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Describing trait evolution across a very small phylogenetic tree
I am very new to phylogenetic comparative methods but I want to explore the evolutionary patterns of a number of quantitative traits I have across a small sample (5) of closely related species (between .45mya and 4.3mya divergence). I am confident in the structure of the tree, but I only have phenotypic data for a small sample of the tree. I want to measure how correlated the evolution of the traits are across this small phylogeny and test the traits to neutral evolutionary models.
Should I even attempt this?  I know that there will be limits for what I can infer about evolution of these traits, but I’m not sure where to start in terms of identifying the specific weakness. I know it will depend closely on my trait measurements, some traits display notable divergence and others do not change much across the phylogeny.
Are there any approaches that would be useful for describing the evolutionary patterns for this small sample?  What references would be useful for convincing me to hold off until I have a larger phylogenetic sample?
Thanks in advance for any advice!

Welcome to Bio.SE! It's early in the morning for me and I'm having a little difficulty understand the question. You have 5 species and you want to build a tree. If there is a clear progression of the phenotype through the divergences then you could infer the history of the phenotype and maybe pin it down at a genetic level? I don't see why there would be any problem with this as a preliminary study whilst you wait for larger datasets.

Are you saying that you have phenotypic data for 5 species in a much larger phylogenetic tree? This will clearly limit the types of conclusions you can draw, and all conclusions will be extremely uncertain. As a first step, it would probably be useful to estimate the phylogenetic signal in the different traits (Bloomberg's K, Pagel's lambda), to see what you have to work with. Plotting the traits on the tree is also useful, but I assume that you've already done this.


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Do we actually get more sick (flu/cold) during winter?
The word flu derives from the Italian phrase "influenza de freddo" meaning "influence of the cold".
Indeed it is that time of the year when my colleagues seem to have the flu/cold more often than not. I remember during university, winter lectures would be riddled with people coughing and sneezing - the so called "freshers flu"
Questions

Is there statistical evidence for this claim?
If so, what are the causes/factors involved?
Another post asks why our noses get runnier during cold whether, is this related?

As a sidenote: looking at the kind of questions you ask, you might be interested in this book

Cheers, I think so far you, @GriffinEvo and biogirl have suggested too many books for my wallet to handle. Will keep this in mind until i progress through them :)

@Remi.b Oh yes, I read about that book in the book "the blind watchmaker" and Dawkins says it's nice too. :)

The combination of these two reports from the CDC give information about the comparative prevalence of flu infection in the winter (September '12- May '13) and summer (May '13 - September '13). I'm going to assume that 2012-2013 was a fairly representative year as far as the level of detail of "do we get sick more in the winter" goes. Particularly striking are the graphs linked to in both documents of the number of flu-infected respiratory specimens per week:
Winter (infected specimens out of 311,000 tested):

Summer (infected specimens out of 52,000 tested):

Together these two figures cover data Sept '12 - Sept '13. Note the difference in scale on the vertical axis. Forgive me if I don't run any statistical tests, but I think you can spot the trend.
The sum of all the Winter cases represents 23% of the 311,333 specimens tested from Sept '12 to May '13, and the sum of all the bars in the Summer figure represents 3.9% of the 52,150 respiratory specimens tested from May '13-Sept '13.
Still left to answer: Why is this the case? In my preliminary research it seems like we still don't fully know the answer to this one; I'll leave someone else to speculate.

Edit: Some tentative answers to why is there a seasonal flu outbreak:
This review (1) does a nice job of laying out some of the current ideas about the cause of the seasonal flu. One interesting note is that seasonal flu is a phenomenon of temperate climates: in tropical regions flu outbreaks occur on a much less regular periodic schedule. Some possible causes mentioned by the authors (paraphrased from the article):

It takes time for virus to mutate enough to be infectious again to people who were already infected with it.
The efficacy of the immune system may vary seasonally, say, due to changes in daylight hours/vitamin D and melatonin levels (which have been shown to affect immune system function in hamsters)
Flu is transmitted better in more crowded conditions + in winter people are more crowded together. This is a popular explanation, but the authors claim that it has not been satisfactorily tested. It has been argued convincingly that the 1918 flu epidemic was exacerbated by the crowded condition of army barracks in WWI (see citation in paper).
Indoor heating encourages air recirculation, which allows virus to persist in the air around you longer.
Viruses survive/persist better in cold, dry conditions. This may allow them to spread in the atmosphere longer during the winter, and be more easily transmitted from person to person via "bioaerosols" (sneezes).

Ultimately, as I said before, we don't really know yet. Reading that list you can imagine several ways in which a few of those factors are not at all causal and are rather just strongly correlated with the "true" cause of flu seasonality.
(1): Lofgren et al. Influenza Seasonality: Underlying Causes and Modeling Theories. (2007). J. Virol. 81(11): 5429-5436. doi:10.1128/JVI.01680-06

nice find and summary! I'll wait a bit to see other people's answers before ticking, but upvoted of course

As this answer cites my paper, it is clearly correct ;). I would note that it's true for influenza, and a few other winter-circulating diseases (Norovirus comes to mind). Other infections are more prevalent in the summer (many bacterial GI infections for example) and some don't care at all.

"Viruses survive/persist better in cold" -
Could you provide proof links on that?

@ctapobep, I am mostly just paraphrasing the open-access article cited here. In that article they make the claim several times that viruses are more stable in cold, dry environments. They cite this paper: Hemmes et al. (1960). Virus Survival as a Seasonal Factor in Influenza and Poliomyelitis. Nature 188: 430-431, which appears to investigate the stability of certain viruses in cold, dry environments.

@ctapobep, furthermore, This result isn't surprising: viruses are inert particles made of proteins in a relatively ordered/low entropy configuration. If you increase the temperature, you make it more thermodynamically favorable for the protein making up the viral particle to loosen from their ordered configuration and move freely, which effectively destroys the particle.

Has anyone investigated the possibility of migrant birds carrying new strains?

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How easy is it to carry out de novo sequence assembly?
Today a colleague of mine asked the following question:

" Assuming I need to build from 0, a chromosome of a fish, with short reads
but no other reference whatsoever [de novo assembly]:

how much work is that?
Is there a generic software (like SAMtools) that will align the reads in a
scaffold one can use?
Basically, given a reasonably clear pipeline in terms of software, is it still blood sweat and tears or is it just a matter of getting it on a cluster?"

Very grateful for any suggestions, sources of information, software etc.

tl;dr: It’s blood, sweat and tears. I haven’t been involved in this myself yet but I know people who are. Depending on the complexity of the genome, you’ll get tons (they got in the order of 1M) non-overlapping contigs.

would it really be necessary to use 30bp reads? that's very short.

cheers guys, actually I pressumed ~30bp to give an idea but perhaps it is more flexible what lengths do you have in mind @ThomasIngalls? Hmm I wonder what the blood sweat and tears would be caused by? I presumed there would be some standard pipelines to automat the whole shebang?

De novo sequencing without using some long-read techniques for cleanup (like Sanger sequencing) requires a lot of coverage, and you still end up with substantial uncertainty in the results, due to the large amount of repetitive sequences that are longer than 30bp in most genomes. The reply by @bitwise gives a great idea of what I was thinking.

If you only want to use only sequencing techniques, you have a problem.
To get a feeling of what kind of results to expect, consider this paper published recently in Nature Genetics. They tried to assemble a whale genome de novo. They had 7 (!) paired-end libraries with different insert lengths ranging from 170bp to 20kb. Read lengths were mostly 100bp and in some cases 49bp. Average genome coverage was 91x.
Assembling this extensive data, they end up with over 100,000 contigs when the assembly is done.
So you really can't get a high-quality complex (i.e. large) genome assembled from only short-read sequencing data using the standard techniques.
That said, recent approaches such as libraries with much longer reads lengths (here) or the use of Hi-C data (here and here) do offer a way of getting high-quality complex genome assemblies using only sequencing data.

"If you only want to use only sequencing techniques, you have a problem." -- Do you mean resequencing techniques, or high-throughput sequencing techniques?

@ThomasIngalls I mean assembling a complex genome de novo using high-throughput sequencing. Resequencing assembly is not de novo assembly.

You can try looking around biostars.org, which is like stackexchange, but for bioinformatics.
Velvet is one example of a de novo assembler.
But 30 bp is really short, and animals have big genomes (not as tough as lots of plants and fungi, but still tough)
What you would get is a bazillion short contigs.  It would not be pretty.

cheers for the Velvet recommendation

I really like the genious software suite. It can multithread and really use the performance of your computer. Even complicated things like De Novo assembly are very very intuitive.

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Why do human eyes glow red on a photo and dog's eyes green?
Previous Research
I know that cameras sometimes come with an anti "red eye" functionality that involves two flashes, presumably the second flash coincides with the shutter opening.
Question
Why do camera flashes sometimes lead to photos of humans with red eyes? And why do dog's eyes appear green?
Related
The reason for the green dog's eyes has been answered quite shortly under the question "why-do-dogs-eyes-glow-green-on-a-photo", but that question does not answer my specific question: Why do humans have red eyes on flashed photos and why are dog's eyes  green?

It's considered a requisite on biology.se that at least some sharing of your reading/research is presented with your question. Why do you think the retina is red? Otherwise it will be closed. The site tour and the help center  provide guidance on how to use this site. Please take a few minutes to read about the kind of questions which are on topic here.

I have edited the question to emphasize the difference between the dog's green-eye effect in the linked question and the human's red eyes. The answer still talks a lot about the human situation, which was the original question

@anongoodnurse let me know if my edit is sufficient background

@ChrisStronks TQ I did notice the dog question had a very weak implication of an answer to this question, but felt the human version deserved its own thorough answer

@hello_there_andy - I totally agree with both your remarks. The other answer was kind of vague, and the human red-eye was never asked before on Bio.SE as far as I am aware. The combination of both in one question makes it a nice new question definitely deserving to be asked! Hope my answer helped.

Short answer
In humans it is basically the red choroid plexus in the back of the eye you are seeing on a flashed photo, while it is the green-reflecting tapetum lucidum in dogs.
Background
The red-eye effect in humans was explained nicely by Yale Scientific Magazine, and I adapted the following text from that source:
The human eye can effectively adjust to different light conditions, but this adaptation is also what leads to the red-eye effect. The eye regulates the amount of entering light by contracting or expanding the pupil. At night, your pupils will accordingly enlarge to extract more light from their surroundings. However, this dilation also leaves your eyes unprepared for the sudden burst of light from a camera flash.
When light from the flash enters your eyes under these conditions, your pupils are unable to contract fast enough (full constriction takes a few seconds) to prevent the light from reflecting back, off of the red blood vessels of the choroid. The choroid plexus nourishes the retina, and therefore contains ample blood supply. As a result, the camera will pick up the red reflection, resulting in the red-eye effect. Interestingly, due to their increased “dark adaptation,” children more commonly have red eyes in photographs.
The amount of melanin, a light-absorbing pigment in the eye, also has a role in the red-eye effect. Individuals with lower levels of melanin will absorb less and thus reflect more light, explaining the high incidence of the red-eye effect in albinos.
Though the cause of this effect is wired in the biology of the eye, some cameras can reduce red-eye by sending a few preliminary flashes before the final flash to give the pupils enough time to contract and adapt to the increased-light conditions. Another way to reduce the effect is to avoid looking directly into the camera lens, which will reduce the reflection of light. Finally, if all else fails, modern image editing software, such as Photoshop, can remove the red discoloration.
With regard to why dogs and other animals may not have red-eyes but other colors, this was indeed answered in your linked question: some animal species have a tapetum lucidum, which is situated in front of the choroid and reflects light back onto the retina thereby increasing light sensitivity. In dogs it is green, as aptly shown in the linked question's answer. The following figure shows the anatomy and the position of the tapetum in front of the choroid. It was adapted from Pets.SE with the related question "Should I be concerned that my dog's right eye is reflecting green in the dark when his left eye doesn't?"

Hence, the reason why animals with a tapetum lucidum have another eye color is that light does not reach the choroid in these species, giving rise to green-eye effects in dogs and cats (picture taken from Ask Nature):

worth noting not all dogs have tapetum, some breeds have lost them, they also have red eyes on photos.


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Consuming animals by slaughtering vs injecting barbiturates?
In "Least painful way to die" we get an answer ...

Companion animals (e.g., dogs and cats): injected barbiturates are recommended
Laboratory animals (e.g., mice and rats): injected barbiturates are acceptable as are inhaled agents (isoflurane, carbon dioxide).

And assume the butcher guy as soon as he comes to know the animal is gone, he will do the following....

A very sharp knife is used in this process: the point of the knife cuts into the animal's throat and cuts through the dewlap, trachea, esophagus and jugular vein immediately below the jaw-line to allow the blood to flow out.........Animals are bled out before being dressed because it prevents blood from coagulating in the tissues and thus making the meat go rancid. (Source Slaughter Cattle commercial method - Step 6)

Here's my question... What if the animal was killed using 'barbiturates', then is that animal safe for eating by humans or the high levels of 'barbiturates' in that body cause unwanted results in humans too (if they consume it)?

I'm new to biology. :)

even if it is OK, drugs might be too expensive for large-scale food manufacturing

but at the cost of the pain of animals... suppose if people become merciful enough to spend more bucks to eat a hen... then? @aandreev

I know for many antibiotics the animal cannot be slaughtered for consumption within a certain time (some can be upwards of 60 days I think). Even NSAIDs like banamine (flunixin) require a brief withdrawal period (1 week if I remember right). I'd imagine barbituates would also require such restrictions.

"the animal cannot be slaughtered for consumption within a certain time" a little explanation about that and confidence about what you said would make it a good answer in the answer box @canadianer :)

Sure, I'll check some drug bottles for the actual time frames and post an answer when I get a chance. I really can't say anything about barbiturates though.

"cost of the pain of animals" does not exist. Only real alternative is free-range meat gunned down in forest,but it is not as tasty

Barbiturates are narcotics.. they will have even more stringent restrictions compared to NSAIDs and antibiotics.

It is important to note that farm animals are not protected under the animal welfare act

so you mean to say the answer is 'no', it is not at all possible.???. @WYSIWYG

so you mean to say we can play with them anyway we like is it ?? @CactusWoman

Yes and no. To be more specific, there exists a "common farming practices" exemption in the animal welfare act, meaning a practice that is considered a common farming practice, such as using a knife for slaughter, can be performed legally on farm animals when it would be illegal to perform it on, for instance, a dog. So, it's not that you can do whatever you want to farm animals, but rather you can do any common farming practices to them. It is also important to note, as WYSIWYG said, that barbiturates are narcotics and not necessarily safe for consumption in any case.

@servantofWiser I think chemicals can be used to numb an animal after which it is killed by regular slaughtering practices. CO₂ and other gases are used to asphyxiate and make the animal unconscious before it is slaughtered. Inhaled anaesthetics may also be fine because they won't be resident in the body for a long time. But I don't think injected anaesthetics and barbiturates would be a good option. Xenon is a safe anaesthetic but is very costly.

I really appreciate the effort everyone has put in here in helping me sort things out! :)

Actually, slaughter with a sufficiently sharp knife, and sufficiently skilled butcher, is supposedly nearly painless (e.g. Hebrew/Islam ritual slaughter). Think about how you don't notice a paper cut right away, then imagine that you suddenly pass out from blood loss. The reason knife slaughter is often frowned upon is because large operations tend to start cutting corners on the knife and/or butcher.

For many drugs, the animal cannot be slaughtered for consumption within a certain time. Here are the slaughter withdrawal periods for some common drugs when used on cattle. There are also withdrawal periods for lactating dairy cattle, but I won't list them for brevity.

flunixin (NSAID) - 6 days
florfenicol (antibiotic) - 36 days intramuscular, 55 days subcutaneous
penicillin G procaine (antibiotic) - 10-14 days
tilmicosin (antibiotic) - 28 days
oxytetracycline (antibiotic) - 28 days intramuscular, 48 days subcutaneous
enrofloxacin (antibiotic) - 36 days, do not use in veal calves

More importantly for your question, I have found this report on pentobarbital used for euthanizing cattle. It says:

Adequate measures should be taken to ensure that carcasses of animals treated with this product and the by-products of these animals do not enter the food chain and are not used for human or animal consumption.

Barbiturates are more dangerous than many other drugs and, furthermore, dead animals cannot metabolize them and they can be quite heat stable (ie won't readily decompose during cooking).

seriously! you answered this? Cool! ......I know a simple 'thanks' is not sufficient, but still, a simple 'thanks'. :)

@servantofWiser You're welcome.


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What is a "marker-matched" plasmid?
I see this term used a lot in papers and have trouble understanding it. From what I have gleaned it seems they are used during control experiments, perhaps with the goal of making the control plasmids as similar as possible to the experimental ones to limit confounding variables?
Here is an example from I paper I've been trying to understand.
"Cells containing an ARS1 plasmid, or a marker-matched ARS-CEN plasmid, were subjected to life span analysis." - David Sinclair & Lenny Guarente, 1997
Let me know if you need more info. Thanks!

It is where a control plasmid is used - this is usually an empty vector or a non-target vector with the same "marker" on the plasmid.
The marker is often one that is either used for purification of a resulting protein (e.g. His, GST etc) or immuno-detection (FLAG, HA etc (these can also be used for purification, as can His and GST for immuno-detection)) or fluorescent (GFP etc).
In addition and as per comment from @MaximillianPress markers can also be selectable, so used to ensure that the plasmid is maintained in the cells and that all cells contain the plasmid. This is often done through expression of a marker that confers resistance to an antibiotic such as ampicillin for bacteria or geneticin for mammalian cells. In yeast nutrient deficient media can be used and the yeast will only grow if they contain a plasmid that allows metabolism or production of an essential compound (e.g URA gene for Uracil production).

I would actually expect that the marker be a yeast selectable marker, such as an auxotrophy marker like the URA3 / KANMX, that can be used to select the plasmid on dropout or antibiotic plates.

@MaximilianPress good point - I don't use selective markers very often, so I forgot about them. I'll edit that in.

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Role of Automata Theory in Biology
Lately I have been taking an interest in mathematical biology. While reading "Evolutionary dynamics" by Martin Nowak, I came across this reference, where the author describes in short how John von Neumann had described a self reproducing automata which increased in complexity over time; the structure of which was equivalent to the central dogma of biology.
This leads me to my question - what is the role of automata theory in today's biology ? Is it still relevant ? Was there any role that it played in the development of biology ? I couldn't find very comprehensive answers on the internet, so if you know of any sources, please do link them.
Thank you.

There is no central dogma in biology. Over 60 years ago as molecular biology was emerging, Crick explained the working hypothesis of those at the forefront of the field of molecular informatics as that information in DNA could be expressed as protein but not vice versa. Experimental evidence has rendered this idea a trivial commonplace — neither central nor a dogma. Anyway, how could the structure of machine be equivalent to a *concept"?

Can you explain what you mean by "the development of biology"? Louis Pasteur was certainly a biologist, and his work predated Nowak's by almost one hundred years, as did Gregor Mendel's.

@David Thanks for your response. As far as I am aware the process of DNA coding information for how proteins are synthesized is referred to as central dogma. I was referring to the process by this name, and not saying that this a 'dogma' that is 'central' to molecular biology.
I should perhaps clarify what I mean by structure of a machine, I didn't mean physical structure, but the logical structure of it. Basically the way the von Neumann's machine works, it's components, and the relationship they bear with one another, is equivalent to central dogma. I hope to have clarified your doubt.

@anongoodnurse what I mean to ask is has the development of automata theory contributed to biology in some way? If so then could you give me an example ? For example, game theory is applied to understand evolution.

You awareness was faulty. See this answer from me on this topic: https://biology.stackexchange.com/questions/49201/crick-s-central-dogma-counter-cases/49210#49210 and for confirmation check the Wikipedia article on the topic. It would seem that the analogy you want — good or bad — is with DNA replication, that the structure of DNA is such as to allow self-replication, although not without the participation of other components. This is quite different from the relationship between the information between DNA and proteins of Crick, which is essentially a dead end.

Interpretation of the question
From the responses of the poster to questions in comments and the revision of the question my understanding of the comparison it makes is as follows.

The the structure of DNA with its two complementary strands gives it
the logical potential for self-replication (by each separated strand
being able to serve as a template for a complement). This is formally
similar to the von Neumann’s idea of a self-replicating automaton.

The main question would seem to be “whether the ideas of von Neumann (or similar ideas that preceded it) had any influence on the discovery of the potential of DNA for self-replication.”
Answer
No.
Biology, both cellular and molecular, is an experimental subject. Biologists of the traditional kind had long known from direct observation that simple cells could replicate, but their ideas on how this occurred were vague and made no contribution to the deciphering of the replication mechanism.
DNA was investigated by other scientists who had concluded that the evidence indicated that it was the genetic material (an idea that was still contested in the 1940s), and felt that it was important to determine its structure. Neither Watson nor Crick anticipated how the mechanism of self-replication would fall out so beautifully from the structure. There was no theory driving their work, just a desire to see things at the molecular level.
Conclusion
Automaton theory was never relevant to biology, so the question “is it still relevant” falls by the wayside. Computation has a role to play in biology, but more in analysis and technology. The ideas that are the context for the design of experiments emerge mainly from jigsaw puzzling together of previous experimental observations, rather from theoretical concepts divorced from practice.
Bibliography
I recently wrote an account of the history of the discovery of the structure of DNA in answer to a question on SE History of Science and Mathematics. Although the main focus of that question is not relevant, it includes an extensive bibliography.

thank you very much for your answer! This was helpful.


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Sources of chlorophyll fluorescence
I have been reading this article recently, which claims that photoinhibition of photosystem II can have measurable impacts of chlorophyll fluorescence. This confused me, however, because photoinhibition (at least as the article describes it) occurs mainly in the PSII reaction center, and I had thought that the majority of chlorophyll fluorescence was caused by excitations that form in the antenna and don't reach the reaction center in time before they decay (after all, there are many more antenna chlorophylls than reaction center chlorophylls). With this in mind, how can it be that photoinhibition of the RC modifies the F0 value of chlorophyll fluorescence data?

Not an expert in this field, but a dig through the literature seems to indicate that the chlorophyll fluorescence that is generally referred to for measuring photoinhibition is indeed localized to or associated with the PSII reaction center. In case it is in question, there are estimated to be ~100 chlorophylls directly positioned within the PSII.
I don't know the basis of your supposition about the excitations that never reach the reaction center, so I'm not really sure how to address it. This paper writes that the efficiency of excitation reaching the reaction center is actually quite high in realistic physical simulations. A quantity of interest here is $L_D$, the parameter controlling how far an excitation can travel readily through a photosystem before being lost; I was not able to readily find their estimates for this value though:

Most of the LHCIIs in the mixed membrane are surrounded by PSII-S within a radius of $L_D$, which led to the 82% maximum quantum efficiency of the membrane upon uniform chlorophyll a (ChlA) excitation.

This review links chlorophyll fluorescence to PSII phenomenologically and theoretically but does not directly address the mechanism:

Changes in the yield of chlorophyll fluorescence were first observed as early as 1960 by Kautsky and co‐workers (Kautsky et al., 1960). They found that, upon transferring photosynthetic material from the dark into the light, an increase in the yield of chlorophyll fluorescence occurred over a time period of around 1 s. This rise has subsequently been explained as a consequence of reduction of electron acceptors in the photosynthetic pathway, downstream of PSII, notably plastoquinone and in particular, QA. Once PSII absorbs light and QA has accepted an electron, it is not able to accept another until it has passed the first onto a subsequent electron carrier (QB). During this period, the reaction centre is said to be ‘closed’. At any point in time, the presence of a proportion of closed reaction centres leads to an overall reduction in the efficiency of photochemistry and so to a corresponding increase in the yield of fluorescence.

In one rather blithe review, it is suggested that other sources of fluorescence are close to zero at relevant wavelengths, though they only mention PSI as a source:

At room temperature, we assume the variations in the fluorescence signal arise from PSII only and we ignore emission from PSI largely because the signal does not make a significant contribution below 700nm (Butler, 1978; Pfündel, 1998; Baker, 2008)

Looking into the Pfündel paper, they write in turn:

At room temperature, a small fraction of the absorbed light energy is re-emitted as chlorophyll a fluorescence. It is usually assumed that most of this
fluorescence is emanated by PSII, and that the PSI contribution is negligibly small (Krause and Weis 1991; Govindjee 1995)

Without following the citation trail any further, it seems that the general assumption in the field is that excitation "lost" to fluorescence of ChlA without a reaction center accepting the energy is pretty negligible. No one seems to be interested in distinguishing the total PSII fluorescence from the PSII fluorescence actually associated with reaction centers. This probably indicates that the two amounts are pretty close to identical.
For some validation of your intuition, this paper writes:

FV/FM works well for plants with Chl a/b antenna systems in which in vivo fluorescence is dominated by emission from Chl a associated with PSII. In phytoplankton, with their diverse antenna systems and thylakoid configurations, FV/FM must be interpreted with more caution [36], [52]. Taxonomic differences in FV/FM can result from contributions to the minimum fluorescence (F0) from pigments outside PSII (see e.g. [53]). Due to the fluorescence from such pigments, the measured values of FV/FM may depend on the excitation and emission wavelengths (unpublished data).

In other words, you need to be careful to account for fluorescence from non-reaction center-associated pigments but it's quantitatively not a large amount (though I haven't yet found a direct estimate despite a lot of looking!).


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Primary charge separation in Photosystem II
I was reading through an article about primary charge separation in Photosystem II when I came across the following graphic:

I assumed that the axis is measured with respect to the unexcited system, which implies that the primary excited state (ChlD1*) has energy of 2 eV more than the baseline PSII-RC. However, I also know that the light absorption of PSII peaks at $\lambda=680$ nm, and light with a wavelength of $680$ nm only carries $1.8$ eV. So how is it possible that the incoming photon seems to excite the Photosystem II reaction center to a higher energy than the photon itself carries?

Did you consider the quantum efficiency (QE)? The absorption peaks - yes, but nevertheless it's a distribution over wavelength (energy).

Oh please — "an article". If you reproduce a figure from the article, please do it and us the courtesy of citing it, preferably with a link.


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Absorption bands of chlorophyll
I am currently reading this article, which discusses the functional impact of the $Q_x$ and $Q_y$ absorption bands of chlorophyll in photosynthesis. However, the article didn't say where on the spectrum these bands exactly are. It did, however, say that the $Q_x$ band is also known as the $S_2$ band, and the $Q_y$ band as the $S_1$ band. I tried to resolve my question with some Googling, and found the following two pictures on the Internet. The problem is that these pictures seem to imply opposite things: one is claiming that the $Q_x$ band is the blue/violet part of the absorption spectrum while the $Q_y$ band is the red part, while the other claims that $Q_x$ and $Q_y$ are both red and practically superimposed on each other. So which one of these graphics can I trust? And can you point me to any articles that explain the $Q_x$ and $Q_y$ bands definitively?

Did you see this para in the article: "Historically, two different assignments of the spectra of Chl-a have
been proposed: the "traditional" 1960’s assignment identifies the
higher-energy component as the Q x origin 10,13–16
, while the "modern"
1980’s assignment selects the lower-energy one, see Fig. 2"

I don't pretend to understand the physics or chemistry of it, but I think you'll find that the Qx and Qy are vibrational states, sometimes referred to as S1 and S2, not absorption bands. Are you asking about the absorption spectra of chlorophyll or the transitional states?

@bob1: yes, but I thought that the article gave the bands in terms of $\Delta v$, a parameter in Magnetic Circular Dichroism measurements, which doesn't directly correspond to a given wavelength (I think). Am I wrong about that?

Mu might be wavenumber rather than a spectral measurement.


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Are there internal systems of organisms which acquired the functions which they were not evolved to perform?
In his research on the issue of belief formation Daniel Gilbert (1991. How Mental Systems Believe) claimed that cognition "is an evolutionary outgrowth of [perception]." What he meant is that the cognitive system processes propositional information the same (or similar) way the perceptual system processes visual images. I assume his claim implies that, apart from some of its components, the cognitive system of comprehension of communicative stimuli (utterances) uses the same subsystems of the brain which are used by the perceptual system to comprehend visual stimuli.
If my interpretation is correct, from the evolutionary point of view comprehension of the above-mentioned types of information is embodied in the same neural structures. Given that visual perception precedes perception of language, we can plausibly conclude that there is a neural structure in the brain which had evolved to process perceptual stimuli which later also begun to function as a system of processing of verbal stimuli.
Regardless of the correctness of this view, I wonder if there are any examples of the systems of an organism which were evolutionarily formed to perform some specific type of tasks and subsequently acquired an ability to perform another type of tasks? Could anyone advise on some literature related to this topic?
P.S. I hope it is clear that I don't mean the sort of acquisition of new functions which can be attributed to our motor system, which was formed to perform such functions as walking, running, grabbing, throwing, etc., and now is used to play musical instruments or paint pictures :)

Converting my comment to an answer because apparently it was what OP wanted.
The technical term for this is a spandrel, a term borrowed from architecture in a classic paper by Stephen Jay Gould.
There is considerable debate about what organismal features exactly might serve as spandrels, which is difficult to decide due to the issues with the fossil record. Examples cited in the wiki page might include the human chin, or language. However if we consider exaptations more broadly (another possible term that includes spandrels), there is potentially a very wide set of traits that might be considered spandrels.

The answer indeed helped me a lot, although the question touched a little bit different aspect of the issue. What is really useful in the approach of Stephen Gould is his critique of what he called adaptationism, which claims that every trait of an organism has some adaptive features. My hypothesis, based on the Gilbert’s account of belief formation, is that some traits are not adoptive, but are emergent characteristics of systems of organisms which really are adoptive. Recently, I have read a similar point made by Jonathan Heidt regarding reasoning and moral judgement (see the next comment).

“Most propose that the building blocks of human morality are emotional [...] and that some early forms of these building blocks were already in place before the hominid line split off from that of Pan 5 to 7 million years ago. Language and the ability to engage in conscious moral reasoning came much later, [...] so it is implausible that the neural mechanisms that control human judgment and behavior were suddenly rewired to hand control of the organism over to this new deliberative faculty.”
(Heidt, J. (2007) The New Synthesis in Moral Psychology. Science 316. P. 998)


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Are there limitations in using DNase I hypersensitive sites (DHSs) to identify candidate enhancers?
Candidate enhancer regions are often defined in studies by DHSs and/or certain chromatin marks. I was wondering if DHSs are exhaustive for identifying possible enhancer regions, and if there is any work out there demonstrating enhancer regions in areas not sensitive to DNase 1.


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Can the concept of fisherian runaway be explained using simple models?
I want to understand the concept of fisherian runaway. Dawkins' book tells about this, but it's not clear enough. It can be seen that the essence of Fisher's idea is that when a male peacock with a large tail leaves offspring, these offspring receive not only large tail genes, but also genes of “love for big tails” in females. But it is not clear how positive feedback follows from this.
Let's consider a simple model. There are 100 males and 100 females in a peacock population. 80 males have long tails, 20 males have short ones. 80 females prefer long tails, 20 short ones. Further, obviously, 80 first males and 80 first females will give offspring with long tails, and accordingly 20 males and 20 females - with short ones. Thus, in the next generation, 20% of cubs will be born with short tails, and since having a short tail is beneficial from an utilitarian point of view, over time, these 20% will crowd out the remaining 80%.
Now suppose that peacocks are not monogamous, but polygamous. 1 male with a short tail will fertilize 20 females, and 4 males with long tails, respectively, 80 females. So far, nothing has changed.
Now suppose that polygamy is even more pronounced, and instead of 4 males with long tails, the harem belongs to one. And here the principle “for everyone who has will be given more, but the one who does not have, even what he has will be taken away from him”, which Dawkins mentioned, can work. Since this supermale with a long tail has 80 females, the fact of his popularity serves as additional advertising for the remaining 20 females. It works that, when all other things being equal, it is better for a female to choose a male that other females have already chosen (such a principle, on average, does more good than harm). Accordingly, this supermale will have additional females from among the remaining 20.
Is this really all that Fisher's model suggests? This argument seems to me not very convincing. Can someone apply my approach (counting the number of males and females) to correctly explain Fischer's ideas?

Remember that Fisherian runaway is an explanation for a thing that happens; in particular, it explains why it's stable when it happens. It's not a claim that this always happens for all traits.

I don't think the last statement of your second paragraph holds true necessarily. The long tail is obviously useful in that it attracts females, therefore mating, so it won't get out-competed by short tails.

Dawkins and Weinstein discussing the topic.

your numbers don't add up, 80 males have long tails, 20 males have short ones. 80 females prefer long tails, 20 short ones. means way less than 20% of the next generation have short tails, because males don't encounter every female but only a small percentage, a large portion of your short tailed males may never encounter a short tail preferring female. thus many will fail to reproduce, likewise female may fail to reproduce or settle for long tailed males because that is all they encounter.

Now consider the simplest form of this, mating calls, making noise that attracts mates also attracts predators, but not finding a female mean your genes die out so even risky behavior that also increases your chances of finding a female will have huge gains as long as the chance of encountering a female without it is low.


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What amount of light energy is required to produce one O2 molecule? How about one molecule of NADPH?
I know that for each O2 molecule, a total of 8 photons are required (4 per photosystem). Would the amount of light energy required be E=hc/wavelength using 680 and 700? Or would the energy from the initial incident light need to be taken into account (as in when light initially hits the photosystem and gets funneled down)?
Additionally, I know that one NADPH  is produced per 2 electrons. I am puzzled as to how this can be transformed into light energy? Would the amount of light energy required be that of PSI and PSII once again, due to the Z-scheme that ultimately leads to the NADPH production?
I appreciate any help.


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Why is it that guttation is most commonly observed in the morning?
Knowing that guttation occurs through a plant's hydathodes due to root pressure forcing liquid water out of the leaves, I am curious as to why so many small drops of water are observable on plants in the morning. Could this potentially have to do with the moisture in the air at night vs day? Since humidity tends to increase at night?
Thanks in advance!

Perhaps you are thinking of the atmospheric phenomenon called dew, which is not caused by plants, or limited to them: https://en.wikipedia.org/wiki/Dew

I don't think so, these are two different phenomena as guttation is water coming out of the plant while dew is condensation of air on the plant! But perhaps their cause is related.

I understand the difference.  What I'm saying is that dew is a far more likely explanation for those small drops of water you observe, especially if they are on things other than plants.

You should add an image if you're trying to convince us that you're talking about guttation vs just dew formation.

I am asking due to a specific question brought up in a lecture, where the professor gave us a prompt of "why is guttation observed most commonly in the morning?". Here is a picture of the slide as well as the portion of my textbook discussing this phenomenon, I am confident I am speaking of guttation. https://imgur.com/a/Pdk7g

@jamesqf I know it's just anecdotal evidence, but I have a Monstera deliciosa in my room and I see it guttate way more in the morning, sometimes by night, never by day. In this case, it just cannot be dew.

Guttation is commonly seen at night and early morning. Plants release excess of water via the guttation. During day time as the transpiration rate increases, excess of water is released via transpiration and hence guttation decreases. Also due to high temperature these small droplets are quickly evaporated during day time.

The stomata are mostly closed at night and early morning. Early morning rising temperatures cause efflux of H2O from the hydathodes while stomata are still closed, and by the time the stomata are opened, the efflux switches to the shorter route through the stomata.

Hello! I fear that your answer isn't really different from the Jim Young one, and, as such, it may attract downvotes. If you like it (as it seems) go upvote it :) and elaborate on something that has not already covered by existing answers (for instance none of the answers provide references).


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Lab technique to distinguish between single stranded and double stranded DNA?
What lab techniques exist to differentiate between single-strand and double-stranded DNA?

Welcome to Biology.SE! We encourage you to do some research on your own and then ask questions informed by what you have learned (ideally with references to reliable sources). For instance searching with "differentiate between single-strand and double-stranded DNA" led me to this. ——— Please also take the time to go through the [tour] and the help pages starting with [Ask] questions effectively on this site. Thanks!

Single and double stranded DNA have different electrophoretic mobilities, ssDNA will move faster on an agarose gel, so if you know the length of your DNA and it moves further than you expect
 relative to a dsDNA ladder it's probably ssDNA. The hyperchromic effect means that ssDNA also absorbs more strongly than dsDNA, so you can heat up your DNA and if the absorbance changes it was dsDNA and if it doesnt then its ssDNA (you should take an aliquot for this so that you have the rest of your sample in tact). You could also take an aliquot and add a single stranded exonuclease and run the products on a gel together with the DNA before the digestion, if nothing is present after in the digested well then you had ssDNA if there is still a band after then you had dsDNA (i don't think this method is really used as you could just run it on a gel which is simpler and you lose less sample, but it should still work).

+1 but I'd like to add an important caveat:  intercalating dyes that allow visualization of dsDNA on a gel may not bind strongly or at all to ssDNA.  So if OP does plan on doing gel visualization of mixed single- and double-stranded nucleic acids, consider using a dye like ethidium homodimer-1 or -2. Good source for dye selection here.

yes thats true you do definitely see a weaker band, so you do have to load more DNA or use a more sensitive dye. I've done with a couple of 100 ng with sybr safe and that has been fine, but it depends if you have that to spare.

@Dirigible Actually the fact that certain dyes bind ssDNA & dsDNA with different strenght can itself be used to differentiate between them. (As long as concentrations are known / comparable). Many qPCR systems also rely on that to measure melting curves, i.e. using dyes like SYBR

@pepsiandsoda I have a doubt...Wouldn't the absorbance also change for ssDNA as we heat it because it is also in some weird coiled shape and that shape must be due to hydrogen bonds which might not let the ssDNA to absorb the light fully. With increase in temperature, these bonds will break and absorbance must increase, although the increase might be small...


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Are controls needed for urine cultures?
If testing for bacteria (gram-negative) in a urine culture, are negative or positive cultures needed?
I could not find anything that says controls are needed unless results seem to be contaminated. I thought since controls are used in Gram stains, they would be used in cultures as well. Thanks!

No, controls aren't needed for a diagnostic test of that kind, since the only concern is about that urine specimen. The result will be either positive or negative; if positive, the urine will be plated and the bacteria will be tested for antibiotic sensitivity. The same is true of blood tests, MRIs, Xrays (although in some pediatric cases, the unaffected side acts as a comparison), etc.

that makes sense, thank you so much!


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Why does atrazine kill photosynthetic bacteria and not nonphotosynthetic bacteria?
Atrazine was found to bind to Qb, which is involved in electron transport to create ATP in photosynthetic bacteria.
Why does this herbicide kill photosynthetic bacteria, while having little to no effect in nonphotosynthetic?

Is this possibly just because electron cycling creates energy in photosynthetic, and non-photosynthetic heterotrophs use a different mechanism to create ATP?


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Searching for reference regarding the impact of famine on a woman's grandchildren
I was once told that if a woman experiences a famine, her grandchildren will show epigenetic changes because the egg that the intervening mother came from also experienced the famine.
In other words, the grandchild would be more susceptible to obesity, due to the grandmother's nutritional environment, even though the famine might have been 40-50 years distant.
However, I can't remember where I heard this, and could not locate a reference.

Welcome to Biology StackExchange. Take a look at Transgenerational epigenetic inheritance. Plenty of explanations and references.

Here's an article in Science about the phenomenon:
https://www.science.org/content/article/moms-environment-during-pregnancy-can-affect-her-grandchildren
It references a variety of different studies, not sure which you are most familiar with, but they include a population study of Dutch children whose grandmothers were pregnant with their mothers in 1944 and some more mechanistic studies in mice.


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What really causes the toxicity of wrongly-thawed meat?
(Note: I've seen multiple related questions over at Cooking.SE, but I'm looking for a scientific explanation, not cooking advice!)
I've been researching this for a couple of hours but the more I read, the less I seem to understand the situation. Many sources claim that thawing meat in warm water is wrong and that I should instead opt for cold water to prevent bacteria from growing and producing toxins. I found a wide variety of toxin-producing bacteria that can live and reproduce in meat, such as Escherichia coli, Salmonella, Corynebacterium diphtheriae, Listeria monocytogenes and Clostridium botulinum.
There are two things I don't understand:

If I thaw the meat quickly, the bacteria have less time to reproduce before I cook the meat. This is especially true for Listeria monocytogenes which seems to be able to quickly reproduce in cooler temperatures. Why is it bad to thaw meat in warm water?
If the sources I've read are true, it leads me to believe that Listeria monocytogenes is not a bigger issue than the other species of bacteria growing in the meat. I suspect that bacteria compete for resources and that it is probably only one of them that is the main factor in making a piece of meat toxic for consumption even after cooking. What is the primary cause of meat toxicity?

Or is it possible that I've been overanalyzing the situation and the exponential relationship between bacterial growth and temperature is the main reason?

Not a full answer, but my impression was always that it was a temperature gradient problem. Thawing meat in warm water or at room temperature puts the outer layer of meat in the "danger zone" while the inside stays frozen. By the time the center is defrosted, the outermost meat isn't well-refrigerated anymore.

This is a really fascinating question and got me reading stuff all through the night. If my response seems tl;dr, then please skip to the fourth paragraph.
From what I've found in literature, it may be the case that prolonged exposition to certain temperature ranges may prove lethal to some pathogens. Shortening this time or shifting the temperature may cause suboptimal death rate of microbes. El-Kest et al. have found that Listeria monocytogenes would be most effectively killed by 5 to 6 freeze-thaw cycles with 35 degrees C as the thawing temperature and -18 degrees as the freezing temperature. Freezing at -198 degrees proved way less successful in killing the bacteria. This suggests that not only the thawing temperature and rate have the influence on microbial diversity in meat but also the actual temperature of storage!
Here is the link to the publication by El-Kest et al.: http://jfoodprotection.org/doi/pdf/10.4315/0362-028X-55.8.639?code=fopr-site
Freezing rate also has a significant influence. If freezing occurs slowly, ice crystals will mostly appear mainly outside cells with rapid freezing having the exact opposite effect. It is quite logical why it happens: spots within the food that are freezing will slowly make the unfrozen surroundings rich in ions and osmotically active substances, the water will gradually seep out from bacterial cells to the surroundings and subsequently freeze up. (https://books.google.pl/books?id=o6kJCAAAQBAJ&pg=PA25&lpg=PA25&dq=Inactivation+by+cold.+In+Inhibition+and+Inactivation+o+f+Vegetative+Microbes.&source=bl&ots=zlH-dMFiqo&sig=AfglM7piuvMnjI3q3JV0ovHy-FE&hl=pl&sa=X&ved=0ahUKEwjS-6fAypTYAhWiJJoKHe-gDJAQ6AEIQTAE#v=onepage&q=Inactivation%20by%20cold.%20In%20Inhibition%20and%20Inactivation%20o%20f%20Vegetative%20Microbes.&f=false)
From that perspective slow freezing is more likely to get microorganisms killed, as there is no cold-shock response and the cells do not become desiccated prior to freezing.
Now, let's look at the big question: why can't we use warm water to thaw meat. As one of the commenters pointed out, there is something called "danger zone" in frozen food safety, in fact USDA keeps talking about it all the time. This might be counterintuitive but by rapidly increasing the temperature in outer layers of meat, you will quickly provide microbes with ideal conditions for cellular division. As time progresses each next layer will be infested by bacteria from the outer layer as well as those that will just start undergoing cellular division, and so on, and so on, until you reach the very center. You end up with a pretty nice bunch of bacteria throughout your meal, though you shouldn't probably worry to much about it, unless you like your meat half-raw.

What happens during cold-water thaw or refrigerator thaw is different because you essentially increase the temperature of each consecutive layer but without providing enough thermal energy to give microbes a near-optimal temperature for intensive cellular division. Sure, they will start dividing anyway but to a much lesser degree. The temperature increase is not rapid therefore there is no abrupt resumption of life-cycles of microbes. Think of it as waking up on a cold winter day vs. warm, pleasant summer morning.

Still, you can use hot-water thaw safely if you're dealing with thin cuts of meat, if fact USDA approves it: http://onlinelibrary.wiley.com/doi/10.1111/j.1750-3841.2010.02037.x/full
Further reading:
https://www.fsis.usda.gov/shared/PDF/Big_Thaw.pdf
https://link.springer.com/content/pdf/10.1007/978-1-4615-5975-7_10.pdf
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4662152/

Now, regarding your second question, I'll mostly answer from my own experience. We used to test meat in our microbiology lab during studies and we tested different kinds of meat. Teachers who teach the subject for 10+ years, when asked, admitted that there is generally a pattern of how many bacteria and what types of bacteria populate different kinds of meat, so there is no safe way to say that there is a single major pathogen that is responsible for food poisoning from meat in general. I'd say what's most dangerous are exotoxins produced by those bacteria, e.g. botulinum toxin is the most potent toxin known to mankind and Clostridium botulinum loves to populate meat stored at room temperature. Listeria is a popular example because of its great survivability in cold temperatures. But it really depends on the kind of meat and even on the specific batch of meat. You simply never know what you'll get with it.
Either way, you were not just overanalyzing the topic. There are really many factors to the quality of food preparation safety, especially when it comes to meat. To summarize:

Hot-water thaw can be used for thin slices of meat (I still use it for bigger slices as well, but only if I'm certain I'll fry the meat very thoroughly)
Cold-water thaw is better due to lower probability of serious bacterial infestation, especially recommended for thicker slices of meat
Freezing as well as thawing rate both influence meat quality
Freezing temperature cannot be too low, nor too high to ensure optimal death count of certain species of bacteria
Meat toxicity is generally caused by pathogenic bacteria that multiplied within or were previously present (e.g. due to improper meat handling by the producer), in most cases due to the toxins produced by the bacteria

Hope I helped a bit :)
[EDIT]
There was a request in the comments to include some more info about the toxins produced by food-borne pathogens. There's a good review here:
https://www.ncbi.nlm.nih.gov/pubmed/8750662 (not sure if paywalled though, I'm using library internet right now). You could group those toxins into 4 arbitrarily defined groups:

heat-liable enterotoxins – these generally can be destroyed in the process of cooking or frying; produced by Salmonella spp., E. coli, Campylobacter spp., Vibrio cholerae (yes, this one causes cholera)
heat-stable enterotoxins – these cannot be efficiently removed by heat preparation of food; produced by Yersinia enterolytica and some strains of E. coli
Shiga-Like toxins – they resemble verotoxin of Shiga spp.; produced by E. coli O157:H7 (this strain is very pesky, as it induces hemorrhagic diarrhea and kidney failure)
Unique toxins – some bacteria produce unique toxins, e.g. Bacillus cereus, Clostridium botulinum, Clostridium perfringens

Generally E. coli strains have many subtypes of heat-stable as well as heat-liable enterotoxins and some strains have other types of toxins like the O157:H7. The name "enterotoxins" refers to toxins that are secreted by microorganisms targeting intestines and generally they are cytotoxic, which essentially means they cause cell lysis of the host. Mechanisms of action are varying, e.g. cholera toxin triggers a cascade of reactions that overdrive CFTR channels (chloride ion transporters) and alters osmotic balance, which macroscopically manifests itself by a production of characteristic watery stool.
Worth noticing: some of those pathogens require other factors to cause disease, e.g. Vibrio cholerae requires a toxin-coregulated pilus to be pathogenic and some even do not produce any toxins directly (for instance Listeria monocytogenes overdrives lysosomes and doesn't let them take the bacterium apart, then it spreads from cell to cell by the means of actin filaments).
In the context of detox diets, there is a large dispute going on about their effectiveness whatsoever. I'd recommend confronting these two articles, which, to me are well written:
https://link.springer.com/chapter/10.1007/978-3-319-49929-1_33
http://onlinelibrary.wiley.com/doi/10.1111/jhn.12286/full
Some animal models have indeed shown some anti-toxic effects of certain foods, other researchers argue that most of the toxins eventually get to the liver and get broken down. The liver does its job pretty well, so running for two weeks on a "kale juice" would be a bad idea. People seem to forget that usually the dose is the poison: if you ingest highly diluted cyanide, it won't harm you, while drinking 7-8 liters of water at once could kill. Switching to an unbalanced, monotonous diet could be actually detrimental to health a lot more than those minuscule amounts of food-borne toxins ingested. The best way to live a healthy life is still: move, eat well and diverse, follow food safety guidelines, take care of your physical and mental health.

Thanks, that's a great answer. Did you learn something about the toxins which you didn't include? If so, could you add it? The reason I'm asking is because I think the internet is full of posts mentioning unspecified toxins (especially on non-scientific forums), but no one ever bothers to do the research or there are no toxins in the first place (detox diets etc.). Your answer is different, which is awesome, but if you can add more, that would be great.

I've updated the answer with what I found on the topic, hope you find it helpful ;)

Thank you, here's your bounty, you very much deserve it. And I learned some pretty cool stuff too!

Thanks for the bounty and for the question. I love questions that make me learn too, so this one was splendid ;)


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Is swimming pool water actually a weak topical medication?
I was inspired by this question.
Given that the chlorine levels in swimming pool water are so high that they can seriously harm amphibians, it seems logical that the water should also kill various microorganisms, fungi or skin parasites.
Is the swimming pool water a weak disinfectant? Are there any illnesses for which a doctor would prescribe a full-body bath in a swimming pool for this reason?

No, there are not. If a doctor wanted to treat a patient with dilute chlorine, they could have the patient put several drops of household bleach into a cup of water (or an ounce into a full bath) and soak in that. However, bleach damages skin as well (if you put your fingers in bleach, they feel slimy afterwards. That's dead skin cells that have been broken down by bleach.) So usually we don't disinfect humans (just materials) with bleach. There are less damaging disinfectants for skin and wounds.

@anongoodnurse Your comment is probably a sufficient answer for this question, so maybe you should post it as such so that I can answer.


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Sound volume drop when falling asleep in an airplane
Note: This question has nothing to do with pressure change.
When I'm flying in an aircraft at cruising altitude, the monotonous sound often lulls me to sleep. I've noticed that just as I am on the verge of drifting off, the perceived sound volume drops significantly. I then notice what is going on and the thought awakens me a bit and the volume snaps back to normal. I verified that the actual noise in the airplane stays constant while this happens.
I always try to hold on to the state where the sound is quieter, but it is very difficult to do while at least a bit conscious. That's why I suspect that it could be part of the process human brain goes through normally when falling asleep. Perhaps it happens every time, but I do not notice because I only ever sleep in such a noisy environment when flying.
I asked a bunch of friends and some of them experience the same phenomenon. I was unable to find any relevant scientific literature mentioning it, though.
What causes this fascinating phenomenon? Does it have a name? Has it been studied?

Cruising planes do throttle down sometimes which does decrease the sound level. Is it possible that the causality is reversed? That is, you are trying to sleep and are finally able to drift off when the noise level decreases.

@CharlesE.Grant I have ruled that out. The actual volume stays constant the whole time. The people sitting next to me never perceived any change. If the plane's engines were throttling up and down like that, it would be called surging and the plane would be in big trouble. I am absolutely certain that this is something that happens to me, not the airplane.

Have experienced this myself.  It is as if the part of the brain responsible for sensing or initially processing the sound falls asleep a bit faster than other parts involved in monitoring that sound consciously.  Sound fades out then suddenly slams back to full volume along with full awakeness.

Is it possible that you are equalizing the  pressure in your ear canal unknowingly when the perceived volume changes? The pressure differential between the external and middle ear is an important factor in hearing ability (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3985947/) , so that might be related.

@ASimonis Not unless drifting in and out of consciousness changes the pressure somehow, which I doubt. Moreover, this is happening during the most boring parts of the flight at cruising altitude when the pressure is unchanging and I'm already accustomed to it. It also felt distinctly... software-caused.


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How does one calculate Rx/a in population genetics?
The ratio of sex-linked to autosome mutation frequencies (R) is Rx/a =(2/3)(2+ α)/(1+ α) for X-linked genes and Ry/a = 2 α /(1+ α) for Y-linked genes. How does one calculate Rx/a, in order to find α?


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Does inoculum volume affect spread plate outcome?
Background
The spread plate method is a technique used in microbiology to enumerate and isolate bacteria or other microorganisms present in a sample. It involves evenly spreading a liquid sample containing microorganisms onto the surface of a solid agar medium in a Petri dish.
Inoculum Density: Inoculum density refers to the concentration or density of microorganisms (bacteria, fungi, etc.) present in the sample that is being plated onto the agar surface. It is typically measured as the number of colony-forming units (CFUs) per unit volume of the sample.
Inoculum Volume: Inoculum volume refers to the volume of the sample that is spread or plated onto the surface of the agar medium during the spread plate method. It is typically measured in microliters (µL) or milliliters (mL).
Question
Does inoculum volume affect spread plate outcome?
If I pipetted 0.1ml 0.5 McFarland of bacteria into the agar plate before spreading, would it differ from pipetting 0.5ml of the same density?

Theoretically, for CFU determination the volume of the inoculum shouldn't matter as long as you plate a dilution series and find the plate with a countable number of colonies. It also shouldn't matter if you use the spread-plate method or the pour plate method or something else (like drop plates or spiral plates). But all of that assumes ideal conditions where you are able to get a perfect and uniform spread over the whole plate every time. In the real world there are practical limitations on the range of usable inoculum volumes when spreading liquid onto agar plates.
When making spread plates it's best to maintain continuous spreading motion until all (or almost all) of the liquid from the inoculum has been absorbed by the agar medium. If you don't, you can end up with unevenly distributed colonies, which can make otherwise countable dilutions difficult or impossible to count accurately. If the volume is too large, it may take an impractical amount of time for the liquid to absorb. On the flip side, the volume still needs to be large enough to cover the whole plate evenly. If it's too small (say 10µL) you may have trouble spreading it evenly across the entire surface.
There's also some potential for variation in consistency when dispensing different volumes. Most micropipettes are slightly more accurate at the high end of their range than the low end. So, IF you were using the same p1000 pipette, your replicates could be slightly more consistent with larger volumes than small ones. But, properly calibrated, the dispensed volume should vary by less than 10% even at the lowest setting of most pipettes, and if this were a concern, it could be remedied by switching to a more appropriately sized pipette.
Lastly, if you are trying to make a bacterial lawn, for something like a Kirby-Bauer test, changing the inoculum volume can affect the outcome of the test. McFarland standards aren't always perfectly calibrated for every organism, but overloading the plate with 5x the standard inoculum certainly has the potential of skewing the test results. The methods for these tests are standardized to improve repeatability between labs. Essentially, a denser inoculum will reduce the size of the inhibition zone, while a reduced inoculum will increase the inhibition zone. Since the inhibition zone determines whether a particular isolate is classified as resistant or susceptible to a given drug, inoculation protocols are standardized to make sure patients receive the appropriate care.
Source: EUCAST Disk Diffusion Method for Antimicrobial Susceptibility Testing  - Version 9.0 (January 2021)

Thanks for the great answer. I'm trying to do the last: bacterial lawn for Kirby-Bauer test. Could you reconsider that it won't affect kirby-bauer test? I'm saying this by gut feeling. It must have to do something with the McFarland standard concentration being fixed at 0.5 for the kirby bauer.

@FreezingSoul I see. It's worth mentioning that AST protocols typically call for inoculating lawns with sterile cotton swab dipped in the bacterial suspension, rather than spreading a specific volume on a plate. I'm sure there's some variation in the actual volume transferred from the swab to the plate, but probably not on the order of the 5-fold difference specified in your question. See updates to my answer for more specifics on how inoculum density can impact the observed inhibition zones (I confess that I haven't evaluated those statements personally).

I tried to keep the question as abstract as possible so more people would benefit from it. But, my problem is that I think my agar soaks the 0.1ml so fast that I don't have time to spread it. Maybe because I dry them by incubating them for 24 hours after pouring, which I don't plan to give up, because it's primarily a sterility check. Is there any problem if I add my 0.1 inoculums to some 0.5ml saline before spreading and spread the whole 0.6ml, since i can't withdraw more inoculum volume?

i think nevermind, the problem may be that i waited to too long for the spreader to cool, it says in a textbook that you got 15 seconds after pipetting the inoculum to spread otherwise the water will be soaked.

To add to the answer by @MikeyC . The spread plate technique for calculation of colony forming units has volume plated as a variable:
CFU/ml = (number of colonies x dilution factor) / volume of culture plated
This means that you account for the volume in the calculation performed after doing your counting.
Of course, as MikeyC mentioned, the volume matters to some extent as if you add too much of too high a density suspension, then you will have an uncountable plate. To compensate for this, what is usually done is a dilution series, where you choose which dilution is used for the calculation This also provides a secondary check on your count, as a plate below (lower dilution) the countable dilution should be TMTC and the one above should have approximately 1/(dilution factor) fewer colonies. For example, in a 10-fold dilution factor series, your countable plate might have 50 colonies, the one below should have ~500 (TMTC) and the one above should have about 5.
You should also note that the dilution factor is also compensated for in the equation.


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What's pooling in the spread plate technique?
"Distributing the organisms by rotating the spreader rather than the plate tends to cause more pooling of the inoculum."
https://asm.org/ASM/media/Protocol-Images/Preparing-Spread-Plates-Protocols.pdf?ext=.pdf

Forming a pool (second definition in link); forming a small amount of liquid on a surface. A la "I knocked my cup over and the coffee formed a small pool on my bench"
Basically this results in a concentration of the organisms in one area, rather than an evenly distributed spread.


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Is there a reliable method to determine if heat fixation was inadequate before proceeding with further staining steps?
Background
Heat Fixation: Heat fixation is a technique used in bacteriology and other biological sciences to affix bacterial cells or other microorganisms to a microscope slide. This is achieved by carefully passing the slide, smeared with the specimen, through a flame. The heat kills the microorganisms, causing them to stick to the slide. Heat fixation helps to preserve the cellular structures and prevent them from being washed away during subsequent staining procedures.
Simple Staining: Simple staining is a basic microbiological technique used to enhance the visibility of microorganisms under a microscope. It involves the application of a single stain (usually a basic dye) to the specimen, which imparts color to all cells, making them easier to see. This technique is called "simple" because it involves only one staining agent. Simple staining provides contrast between the microorganisms and the background, allowing for better visualization and examination of their morphological features. Examples of basic dyes used in simple staining include crystal violet, methylene blue, and safranin.
Question
Is there a reliable method to determine if heat fixation was inadequate in bacteriology before proceeding with further simple staining steps and microscope inspection?

I work with a teaching group who has looked at this, specifically for the aim of making things easy for undergrad labs in under-resourced countries, where gas and/or Bunsens or alcohol burners might not be available.
It turns out for most commonly used bacteria (E. coli, Staphylococcus, Streptococcus, Bacillus etc.) and on regular glass slides with common stains  such as Gram stain, crystal violet, endospore etc. it is the drying that is most important, heat "fixation" just ensures that it is dry enough to not wash off during the subsequent staining steps. The vast majority of stains contain a step (often involving alcohols) that will kill many of the common pathogenic bacteria adequately for most purposes. The step where you are more likely to contaminate yourself is usually during the picking and spreading on the slide, before the heat fixation anyway.
Thickness of film helps here, if you have a thin film, it will dry quickly and adhere, but a thick layer (which you usually don't want anyway) won't dry adequately, and (assuming using the drop technique, not Coplin jars) acts as a barrier for liquid flow which means it is more likely to wash off during wash steps.
Most bacteria are too small to make out a lot of internal structure with basic stain techniques and using 100x oil immersion objectives.
So; let it dry. Instead of a 10 min wait, this might be a 30 min wait, but it works!

wow one of the most valuable things that i learnt on this site, and I forgot to accept the answer, If a bad thing happens to me, i had it coming.


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What are pit fields?
I found this statement from my biology text book,

"The sieve tube elements and the companion cells are connected by pit fields present between the common longitudinal walls".

Is the pit field same as Plasmodesmata ?

Pit vs plasmodesmata
From wikipedia > pit

Pits are thin portions of the cell wall that adjacent cells can communicate or exchange fluid through, utilizing plasmodesmata.

The definition of "pit" is therefore very related to the one of "plasmodesmata". From wikipedia > plasmodesmata

Plasmodesmata (singular: plasmodesma) are microscopic channels which traverse the cell walls of plant cells and some algal cells, enabling transport and communication between them.

I think the following quote (from wikipedia > plasmodesmata again) will help you to distinguish pits from plasmodesma

Primary plasmodesmata are formed when portions of the endoplasmic reticulum are trapped across the middle lamella as new cell wall is laid down between two newly divided plant cells and these eventually become the cytoplasmic connections between cells. Here the wall is not thickened further, and depressions or thin areas known as pits are formed in the walls. Pits normally pair up between adjacent cells. Plasmodesmata can also be inserted into existing cell walls between non-dividing cells (secondary plasmodesmata)

Pit field
A pit field however is just an area where there are plenty of pits! From Merria-Webster

[A pit field is] an area in the wall of a plant cell in which one or more pits develop

Pit field is thin depression in primary cell wall whereas pits are depressions in secondary cell wall. For example Companion cells and sieve tube elements are living cells having primary walls. They are connected by pit fields. Note that pit fields are also characterised by presence of plasmodesmatal connection.

Welcome Mudasir, in addition to the advice in the answer banner, you should take our wonderful [tour] and refer to the [help] as and when for guidance. Enjoy the site.


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Difference between bacteria and bacteroids?
During nodule formation Rhizobium is converted to bacteroids. What's the difference between them?


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Are mesophyll cells the same as parenchyma cells?
I read in my biology textbook that ground tissue is constituted by parenchyma, collenchyma and sclerenchyma.It was also mentioned that, in leaves the ground tissue was made up of thin walled chloroplast containing cells called mesophyll cells.


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Can crocodilians differentiate their offsprings from other young crocodiles?
I read that some species of crocodilians can take care of their young for as long as a year.
How do parents differentiate their offsprings from other young crocodiles? Smell, appearance, sound?

Crocodiles have very keen hearing and can hear their babies calling from inside their egg. I believe mother crocodiles recognize the sound of babies after they hatch also.

Why do you think they differentiate?

So there's actually a master's thesis about this:
Giddings, Lydia Dashley. 2019. “Behavioural Response to Juvenile Distress Calls as a Measure of Extended Care in Crocodilians.” Master of Science, University of Bristol.
Crocodylus siamensis mothers respond to playbacks of their own offspring's distress calls about 86% of the time, but to unrelated conspecific offspring distress calls about 5-14% of the time. (I couldn't easily figure out the sample sizes, anyone who wants is free to dig through the thesis themselves ...)

Table 3.15. GEE (binomial model) output for C. siamensis response rate to unrelated young distress calls (20 cm, 60 cm and 160 cm) compared to offspring distress calls (55 cm). Note: B= unstandardized regression coefficient. S.E.= standard error.

(Table is slightly abbreviated; B is in log-odds units, EMR = "estimated mean response".)
Caller body size   B   S.E.  lower_CI upper_CI   p       EMR lwr_EMR   upr_EMR
20 cm            -4.71 1.49 -7.62     -1.79      0.002   0.05     0.01  0.18
60 cm            -4.54 1.45 -7.38     -1.69      0.002   0.06     0.02  0.19
160 cm           -3.64 0.88 -5.36     -1.92      <0.001  0.14     0.12  0.16
offspring                                                0.86     0.57  0.97

Interesting paper! It looks like for some species there were 1 or 2 adults tested (not necessarily breeding pairs), and as few as 1 juvenile of each size. The author also says: Both relatedness and species likely influence C. siamensis’ responsiveness to distress calls. However, due to time constraints the influence of kin discrimination within same species calls on C. siamensis responses could not be conducted in this study.

When we carried baby crocs through the holding area at my first zoo, which has 24 species of crocodilians, adults of all species would react to their little distress calls, which are very specific to the hatchling age: https://www.britannica.com/video/22026/Crocodiles-hatchlings-produce-sounds-mother.
Adults of any species will protect very young hatchlings (under about a year) but once they get over a certain size, they are fair game. I've never seen evidence of parents differentiating their own offspring from others. There are mixed species exhibits of young and adults: https://www.alligatorfarm.com/crocodiles-as-parents/.


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Insect identification - Possible grasshopper or grass beetle
We found a small insect on our window and we cannot decide whether it is a type of grasshopper or grass beetle. It doesn't seem to want to fly, but was on a first floor bedroom window, and walks slowly and has a strong grip on the window and petri dish. We live on the outskirts of a town in Essex, UK and it could have come from a field, but they are on the other side of the house. It is a small brown insect (the main body is approximately 2cm long) with 6 legs, and the back 2 legs seem to bigger than the others.

Neither beetle nor grasshopper, it is a hemipteran, Coreidae. Leptoglossus occidentalis or
Western Conifer Seed Bug.  https://www.britishbugs.org.uk/heteroptera/Coreidae/leptoglossus_occidentalis.html

This idenification looks good. Insects of this genus seem to have  variable spine arragements on their femurs. I'd like to know more about that.


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What is known and what can be measured of biofilms?
Context for the question
I am a mathematics researcher working on the mathematics of imaging and parameter estimation (inverse problems). I found an interesting diffusion equation that models the growth of biofilms. A question I am interested in: Given some measurements of the biofilm, and assuming the mathematical model is accurate, can we deduce the coefficients in the model? This, however, is not the question I want to ask here.
Please pardon nonstandard use and misuse of biological terminology and gaps in knowledge; this is by no means my field. I have never done biological experiments in a laboratory, for example, or studied any university-level biology.
The model
Let us assume a simple scenario where we have a biofilm and some substrate it consumes to grow. We consider a surface where the model should tell how fast and to where the biofilm grows. The parameters in the model are:

$d_1$ substrate diffusion coefficient;
$d_2$ biomass diffusion coefficient;
$K_1$ maximum specific consumption rate;
$K_2$ biomass decay rate;
$K_3$ maximum specific growth rate;
$K_4$ Monod half saturation constant (relative to initial data $S_0$);
$a$, $b$ biomass spreading parameters.

The quantities that are solved from the equations are the following, both of them scaled so that $0 \le M, S \le 1$. Both of them are functions of space $x$ and time $t$, which I omit from the notation.

$S$ is the concentration of the substrate that the biofilm feeds on
$M$ is the biomass density

The governing equations are the following, with some boundary conditions I will not specify here:
$$
\begin{cases}
\partial_t S = d_1 \Delta_x S - K_1 \frac{SM}{K_4+S} \\
\partial_t M = d_2 \nabla_x \cdot \left( \frac{M^b}{(1-M)^a} \nabla_x M \right) - K_2 M + K_3 \frac{SM}{K_4+S}
\end{cases}
$$
The questions
Can both $M$ and $S$ be measured with fair accuracy in laboratory conditions? How is it done and how reliable is it? Can the experiments continue afterwards, or does the measurement significantly alter the experimental set-up in some way (by for example destroying the biofilm or mixing the entire thing etc.)?
Of the parameters in the model, which are well-known?
I suppose the answer to last question depends on whether the biofilm is of known or unknown nature, and in the case of an unknown substance, only $d_1$ might be known. What about a known kind of biofilm?


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Why do bananas grow curved?
This old common question is still not clear to me. I got this explanation:

Bananas go through a unique process known as negative geotropism. Instead of continuing to grow towards the ground, they start to turn towards the sun. The fruit grows against gravity, giving the banana its familiar curved shape.
But why? The answer lies in the botanical history of the banana. It originated in the middle layer of the rainforest, where there is little sunlight. If the fruit were to grow towards the small amount of light that penetrates sideways through the vegetation, the plant could overbalance and topple over.
So bananas developed a way of growing towards the light without destabilising the plant.

source
So, evolutionarily, the bananas are 'forced' to grow towards the light. But how is this capabilty 'grown into' the banana? Is it something epigenetic or is it just light that attracts them? So how does this mechanism works?

The last paragraph makes the question a little unclear. Are you asking "why" in the sense of "what are the evolutionary forces that pushed the banana to grow like that?" or in the sense "what are the physiological mechanisms that causes the banana to like that?"?

Note by the way, this is what a wild banana look like.

Note that this curved growth is hardly unique to bananas.  Cucumbers, some kinds of chili peppers, pea & bean pods, and many others can all have similar shapes.

The "proximate cause" would be a differential rate of growth on the different sides of the individual bananas. If the cells on the underside of the banana are dividing faster than those on the top, that will cause the upward curvature.
As to what causes the differential growth: I'm not a banana biologist, but I would suspect that a growth hormone of some sort finds itself more highly expressed in the part of the fruit that starts out closest to the stem.
Why that hormone might have decided to start doing that, and what selective advantage it might have given the early wild bananas, I have no idea. But our modern cultivated bananas have probably been strongly encouraged to do it, for compactness of shipping, if nothing else!


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Are there hybrids that emerge as a new species?
We know a couple of hybride (mammal) animals (http://www.rantpets.com/2015/06/03/15-strangest-hybrid-animal-breeds-you-didnt-know-existed/) and perhaps even more and perhaps even insects like the Drosophila.
But are there animals which arise as a new species? And by species I mean animals who can't breed with the species of their parents but can interbreed succesfully with their own species ('brothers' and 'sisters'). Only leaving out pre-mating mechanisms in case they don't get offspring (so that only Post-mating isolating mechanisms counts)
See also: Have we ever observed two drosophila lineages that evolved reproductive isolation in labs?
Have scientists ever produce a new species in laboratory by means of natural selection?

While it is an interesting question, since the operational definition of species is the inability to interbreed with other species, the fact that hybrids are viable suggests the two initial "species" are almost the same.  By post-mating I assume that you mean chromosomal problems during meiosis (e.g., aneuploid gametes)?

Yes, this is called hybrid speciation.

Hybrid speciation is a form of speciation wherein hybridization between two different species leads to a new species, reproductively isolated from the parent species

There has been a fair amount of work on hybrid speciation (see here). Hybrid speciation is often thought to be more frequent in plants than animals. In ferns for example, we estimate that 7% of species emerged through hybrid speciation (Otto and Whitton 2000). Typical cases of hybrid speciation include changes in ploidy levels (examples include sunflowers). Hybrid speciation also occurs in animals such as the lonicera fly to cite just an example.

In my initially question I asked (before it was edited) species created by human. Are new species created by human?

The post did not match the title (the post made absolutely no reference to humans). Now that the broad question of "is this a thing" has been answered I would recommend that you open a new post to ask specifically about humans. You will be able to use the term hybrid speciation which will make your post short and clear.


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Considering Two Genes, Are There Only Two Possible Outcomes for the Four Gametes Produced After Meiosis, Regardless of Independent Assortment?
Is it true that for a single meiotic event when considering only two genes, there are only two possible genetic outcomes among the four gametes produced, regardless of whether the two genes are found on the same homologous pair or on two different pairs?
To simplify my question I am disregarding recombination, but feel free to mention the importance and implications of recombination and other factors that I may be disregarding, in gamete formation.
To explain my thought process further, I will use an example. I think that if one daughter cell produced from meiosis I gets the alleles A and b for example, then the other daughter cell must get the alleles a and B, because each gene only has two alleles, one of which is given to each daughter cell in meiosis I. Thus, 50% of the gametes will be the same as one another, again this happens only theoretically, when considering only two genes and disregarding recombination. In this case, two gametes will have the alleles Ab and the other two will have the alleles aB, irrespective of whether the two genes are found on the same homologous pair or on two different pairs. Of course my example is only considering two alleles. Below is an image which illustrates my thinking:

I take it each band represents an allele and the colour of the band represents the gene. I think the image is overcomplicating my question, but it does seems to be consistent with my above simplified description.
I think when people say there are four unique gametes resulting from meiosis e.g., Ab, AB, aB and ab, when considering two genes and assuming independent assortment, they need to be more specific and emphasise that there are four possible gametes per meiotic division, or maybe more depending on whether recombination is considered. Now, that I think of it there are probably more than four possible gametes if you add recombination to the mix.
Regardless of independent assortment, I take it that the result of the meiotic division will actually be two genetically unique gametes, if you disregard recombination and only consider two genes. However, the number of possible unique gametes will be greater.
In summary, I think we need to specify whether we are talking about the observed number of genetically unique gametes resulting from one meiotic event or the possible number of genetically unique gametes, which could be observed given more than one meiotic division, and obviously we need to specify how many genes we are considering in order to determine the genetic uniqueness of the gamete. Lastly, we need to state whether we are assuming recombination or not.
Again, I am assuming everything in I have written based on what I have learned so I may be wrong at any point, I am just a Biology student at University.
To add to my confusion, I assume there are actually two possibilities for the specific combination of alleles found on each chromosome, when two genes are found on the same homologous pair. But these possibilities only express themselves at the individual level, rather than at the 'meiotic event' level. For example, if two genes are found on the same homologous pair, one individual may have the alleles Ab on one homologous chromosome and aB on the other homologous chromosome, whereas the other individual may have the alleles AB on one homologous chromosome and Ab on the other homologous chromosome. However, there is only one possibility for the gametes produced from each meiotic division for each individual. So, in this case, considering only individuals with these two specific genes on the same homologous pair of chromosomes, the gametes produced will be different between individuals for the two genes, whereas the gametes produced for individuals that have these two genes on different homologous pairs can be different between independent meiotic events.
My last inquisition is on how one would calculate the probability of a specific allelic composition for a gamete, with the correct interpretation. If two genes are found on different homologous chromosomes and if we disregard recombination, I assume there is a 50% chance that 50% of the gametes will be Ab and 50% will be aB or 50% will be AB or ab? Is this the correct interpretation?
Apologies for the length of this question!

Yes, correct. But there are many cells to begin with, not just 1, meaning that all 4 end-combinations will be present. Importantly, crossing-over is not a rare optional event, but a necessity with control mechanisms.

I am surprised because to me most of what I said was 'logical' assumptions and I suspect more of the later. Thank you.

A "single meiotic event" would include both meiosis I and meiosis II. So, if you start with an AaBb mother cell prior to any phase of meiosis, then observe one of the resulting final daughter cells, you would have an equal probability (25%) of finding AB, Ab, aB, or ab.
The line of reasoning from OP is only relevant after meiosis I has occurred, and in the absence of recombination. At that point the two intermediary daughter cells have either the genotypes AB and ab (the left side of the figure), or Ab and aB (the right side). From that point the possibilities of the final daughter cells are indeed limited, so if one knew the outcome of meiosis I, they would know the set of genotypes held by the four final daughter cells.
One would also know—again, in the absence of recombination—that a single AaBb mother cell will produce four daughter cells that contain only two possible genotypes among them (but not which genotypes they will be). However, this would only be useful in very narrow circumstances because, first, recombination is integral to meiosis, and second, usually there's a population of mother cells to consider. (And third, it doesn't seem like very useful information in the first place.)
As other comments point out, recombination is not a rare event. When recombination is considered, it is indeed possible to get all four genotypes among the daughter cells

Thank you so much for clarifying Darlingtonia! While the information is certainly not practical, it is very useful to know and helps in understanding the theoretical basis of human knowledge on the subject, especially for a student like me. I came to these conclusions independently because teachers would always 'breeze' past this stuff. Now my understanding is more thorough and I can utilise this. Furthermore, now I understand the mechanisms of recombination, rather than just the implications. Thank you for providing an excellent answer!


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Is there a name for this type of diagram?
Is there any commonly used name for this type of diagram / symbology? I have not been able to find them referred to by any name.

is this what you are looking for https://en.wikipedia.org/wiki/Block_diagram

The glyphs themselves come from SBOL visual: https://sbolstandard.org/visual-glyphs/. You could look in the spec to see if they refer to the diagrams as something other than an SBOL visual diagram.


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What kind of spider is this please? Southern Indiana. Very strong web

It never comes out during the day so it's been hard to get a decent picture. We have been battling over ownership of my mailbox. It's a house box and every morning it's covered in cobweb from it to the siding or across the top of it if the lid was left up. Very strong web, it takes effort to get it off. I was going to put up a new one with a sealed lid but would kind of like to know if it's poisonous before I go messing about the battle grounds.

Even with lightening your photo:

It is difficult to ID this to genus. If you are only interested in knowing whether it is a medically significant spider, you can rest assured that it is not. The (few) markings and shape of it are enough to rule out widows and recluses.
From its shape and habitus, it is likely a cobweb weaver of some kind (family Theridiidae), but there are many possible choices for genus unless you can get a clearer photo. While black widows are also Theridiidae, the medically-significant female widows have solid black legs while we can see leg banding in this specimen. As @anongoodnurse points out in the comments, the legs here are shorter than a black widow's legs, so I would even rule out a male widow. The abdomen here is rounder shape than the tear-drop abdomen with a tapered end that a widow has. (Similarly, recluses do not have banded legs and do not hang in webs like this Araneoid is. And there are no other medically significant spiders you need to worry about in your geographic area).
The leg banding, general shape, and the slight white marking on the abdomen we can see in the lightened photo make this a little reminiscent of Enoplognatha marmorata (like this one https://bugguide.net/node/view/646186/bgimage). It is very rare to find Enoplognatha indoors.
Here is an example of an E. marmorata found in Indiana: https://www.inaturalist.org/observations/107343897

It would be helpful if you could explain how/why you know it's not a widow-type spider, and even better if you could actually identify the spider. I'm not an arachnophobe by any means, but I would approach this one with some caution, as it's habitus is similar (though the legs don't appear to be as long.) Good answers on this site are backed by sources. Thanks!

@anongoodnurse thanks - added additional info with my best hypothesis of a feasible ID.

The globular abdomen, posture in the web and general shape certainly suggest a Theridiid.  The glossy black body and banded legs are consistent with both the pretty harmless Steatoda species of "False Widows"and their more problematic cousins the Black Widows.  In both cases, the abdominal stripes and leg bands fade to black as the female matures, and while it would be unusual, I bet that having an all-black abdomen and still have traces of the brown banding on the legs is not too uncommon. However, Latrodectus mactans, which I think is the more likely Black Widow species in Indiana, would be expected to still show some of the red spots on the abdomen at this point in its growth. So I'm leaning toward a Steatoda.  Both are noted for strong webs, with the real Widows having a particularly strong silk; the simple ID solution is to check the underside - a real Widow will have the classic red "hourglass" marking, while a Steatoda will not.
The image below is Steatoda grossa, the bigger of the common "False Widows".  Steatoda borealis females commonly feature a white midline on the back, but I'm not sure if the photograph shows a real feature or just an artifact of the flash.