or pond snails, which I have numerous of in the same tank, in the slightest. It's only the bladder snails that end up infested.
Location
These snails were gathered in Canada, in a still-water area connected to the Oldman River. The river is accessible by cows and deer.
Reproduction
I have witnessed the snails shedding tons of cercariae into the water, which eventually disappear after a couple of hours (reinfect the snails?). I'm not sure if those are related to this worm, or if the snails are also infected with some other type of fluke.
Update: I now believe the aforementioned cercariae are unrelated to the worm in question. I managed to record an adult worm releasing numerous live young, which resemble tadpoles (trochophores?):

I've recorded a video of the worm giving birth that can be viewed here (left image below). The young seem to be stored in chambers inside of the parent, and then are pumped through the body and out the back end. While the young appear to be still in the video, some of them are quite active (right image below).

My theory at this point is that the young penetrate snails, grow inside of them, emerge and hang onto the host for a while, and then eventually dismount as free-living adults. Adult worms seem to be independent, while smaller worms hang off of the host the snail (feeding off of it?) until they're large enough to live freely.
Treatment
I would like to eliminate these worms if possible (I can't gather more snails any time soon, and they eventually kill off smaller snails). My first attempt was dosing with praziquantel, which is supposedly effective against flukes while being snail-friendly. Unfortunately, three days later, one of the snails died, and the worms appear to be unharmed.
Update: I gathered some more snails, and attempted praziquantel once again. While it did not harm the snails, it also continued to be ineffective against the worms. I have been experimenting with Seachem ParaGuard, and the results seem to be positive for minor infestations, but not against fully mature worms.
Conclusion
After some research, my best guess is that they're trematodes from the class Digenea-- They appear have sucker mouths, can parasitize snails exclusively, can have a free-swimming form, and can shed cercariae. That said, I'm not terribly confident, and would ideally like to be able to identify them more specifically.

Hi welcome to Bio.SE! This is a very well thought out and well written question that shows prior research effort on your part and provides useful pictures and specimen characteristics (including size and your location). These are all excellent qualities we hope to see in all of our questions! Thanks. Unfortunately, I find it unlikely that anyone here will know this answer. My hope is that my bounty (though little, given how unlikely I think a good response will be) will attract someone to dive in and do a little more research for a good answer. We'll see. Good luck!

Thanks a lot! If no one here can provide an answer, I'm not sure where else to turn. Anything to narrow it down a bit would helpful. I've been trying to find any parasitic worms that feature these "legs" (or even what the proper term for them is if not that), and so far my search has been futile.

I would guess the pseudopod/protoleg looking structures and the mouth parts should be the most helpful in narrowing this down...

The oral sucker and association with snails almost certainly makes this a trematode (aka fluke). The cercaria life stage usually has one or more tails, which I don't see on your specimen. However, I don't know of any adult flukes with the leg-like structures seen in your images (though this old drawing identified as Phyllodistomum americanum appears somewhat similar)

This is single handedly the best series of updates I've ever seen on a Stack Exchange post anywhere. Bravo, mate! your answer is much more possible now, I'm sure (though I admittedly don't know the answer). I am not an expert in these things so I'll have to do a bit of digging/thinking etc. -- which will take time when I can find some -- but I will try to see if I can help you with this. If you don't get an answer from me within the next few months, ping me. Boy, I hope you get a great answer for this post!

Could it be the rat lungworm which has a primary intermediate host in snails: Angiostrongylus cantonensis

I have finally figured out what these are, and it turns out I greatly misunderstood their relationship with snails.
These worms are annelids of the genus Chaetogaster, specifically Chaetogaster limnaei limnaei.

Source: Page 653 of "Fresh-water biology" (1918)
Ch. l. limnaei is unique in its genus in that lives on the bodies and in the shells of snails, including Physa spp. like the Physa acuta snails in question. While the relationship was originally thought to be parasitic by early researchers, it turns out that it's actually commensalistic (or even mutualistic in some scenarios).
From this vantage point the worms feed on various microorganisms, such as rotifers and algae, and small particles stirred up by the host snail scavenging for food. They also feed upon the cercariae and metacercariae of fluke species that parasitize the snails, even able to protect the snails from getting infected in the first place.
That said, it's not all good-- Snails with heavy infestations of Ch. l. limnaei have been shown to be less active, spending more time in their shells rather than out and foraging for food (Stoll et al., 2013). Additionally, worms have been experimentally shown to consume tissues of their hosts when food is low or nonexistent (Stoll et al., 2013).
To respond to a few points from the question:

These worms are highly specialized, and do not seem to affect ramshorn or pond snails, which I have numerous of in the same tank, in the slightest. It's only the bladder snails that end up infested.

Ch. l. limnaei is not restricted to bladder snails, and will happily live on pond snail and ramshorn species. It's possible that the bladder snails had more severe fluke infestations which the worms found preferable.

My theory at this point is that the young penetrate snails, grow inside of them, emerge and hang onto the host for a while, and then eventually dismount as free-living adults. Adult worms seem to be independent, while smaller worms hang off of the host the snail (feeding off of it?) until they're large enough to live freely.

This worm is able to reproduce both asexually through budding, but also sexually as shown here. Sexual reproduction often occurs in the winter, where the worm lives freely and reproduces sexually before returning to snail hosts in the spring.

I would like to eliminate these worms if possible

I found a blog post by someone struggling with the same problem:

One day (do not know it exactly, probably few months later) I noticed that all worms disappeared. I did not know why they were gone.
Later I found the reason in the 1974 thesis. Chaetogaster limnaei limnaei is highly sensitive to temperatures above 24 °C. Such a temperature reduces or completely eliminates these worms. Therefore, If you transport worms from their natural environment to your tropical aquarium, there is no need to worry. If you have aquaria with aquarium heater, they are bound to be killed by high temperature. Worms are killed in summer heat as well.

This seems to be accurate, as with the onset of the summer heat, I no longer have any of these worms present on my snails. Now knowing what they were, it almost feels like a shame-- They were protectors, not foes.
References

Density-dependent relationship between Chaetogaster limnaei limnaei (Oligochaeta) and the freshwater snail Physa acuta (Pulmonata)

Awesome job -- glad you figured this out!! Great answer to your wonderful post. I'm glad you're the one to figure it out, too, so you could come full circle with this. Bravo. (Also, very interesting to learn about the ecology of this organism -- thanks!)


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KRAS gene and K-Ras Mutations
This question pertains to the KRAS wikipedia page, and I just want to double check and clarify my own understanding of how this mutation works in cancer.
It states:

K-Ras protein acts like a switch that is turned on and off by the GTP and GDP molecules.

So if K-Ras is a switch, does that mean that when there is K-Ras mutation, it functions defectively so that it does not shut off? So for example when it binds to GTP and converts it to GDP, KRAS does not shut off regardless of GTP is converted to GDP and this would lead to / cause cancer.
So I guess I have several questions to my reasoning above..

Why does excess conversion of GTP to GDP lead to cancer? Is it because this is specifically pertaining to the the RAS pathway?

When I referenced above "it" is the K-Ras binding event the K-Ras protein binding to GTP then converting to GDP caused by the K-RAS gene not being able to function correctly? I'm just confused if its the K-Ras gene causing the problem or the K-Ras protein being the problem, or is it both?

If K-Ras acts as a molecular switch, how to GEFs/GAPs effect K-Ras mutations? Because I know GEFS activate the conversion of of GTP to GDP, but what is its relationship to KRAS/K-Ras?

In the next line it states:

When the protein is bound to GDP, it does not relay signals to the cell's nucleus.

Is this saying when K-Ras is bound to GDP, that the conversion of GTP to GDP won't ever stop? I kind of just don't understand why this was written or what its relevance is. Or is it simply stating K-Ras can only turn on GTP to convert it in to GDP but not the other way around?

NRAS is indeed a molecular switch, as part of the MAP-Kinase signaltransduction pathway it acts in controling the signal which goes downstream and finally will cause the expression of genes. In the case of NRAS this includes genes for proliferation, which is important for tumors. In principle, this looks like shown on this figure (from here):

RAS (this is the same for all three RAS family members) needs to be activated so it can signal downstream, this happens, when GTP is bound to the protein. Since permanent activation is obviously not a good idea, RAS itself has an intrinsic, but slow GTPase activity, which is activated by GTPase-activating proteins (GAP) and will eventually cleave the terminal phosphate group group from the GTP to make GDP + P. GDP bound RAS is inactive. GDP stays bound to the RAS protein and needs to be exchanged against GTP by Nucleotide Exchange factors (NEF) to activate RAS again.
The general principle is shown in this figure (from here):

Mutations in RAS proteins occur in 98% of the time in three locations (see reference 1): In codons 12, 13 and 61. All three mutation affect the ability of the protein to break down GTP by abolishing the intrinsic GTPase activity by the GAP (see reference 2). This leads to the accumulation of RAS protein which is permanently bound to GTP and therefore activated, subsequently activation transcription of genes for proliferation (amongst others). This process can lead to the formation of cancer.
Your questions:

The conversation of GTP to GDP does not lead to cancer. This process stops the activation of RAS proteins. It is the permanent activation which causes the problems.
You have the mutation in the KRAS gene, which is the origin of the problem. The wrong activation is of course done by the KRAS protein.
GEFs facilitate the exchange of GDP to GTP, the break down of GTP is supported by the GAPs. The mutation hinders the GAP to fulfill their role, so they are useless in the mutated form of the protein.
The other way round. If RAS proteins are bound to GDP, they are rendered inactive, unless a GEF exchanges it again to GTP.

References:

RAS isoforms and mutations in cancer at a glance
Guanosine triphosphatase activating protein (GAP) interacts with the
p21 ras effector binding domain.


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What have the L-systems (Lindenmayer systems) been actually used for in biology?
From Wikipedia:

An L-system or Lindenmayer system is a parallel rewriting system and a type of formal grammar.
L-systems were introduced and developed in 1968 by Aristid Lindenmayer, a Hungarian theoretical biologist and botanist at the University of Utrecht. Lindenmayer used L-systems to describe the behaviour of plant cells and to model the growth processes of plant development.

I tried to find biological research that has actually used this system but I could not find any. Perhaps this is because I do not know biology that well.
Are these models important? Still taught?
They do produce pretty pictures (again from Wikipedia)

The Wikipedia article points (in the references at the end) at least to a potential impact in developmental biology with this book (which I haven't read): http://www.amazon.com/Lindenmayer-Systems-Theoretical-Computer-Developmental/dp/3642634745

BTW awesome images.

http://ftp.tuebingen.mpg.de/pub/kyb/bweber/papers_db/2001/Zamir/J%20Gen%20Physiol%202001%20Zamir.pdf

The main point is not that biologists do use l-systems in their research (although those interested in artificial life do), but that plant growth is (in mathematical sense) a l-system.

I've been considering using them to produce realistic branching in neural simulations, but I haven't actually implemented anything yet.

Great photos... here's a paper from Researchgate that may help you. I suggest reading the abstract + intro thoroughly and skimming over the paper. https://www.researchgate.net/publication/27481070_Derivation_of_L-system_Models_from_Measurements_Biological_Branching_Structures_Using_Genetic_Algorithms


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Can I safely handle this caterpillar?
I just found this caterpillar in my garden. I’m about to mow the grass for the first time. Can I safely handle it? What type of caterpillar is it?
For reference, I’m in Leeds, UK. Here are some pictures:

It’s about 5cm long and 1cm wide. Thanks

After a bit of Googling I think I found it. It’s a pale tussock moth caterpillar. https://butterfly-conservation.org/moths/pale-tussock
It says it irritates the skin and can cause a nasty rash so I’m staying away for now.
I might risk moving it with a trowel and small tub though.


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Is there a biological basis for race (re: Nicholas Wade's article)
I just recently read this article by Nicholas Wade on Time Magazine's website about a biological basis for race.  It all sounded very racist, but of course my Western liberal attitudes about racism shouldn't cloud my stronger Western liberal convictions about Science giving every empirical claim a fair hearing.
So, that said, where can I learn more about the evidence supporting and contradicting this view?  I found on his Wikipedia page that a number of scientists have condemned his work, but I'd like to actually know the evidence and arguments underneath all this.
I suppose I should also ask more generally about the state of biological evidence for the reality of race.  I had heard in college that there is no biological basis for race, but I'm wondering if that is an out-dated view in light of recent work in genomics.  I read this stack exchange question but it had more to do with whether there is a consensus rather than on the arguments surrounding the issue.

The linked article doesn't appear to provide any empirical evidence about a biological basis for race. The biology is limited to two paragraphs at the start which are presented as FACT with no citations. The only (obliquely) cited arguments are Darwin, some (economic) historians, and a reference to book in the sociology field from 1975. He can't make scientific arguments without directly linking to the science. These are red flags for me but it's hard to rebut the biological evidence when he hasn't presented any.

Don't you think saying "Western liberal" instead of simply "liberal" is regionalist if not mildly racist?

@WYSIWYG My understanding is that liberal has different meanings in different places.  No attempt at racial division was intended.

Not sure why this was downvoted - it's an honest question about an admittedly touchy subject, but the OP asks it in an open manner and wants a clear, unbiased, scientific answer - exactly what we're here for.

Related: Like other animals, why humans don't have species & breeds?

Possible duplicate of Do humans have enough biological differences to be grouped into races or subspecies? and Like other animals, why humans don't have species & breeds?

I think it's best if you check out Wikipedia article on Race. Race is not a taxonomic term. In a nutshell, you can't define it in a useful way that has anything to do with the usual associations of the word, or gives it a practical value in science.
The problem with arguing about the existence of races in humans is that this is an argument about a word without an agreed definition, so there's never a true or false. This author is merely making some controversial extrapolations from quite obvious biology: Of course human genomes change over time, and it is also possible to an (impressive) extent to trace genetic lineages geographically. Of course there are subgroups that share a small set of characteristics not found in the rest of the human population. Some of these subgroupings are for example medically relevant.
Essentially, "race" ends up a loosely defined term that has something to do with subgrouping a species based on whatever criteria chosen. The reason why it's not a useful word to argue about in humans is because whatever subgrouping you might make, and for whatever purpose you are subgrouping, there are better, more meaningful (and quite importantly, less controversial) terms to describe those subgroups.

You will probably be interested in the American Association of Physical Anthropolologists' statement on Biological Aspects of Race. It's rather long and detailed, so I won't attempt to reproduce it here, and it's rather well written, so my summation wouldn't really do it justice.
In science, when we classify something, we need to have inclusion and exclusion criteria. You either carry a certain gene variant that has a deletion mutation that increases your risk of cancer, or you don't. To be a zebra, you need four legs and stripes. If you have stripes, but six legs, you're not a zebra. If you have four legs, but spots, you're not a zebra. So how then do you classify a race? Taking the three major old (and racist) classifications, people were either thought to be mongoloid, caucasoid, or negroid. How do you tell if someone is negroid? Well, their skin is dark brown! Caucasoids have white/pink skin. But where's the cutoff? How would you classify someone of Arab descent, with skin darker than a northern European, but lighter than a sub-Saharan African? How would you classify the offspring of a northern European and a sub-Saharan African?
People are a blend of phenotypes. While you can always define a group of people that look one way, and another group of people that look a different way, you'll always be able to find people somewhere in the middle. We are all the same species; every single fertile male on Earth can reproduce with any fertile female, regardless of social class, national or geographical origin, ethnicity, culture, skin color, or any other factor. This is not true of robins and cardinals, or elephants and zebras, or dogs and cats. (Yes, some species can form hybrids with other species, but that's a different topic.)
Within our species one can define certain groups based on physical characteristics, such as those of Han Chinese descent, that are grossly similar to one another, but far from identical. This group may share some common gene alleles, but there will still be (sometimes significant) variations from one person to another. One of the problems identifying that group as a race is that there is no strict biological definition of the term, with explicit inclusion and exclusion criteria, and the reason for that is it is almost impossible to identify these strict criteria that more than a handful of people would meet, due to the variation I mentioned earlier.
Now, of course there are groups of people with similar ancestry that share certain common gene variations that protect them from or predispose them to any number of diseases or conditions. There are also confounding cultural, socioeconomic, and environmental factors that make absolute connections between these gene variations and the associated diseases tough, as well (African-Americans and heart disease, native Americans and alcoholism, etc.). However, calling these different groups "races" is not helpful, and most of the time not even accurate (again, getting back to the lack of a clear definition of race).
Race is a social construct, based on a long and dark history of misguided attempts at classifying people. The concept likely has some utility to sociologists (I'm not one, so I don't know) so that people can voluntarily choose to identify with a group, and likely other reasons as well. However, because of the vagueness surrounding its meaning, and the incredible genetic diversity and identity between people, the concept really has no biological basis. I can just as easily study why people with certain genetic markers are predisposed to heart disease, for example, as I can study why many African-Americans get the disease, and I actually have a clearer criteria for subjects to include in the different arms of my study because I have a solid genetic definition, not just one based on skin color, which is completely irrelevant to the subject at hand.

Thank you for the link, I'll try to read it in as much detail as I can.  So I've actually been arguing this point with someone who was trying to argue that race is real.  I've made a lot of these same points, granted with not quite as much education or detail as you have.  I've also mentioned that even if we pretend races are well-defined and sample Fins and a certain group in Africa, we find that in-group variation is many times larger than between-group variation--I believe this falls within the statistical theory of ANOVA, yes?

Also, even if races existed we still have no evidence that valuative properties are heritable, like intelligence or morality--again, here, there is a measurement problem just like with the problem of race.  IQ has been found a poor measure for a few reasons, and of course morality is even less possible to measure.  Just wanted to say these out loud to someone who might know more than me in case I'm making any mistake.

@Addem I don't know about the statistics, so I can't judge that claim one way or the other. It all depends on what you're measuring. Regarding your argument with your friend, race is real depending on what your definition of reality is (seriously). If you're talking about police (mis)behavior, then yes, race is definitely very real. If you're talking about biological classification, then it is not - there's just not enough differences between people, and there are no good ways of defining inclusion and exclusion criteria, as I've written.

I'm not quite sure what you mean by "valuative properties". There is definitely a genetic component to intelligence, but the nature vs. nurture debate is very relevant in that area - you can take offspring of two very intelligent people and have them raised by uneducated, economically disadvantaged people in an overcrowded, under-funded school district, and they won't turn out anywhere near as well as if they were raised in a wealthy home with attentive, highly-educated parents with access to the best educational and enrichment resources.


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Could bone marrow transplants help make xenotransplants viable?

So the immune system doesn't calibrate (for want of a better euphemism) to recognize it's own cells until fairly well along in fetal development & the major components of the immune system (antibodies, white blood cells, etc) are all produced by the bone marrow.

Those are the known details that cause me to wonder if this (below) might not be a viable approach.

Introduce the patients cells to a pig fetus before it's immune system has been set & it will be born with an immune system that recognizes both it's own cells & the patients cells as it's own.
Kill the patients own marrow (as per a normal bone marrow transplant) & transplant the pigs bone marrow into him giving him an immune system that recognizes both his cells & the pigs as it's own.

If my understanding is correct you should then be able to transplant any other organs from the pig into the patient without any tissue rejection issues.
I am only interested in the science so (any legal & moral issues aside) are there any major factors I'm unaware of to suggest this approach is a non-starter?

See Xeno: The Promise of Transplanting Animal Organs into Humans By David K. C. Cooper M.D., Robert P. Lanza M.D. Published 23 March 2000 by Oxford University Press, specifically the section on "The Induction of Chimerism Before Birth" from page 117 onward in this link.
That talks about my suggested first step (though in reverse), creating a human with immunity to cell rejection of a donor animals cells, which isn't much use to anyone who's already been born.
So I flipped the idea.

A Thymus transplant might be needed as well.

Comments are not for extended discussion; this conversation has been moved to chat.

I feel I've enough sources & data to venture an answer on this one myself now, so here goes.
Step one: Can we produce the pig in the first place?

Fetal Inoculation With Donor Cells in Cardiac
Xenotransplantation 1996
Perinatal induction of immunotolerance to cardiac and pulmonary allografts July 1997
Induction of donor-specific tolerance to cardiac xenografts in utero: 1998 Sep
Cell Transplantation January 1 2003
IMMUNO-INTERVENTION FOR THE INDUCTION OF TRANSPLANTATION TOLERANCE THROUGH MIXED CHIMERISM: 2011 Aug 11
In utero hematopoietic cell transplantation: induction of donor specific immune tolerance and postnatal transplants: 2014 Nov 12

another link to the same article
In utero hematopoietic cell transplantation: induction of donor specific immune tolerance and postnatal transplants 12 November 2014

First human-pig 'chimera' created in milestone study 26 Jan 2017
Interspecies Chimerism with Mammalian Pluripotent Stem Cells 2018 Jan 26
Interspecies Chimeras and the Generation of Humanized Organs 3 Jan 2019

Yes, an animal can be produced with donor specific tolerance to the patients organs, it's a known procedure & observed effect that has been replicated numerous times in experiments, its immune system would not attack either the patients cells or its own.
Step two : Can we transplant this animals bone marrow to the patient?

Stem cell and bone marrow transplants

Yes, bone marrow transplants involving the complete removal of the original bone marrow is a long established procedure for the treatment of leukaemia.

And now being used for treatment of other severe autoimmune diseases in a way which may make this idea moot, I'll have to look into that further, not read that article in full yet.

Step three : Will we then be able to transplant other organs from this (or a genetically identical) animal to the patient without tissue rejection?
The immune system isn't seated entirely in the bone marrow & its products (the thymus, spleen & lymphatic system also have roles) so for best results some of these may also need to be replaced.
If so it must be hopped the lymph nodes play no role in in the development & tuning of the immune system, there are 500-600 of them around the body so replacing them all would be no small task.
Conclusion :
Still in progress / just saving work so far

No, this will likely never work - but chimeric trans plantations of 'humanised' organs might become possible.
Firstly, the process of injecting human/patient cells into an embryo would - if it works - create a chimera. Experiments of creating pig-human chimeras have (to my surprise) actually been performed, however the amount of humans cells that didn't immediately kill the embryos was very low (~0.001%), so even if they embryos would be able to reach adulthood (which the researchers didn't test) the organs wouldn't be human-like enough to allow transplantation. (source1, source2)
If the chimeric embryo's indeed survive then it might be possible to create animals that have a completely 'human' bone marrow that can be transplanted, by removing part of the pig genome that allows for the generation of bone marrow so that the injected human cells take over that role (this technique has been used successfully in rats & mice for other organs). If organs other than the bone marrow could be 'humanised' this way in pig chimeras is probably unclear since the difference between pig and human is much larger than mice and rat and might cause immune rejection issues.
Transplanting actual chimeric organs will likely never be done, since some of the cells will always be of the 'wrong' species, which would cause a lot of immune issues in some way.
Since chimeras unlike hybrids will never have individual cells that combine two species, it will also not be possible to make a thymus that 'trains' the whole immune system against two species - individual T-cells might only see one type of species during maturation and therefore cause immune reactions later on.

"ethics" please read the question again.

@Pelinore: I read the question, and my answer is a clear NO irregardless of the ethics aspect

"otherwise the pig will die" can you explain why pigs with humanized organs don't die then, we've almost two decades of experimentation doing just that and I don't recall ever reading anything about a problem with pig mortality arising from that?

@Nicolai your post could be improved with more thorough references. Right now you've just linked to the wikipedia page on T-cells, but you make very specific statements about what would or couldn't happen in various experiments.

@DeNovo I'll try to see if I can find some references but it wont be easy since these are mostly hypothetical experiments that noone would actually do (and therefore write about), like injecting adult cells into an embryo.

@DeNovosupportsGoFundMonica I edited (or rather rewrote) my answer with a better sourced foundation.


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About embryonic and genetic evidence of evolution?
My question here is about evidence for evolution from Embryology and from Genetics.

Mammals do have similar Embryos, but is it the case that for each species there is an embryonic development that occurs in earlier species, has such relationship been observed?
What I mean for example if we generally conceive of having species$Sp_1,Sp_2,...,Sp_n$ where each $ Sp_{i+1}$ being evolved from $Sp_i,$ then is it the case that the embryonic development stages of $ Sp_{i+1}$ contains some of the embryonic development stages of all of its ancestor species.

Similar question to 1 but regarding Genetics, is it the case that every species has a genetic thumbprint of its ancestors that lie there in the non-functional sections of its DNA, i.e. is it the case that all the genetic history of our evolution is recorded in the non-functional section of our DNA. So do human DNA have some portions of the DNA of some dinosaurs for example?

In short: Yes and Yes

"ALL the genetic history", most definitely not, genes mutate and get recycled or lost. There is some genetic history of our evolution, and comparing it to other organisms can yield much more.

You seem to want to use LaTex formatting in your post. That's great for having nice layout. Just wrap your format in $ to have it Latex (MathJax actually) format. For example,  $Sp_1$ is displayed as $Sp_1$

Question 1 asks whether ontogeny recapitulates phylogeny. It is striking that the when observing e.g. human embryo development, the embryo seems to go through stages that its ancestral species would go through, but where those 'lower' species would terminate at a specific stage. In other words, embryonic development seems to recapitulate a species' evolutionary lineage.

This is the recapitulation theory, which is outdated and incorrect, but a great example from the history of science. The most prominent of these was Ernst Haeckel's biogenetic law and the Meckel-Serres Conception. There were many problems with this, especially because they focused on noting similarities rather than differences, and several exceptions exist to the rule. They were not very scientific. It also incorrectly presumes that complex organisms have more predecessors. However, it is a compelling piece of evidence to elegantly show that evolution acts incrementally on existing embryological processes.
Question 2 asks whether there is evidence of ancestral DNA in our genome. The answer is yes. Where to begin? We share almost all of our genes with close relatives (e.g. chimpanzees and bonobos) and progressively fewer with more distant relatives. 50% of a banana’s genes (and indeed most other plants') can be found in the human genome. But remember, logically, that doesn't necessarily mean that 50% of human genes are found in bananas, though, because of the way divergence works. The human genome also contains a record of many viruses that have inserted themselves over tens of millions of years. Though they are not ancestors, they have been added 'horizontally' as opposed to the 'vertically' that ancestor DNA is modified over a species lineage.
It's very possible to answer your questions from many, many different angles, and present countless pieces of evidence in favor, but I think this should suffice.

S Pr's answer is very good, I'll just elaborate on a few points.
1) Evolution acts incrementally on existing embryological processes -> the insight here is that organisms don't come out fully formed, they develop. When we say a gene, say, "codes for" a tail, it doesn't make a tail magically appear: its action happens during the organism's development, where it acts on the development process such that the adult organism will have a tail.
This means that when organisms change over time via evolution, the way these changes are actually implemented are as changes to an existing development process; obviously the development process isn't going to be reset each time. So for example, it might make sense that since snakes don't have limbs as adults, they should never have limbs at any point in their development because what would be the point? But they evolved as a variation on organisms that did have limbs, and whose embryological development included the development of limbs. Evolutionarily speaking there's little reason why you should change that by preventing the development of limbs at stage 0, as opposed to, say, halting their development at stage 10 and destroying the limb buds. Either way you end up with a limbless adult snake! On the other hand if you destroy the limbs at stage 10, you're hardly going to have them come back at stage 19. In other words, you can end up with a pattern of later evolutionary changes happening later in development on average even if the changes occur at a random point in development, simply because a change at one stage of development also changes the later stages, but keeps the earlier stages intact. So earlier stages are more likely to be unchanged on average, i.e. similar to how they were in the ancestors. In practice the changes don't happen randomly in the development process of course, which is one reason "ontogeny recapitulates phylogeny" actually has tons of exceptions. This textbook "Developmental Biology" has a cool companion site with a chapter that discusses the history of the idea. This Wikipedia page also discusses some evolution in the view of evolution and development, talking about the "hourglass model" vs the "funnel model". The funnel model is this idea that the earliest stages are most similar to ancestral forms (and thus similar between related species), but the hourglass model points out that actually there is one specific stage (the "phylotypic stage") that stays similar between species, but there are differences both in earlier and in later stages.
2) There is no such thing as "dormant" DNA. There is active DNA (that codes for genes, regulatory regions, etc) and non-functional DNA. Non-functional DNA can be a few mutations away from being functional, and thus become functional as a result of chance mutations, but "dormant" suggests regions of DNA that are deactivated with the intent of reactivating them in the future; this isn't a process that occurs in evolution, which has no such future-looking intent.
Now it is the case that a) all DNA is subject to mutation, and b) we have a whole lot of DNA, and the mutation rate is quite low. This means that a lot of DNA is indeed more or less the same as it was in our faraway ancestors. Having said that, non-functional DNA is less likely to remain the same than functional DNA is, because nothing prevents mutations to those parts from being passed down through the generations. The DNA sequences that are the most unchanged ("conserved") are those that are used in such basic functions of life that they evolved very early in the history of life, and any change to them kills the resulting organism, which means that natural selection will make sure they don't change, or change very little. Here is a paper "The Genetic Core of the Universal Ancestor" that looks at such DNA sequences that are the same in all organisms ("universally conserved") to infer what genes the common ancestor of all living things had.
Finally, while this does mean that humans share a lot of their genome with dinosaurs, those shared genes mostly come from the fact both humans and dinosaurs share genes with their common ancestor, which was one of the earliest reptiles. Dinosaurs are not ancestors to humans.

On the upside those changes in nonfunctional portions also get passed on and make for a better measure of relatedness, since selection is not really doing much with them.

Question 1

Mammals do have similar Embryos, but is it the case that for each species there is an embryonic development that occurs in earlier species, has such relationship been observed?

Technically, we do not observe much from the embryology from ancestral lineages. They don't exist anymore, so we can't make many observations from their embryology. The question is rather whether related lineages have similar embryogenesis.
The answer is yes. Mammals develop like mammals, birds develop like birds, angiosperms develop like angiosperms. For example, in all protostomes (insects, spiders, crustaceans, molluscs, ...), the blastopore becomes the mouth while in all deuterostomes (sea urchins, sea cucumber, vertebrates incl. birds, mammals, turtles, lizards, sharks, etc...), the blastopore becomes the anus.
Question 2
Genetics is our main tool for inferring our phylogenetic trees. So, it makes more sense to ask whether other things match the genetics than the other way around. But yes, things match. Fossil records, ontogeny, phenotypic variation and genetics. Everything match to tell a similar story of the phylogenetic relationships among species.

The important thing about "ontogeny recapitulates phylogeny" is that it is not true,  There was an idea that it perfectly replicated phylogeny, which is were the phrase came from, but that proved false pretty quickly. The phrase has hung around because ontology can provide a lot of useful information about phylogeny.

@John I did not know that it used to mean more than it does today. Thanks for your comment.