text:
What causes motor laterality/ side dominance?
I would like to understand what leads up to motor laterality, or side dominance of motor skills.
I made this assumption that it depends on neuroplasticity and the side in which one first learns the motor skill; whereas the more you practice, the more you strengthen that side. I appreciate your time and patience. Thank you; can't wait to discuss.

I think this question is overly broad in scope. There is abundant literature on the various causes of handedness: genetic, epigenetic and environmental. The following might serve as an introduction: https://www.nature.com/articles/s41598-018-37423-8.

I found this article on forced right-handedness; can I get your opinion on if it supports my assumption, @Adhish? Thank you for your help! https://blog.cognifit.com/ambidextrous-brain/

The available evidence (and the article you shared) suggest that training does play a role. So your assumption is correct to an extent. But inherited factors are important too.

Ah, Thank you! Just one more question, if you don't mind me asking: What "category" of factors would training/practice fall under? Physical factors? My apologies; I'm very new to this field. Thank you for your patience, @Adhish.


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Why are 2 electrons transported from photosystem II at the same time?
I only know that electrons are captured by the primary electron acceptor and then go through the electron transport chain, ultimately ending up at photosystem I. But why do 2 leave photosystem II in the first place? I thought the oxygen-evolving complex only replenishes the electron hole one-by-one?

So refer to the following diagram,

In the photosystem II complex, water is decomposed into oxygen and protons. That's two electrons liberated from each water molecule. Plastoquinone accepts two protons from the stroma by coupling it to the two electrons it receives from the photosystem complex. In this manner, the protons are transported to the lumen, and the electrons are sent into the electron transport chain. So PQ binds in a QB site in the D1 protein, and it's not released until it's double reduced/protonated. Another PQ binds in it's place when PQH2 leaves the binding site. Source
Short answer: Two electrons are liberated in splitting water, and that mechanism feeds into asymmetric lumen/stroma H+ concentrations and movement of electrons through the ETC.

source: Stack Exchange

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sort: votes


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Why does evolution only involve heritable traits?
If natural selection favors a certain behavior that is learnt, then wouldn’t that behavior be found more often among a population (as more offspring will learn that behavior from their parents or their peers)? Since the behavior is not encoded in the genes, it is not heritable, but it is transmitted through other means and will thus accumulate in the population. This, to me, seems a lot like the effects of evolution, yet this is not a heritable trait. So my question is why does evolution concern only heritable traits and not those that can be reproduced by learning?

If offspring learn it from their parents, isn't it heritable by definition? Apparently, not in genetics. It seems to me that this question is mainly about definitions. If you're studying genetics, you want to define "heritable"  so as to apply to genetic inheritance only, and other features passed from parents to offspring may be considered environmental. These other traits would have to be analyzed in a different way.

I assume the definition of ‘heritability’ in genetics is the one used in evolution, unless I am mistaken. My question is why this definition is used rather than one that encompasses environmental factors as well.

There is a lot to say to address this question fully. I will be brief and a little messy to try to introduce you to some concepts and that will hopefully push you to learn more by yourself.
Heritability in genetics
In genetics, heritability is a statistic that describe the fraction of the phenotypic variation that which is caused by underlying genetic variation. Please have a look at this post to understand the concept of heritability as used in genetics. Note that there are two such statistics, named heritability in the broad sense $h_B^2$ and heritability in the narrow sense $h_N^2$.
Basics of non-genetic inheritance
Here, I will refer to "heritability in the broad" as the passation of trait value (such as behaviour for example) and environment characteristic to another organism. One must not confound what I call here "heritability in the broad" and heritability in the broad sense as defined in genetics ($h_B^2$).
Sure, a lot of things can be inherited from one organism to another. Any such heritable (in the broad sense) trait is susceptible to show interesting variation in the frequency at which trait values are found in a population. If, in addition to that, this trait is susceptible to spontaneous changes (the equivalent of mutations in genetics), then this trait can show interesting evolutionary patterns. If in addition to that, different trait values have different aptitude to replicate (the equivalent of natural selection in genetics), then such trait can evolve in an "even more interesting way".
What can be non-genetically inherited?
Two things can be inherited without the use of any sort of genetic information (I also exclude epigenetic information incl. DNA methylation or protein concentration in the yolk).

Environment (Ecological inheritance)
Meme

See more on Ecological inheritance and memes below.
Ecological inheritance
This is probably the first type of inheritance one would think of when not thinking about biology. In humans, it is not uncommon for offspring to inherit "stuff" from their parents when they die. Similarly, beavers can inherit a dam that has been built by their parents. This type of inheritance in generally called Ecological inheritance.
This type of inheritance might eventually be important to evolutionary processes (see literature on niche construction).
Inheritance of a meme
Definition
A meme has been named by the analogy to a gene. A meme is any idea, behaviour, thought or tradition (piece of culture) that can be inherited. The concept of an internet meme is now quite popular, but a meme is more than just an internet meme. While genetics is the study of genes (and much more actually), memetics is the study of memes. Memetics is a very interdisciplinary field of study that attract biologists, philosophers, mathematicians, linguists and archeologists among others. The hypotheses built in the field of memetics rarely offer predictions that can be easily tested, and therefore a good part of the work in this field remains very uncertain.
Analogy to genes
A meme could be a joke for example. If the joke is funny it will replicate easily and enter in new brains. This meme could be said to have high fitness. The joke may come into spontaneous changes (mutations). Be careful with analogies and they may show nothing but similarity. For example the nature of memetic mutation seem to be quite different than from the nature of genetic mutation.
Example
In humans, the examples are very easy to find. As I am writing this answer, I am currently trying to pass on a meme which has been given to me by some other authors. Hopefully I won't mutate this meme too harshly.
Lots of monkeys and apes are transmitting traditions, foraging methods and other memes to their offspring, sometimes through active teaching but often through imitation (or emulation). A classic example is the one reported in Rhythms of Vision in 1975 (I could not find the original peer-reviewed paper). A female monkey, one day had the good idea of washing a sweet potato. This behaviour has since increased in frequency throughout the population so that most monkeys now wash their sweet potatoes.
Pitman and Durban (2011) (and others before them) report that some population of orcas use cooperative hunting while some other population does not. Variation for this trait seems not to be caused by genetic variation.
How does inheritance work?
Inheritance can be "vertical" (parent to offspring) or "horizontal" (between individuals of the same or different species). This holds true for both genetic (consider transduction) and non-genetic inheritance (teaching to offspring or to the neighbors).
In addition to that the passation of a meme can be active (teaching) or passive.

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Mosquito physics
What are the environmental limitations of mosquitos I should know of if I want to avoid getting bitten?
For example:

How fast should I walk in order to be moving too fast for one to bite
me?
Can a fan work to blow mosquitos away from me?
If I'm looking to
buy an apartment, is there a minimum height in which mosquitos will
no longer reach?

Thanks!

Speed of mosquitoes vary from place to place and their current health status.But if there is any such problem, maybe you can run a short distance (some yards) and then they won't harass you for some time till they cope up with you.
Yeah, a fan usually at comfortable speed will be enough to blow the mosquito away. If this doesn't work then set speed at full speed and wrap yourself in a blanket
I don't think there is some height where mosquitoes can't reach but my friend who lives on 12th floor in his apartment hardly has 4-5 mosquitoes bugging him.

Could you provide some references?

I am quoting this web page http://spectrum.ieee.org/consumer-electronics/gadgets/backyard-star-wars which describe a prototype of a system to kill mosquitoes by means of a LASER, for what regard the speed:

Mosquitoes fly up to a meter per second.

This speed is compatible with 1.2 meter per second quoted in the paper
SNOW, W. F. Field estimates of the flight speed of some West African mosquitoes. Annals of tropical medicine and parasitology, 1980, 74.2: 239-242.

There was a relationship between wind speed and catches of Anopheles
  melas and Culex thalassius which attempted to bite man at ground level
  and at 4 and 8 m on  an open scaffolding tower, in cleared bush in The
  Gambia. It was expected that in winds which exceeded their flight
  speed, no mosquitoes would be able to approach  and attack men on the
  tower. Catches of mosquitoes fell off sharply in winds of 120 cm/s,
  which may approximate to their flight speed, although some insects
  were still captured at the highest wind speeds encountered.

For what regard the flying altitude:

The average flying altitude varies among mosquito species but is
  usually only about 2 meters. They will fly over obstacles when
  necessary—even into an upper-story window—but if your virtual fence is
  3 to 5 meters high, it can catch almost all mosquitoes that fly by.

The system is patented and the patent is specific about Anopheles:

For example, more than 99% of Anopheles mosquitoes (which may carry
  strains of malaria that can infect humans) fly at less than 3-5 meters
  of altitude

HYDE, Roderick A., et al. Photonic fence. U.S. Patent Application 14/255,119, 2014.

Environmental limitations of mosquitos can be:
1) Wind. Prefer a windy day for a walk in the marches! Or a large ceiling fan above you bed makes a real barrier against mosquitoes!
Mosquitoes cannot fly against the wind if the wind is more than ~1m/s as you read in your reference.
1) Temperature. Prefer the winter season or AC-rooms!
Some species hibernate during winter (but they still need to take some blood meal from time to time). If it is spring or if spring season doesnt exist where you are, prefer a cold day. It is relative to the normal temperature of the considered location. Some cold-climate species swarm very well at 12°C (Aedes communis  https://doi.org/10.1016/J.JINSPHYS.2021.104233)
2) Humidity. Prefer the dry season or dry locations!
Mosquitoes prefer humid places, otherwise they could die. Again, it depends of the species and some got adapted to arid location. However, they always need water to lay their eggs.
3) Mechanical barrier. Prefer to sleep under a bednet!
Mosquitoes are small and are very good to pass below your door in in a small holes of your window, however they cannot pass if you are in an isolate place. To keep some afresh air, use a bed net. It is a recommended by WHO (https://www.who.int/elena/titles/bednets_malaria_pregnancy/en/)

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Can a person's body produce enough electricity to break a wristwatch?
I know of someone who cannot seem to wear watches without the battery dying or something else about the watch going haywire. this person was told it is because their body is producing too much electricity and that by putting nail polish on the reverse of the watch to block the current the watch would work.
This was tried and it actually worked. My question is, is this a real thing? I couldn't find a legit discussion of this online.

Static electricity (depending on clothes, floor material, air humidity, etc...) seems more plausible.

I would hazard a guess that sweat or something similar would be more likely. (That is a guess, though.)

I'm voting to close this question as off-topic because it is better suited to skeptics SE - I don't view this as a biology question

I do think this has the potential (haha, electricity joke) to be a very interesting question - there's a lot of anecdotal evidence out there about people (a friend of mine included) who cannot wear watches because they are continually dying or otherwise malfunctioning. It would be great if someone could find a study on this.


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Would it be possible to regulate proper phosphorylation so the UPR wouldn't initiate a reactionary cell death in important cells?
In studying the correlation of folded versus unfolded proteins and their impact on neuro-degeneration, it looks like improper phosphorylation in the chaperones (at least, in part) causes the mis-folding of proteins? If so, would it be possible to regulate proper phosphorylation so the UPR wouldn't initiate a reactionary cell death in important cells?

I think it is lot more complicated. Because amyloid and prion develop intercellular space, while chaperones are expressing inside of cells.

Please define UPR.

UPR: Unfolded Protein Response.


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Term for a leaf in a family tree
Imagine a family pedigree.
Mathematically it is a graph, which consists of nodes and edges.
Nodes being family members, and edges - their relationships.
In a clinical setting, what is the proper term for the nodes? Would they be called 'leafs'?

So in a pedigree, Standardized Human Pedigree Nomenclature: Update and Assessment of the Recommendations of the National Society of Genetic Counselors notes that these "nodes" in the pedigree are the "individual symbol" denoting individuals. Although, when you read it, you'd read "Male," "Female," "Gender Unspecified," etc. instead of individual symbol.


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Partial muscle fibre contraction
I'm being taught that: a muscle fibre spans the entire length of the muscle, from the originating tendon to the inserting tendon.
The question is, can a muscle fibre contract only partially? Say, if the fibre is 1m long, can only the first 10cm contract without the rest contracting?
Additonally, to help me understand better:
When a neuron innervates a muscle fibre, does it do it only at one spot, or can a muscle fibre be innervated in several spots? Can several neurons innervate the same muscle fibre?

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What type of factor is practice of motor skills?
I recently asked a question about the cause of motor laterality: What causes motor laterality/ side dominance?
I understand that there can be genetic factors, epigenetic factors, or environmental factors. But in terms of continuous practice of motor skills, what type of factor will that be? Physical factors? Thank you!

Hopefully someone will post an answer to your linked question as well!

@uhoh Hope so! So far I've only been conversing in the comments, as you've probably seen.  •-•


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Does the corpus callosum have a significant relationship with motor memories/ muscle memories?
With the corpus callosum located in the cerebrum, and motor memories having a closer relationship to the cerebellum (which I'm not quite sure about), is there a significant relationship between the corpus callosum and motor memories? Do motor memories process in one hemisphere and are then shared with the other- if so, how? Thank you so much for your time and patience!

Almost all parts of the brain have a relationship, but what deems a neuronal relationship significant? Maybe this will help (pay-wall): https://onlinelibrary-wiley-com.ezproxy2.acu.edu.au/doi/abs/10.1002/cne.902470303

@Andrew thank you for sharing! However, I don't have a user account with ACU . Can anyone sign up or just students? Cheers!

Apologies, try this link: https://pubmed.ncbi.nlm.nih.gov/3722441/

@Andrew got it, thank you so much!

This study tests the time it takes for patients with damaged corpus callosums to perform intermanual transfer motor tasks.
Patients drew a meaningless figure with one hand, then did it again with the other hand (And vice versa). Thus performing intermanual transfer.

All three patients displayed a significant benefit for transfer from the dominant to the non-dominant hand but not vice versa during proximal motor activity.

...the proximal transfer behavior was found to be similar for all patients in the healthy group.

From these results, a relationship exsists.


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What are kinesiological factors?
I am in search of a term that describes movement, or practice of motor skills, as a factor of laterality. Would "kinesiological" be appropriate? I'll leave my two previous questions down below; hopefully it can shed more light. Thank you so much!
What type of factor is practice of motor skills?
What causes motor laterality/ side dominance?

There is no magic dictionary of "factors" that biologists use and that those writing about Biology must draw from. It seems you want to describe "practice", so use that word, "practice".

Hi @BryanKrause! Thanks for the reply; I'm writing a script for a "scicomm" video and wanted to say something to this effect: "Keep in mind, there are genetic, environmental, physical factors, et cetera, but I'll be focusing on the _________."

If you presumably plan to refer to the literature then you can use the language used in the relevant texts.

I understand. Thank you for your time and patience, @BryanKrause .


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The fastest vaccine developed is a mumps vaccine, which took 4 years. Where is the hope that we will find a COVID vaccine in less time?
I understand that doctors and scientists are working hard to find a vaccine, but is there a reasonable chance that we will find one in the time that scientists and politicians are suggesting?
I also understand that we have no choice but to socially distance and bithe our time to find a vaccine if COVID is anything like the flu, but what if it proves to be as hard as finding a vaccine for HIV? The first HIV outbreak occurred in the 1980s, and if I'm correct we still don't have a vaccine for it yet (even though we do have treatment for it so people could just live their life with it).
So my question is with all this in mind, how could there be a chance that we will find a COVID vaccine in less time? Is it just optimism, or is there actually reason to believe the vaccine will be produced say by the beginning of 2022.

@David With all due respect, I don't agree. The tour that you linked me to does not suggest this question is off topic. In fact, this question first came to mind when I saw a Biology.SE question asking why a COVID vaccine wasn't quick and simple. I wouldn't understand why vaccine development wouldn't be considered "general questions about biological concepts" as described by the help center. I also have an inkling that you misunderstood the question as musings of future success for the vaccine candidates. Instead, I was asking why a COVID vaccine could possibly take less than four years.

A question about a biological concept is of the type "what does the spleen do?", "How do eagles fly so high?", "How does insulin regulate metabolism?", "How does coronavirus enter cells?", "What determines an IgG v. an IgA response?"  Your question is about commercial drug development, presumably in a regulatory context as I imagine you are aware that vaccines are already in use in China and Russia. It might or might not be on topic in SE Medical Sciences, although they may question the preparation for the question given the widespread coverage of the topic in serious news media.

Expectations for accelerated vaccine development are based on two main points.

Groups have been working on vaccines for SARS-CoV-1 since 2003, and much of that work is applicable to SARS-CoV-2 (the COVID-19 virus). Here is a review article discussing work on SARS-2 vaccines based on work on SARS and MERS. One example, transgenic mice are available that express the human version of ACE2, the host receptor protein that allows SARS coronaviruses to enter a cell. These mice allow vaccine testing that is much more informative than cell culture tests, and weren't developed until 2006-2007. SARS was eliminated in 2004, so we can estimate it would take at least two years to develop an animal model for COVID if it wasn't already available.

Here is a diagram from the linked review showing timelines for traditional vaccine development and the accelerated SARS-CoV-2 vaccine development:

Several pharma companies have developed "plug and play" vaccine platforms which allow rapid manufacture of vaccine candidates once a molecular target is known. In this case, the target is the 'S' glycoprotein. Once the sequence that encodes for this target is known, it can be inserted into the platform and produced quickly.

Here is another diagram from the same review describing some of these platforms:

EDIT - I wanted to emphasize a third point: If you notice the "Production (at risk)" text in the accelerated development diagram, it means that pharma companies are producing large amounts of their vaccine candidate before testing is complete, and therefore running the risk that their warehouses full of product will be rendered worthless by bad outcomes in the clinical trials. Moderna had started production of their mRNA vaccine candidate by July 15 2020, so this gives them a several month head start if the trials turn out well.

Thank you! Your response was concise and answered my question.


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Are coronaviruses gaining an evolutionary advantage?
So there are 7 known strains of coronavirus that are known to infect humans: 4 that cause the common cold (229E, NL63, OC43 and HKU1), and 3 that have been known to cause acute respiratory infection (SARS, MERS and now COVID-19). They're all beta-coronaviruses except for 229E and NL63.
I can't help but notice the latter 3, which also happen to be the most serious, have all emerged very recently and within less than a decade apart from one another. I tried to find out how long the common cold strains have been around for, but can't find too much information on that (I found one article from science daily that says the common cold could have originated in birds around 200 years ago, but that's about it).
Does anyone have more information on this? Is the fact that SARS, MERS and COVID-19 emerged so close to one another a trend or just a coincidence? Are there any notable scientists who've noticed this and have an explanation as to why?

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. Note, your question is unclear and the title and body of your question don't seem to match. Please only ask one question at a time to improve the chances that you will get answers and makes them more accessible for future users. ——— We also encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!

Thanks for your response! I just graduated from undergraduate school so my biology skills aren't incredible yet so forgive me if my question seems vague and non-specific. I kind of  just dumped whatever information I knew in the description. So the purpose of the question was just to figure out if there was a reason why coronavirus diseases specifically keep popping up. The reason why I mentioned the common cold strains was because I was wondering if there's evidence that they emerged in the human population recently, too.

It is not a coincidence, but it doesn't have to do with sudden evolutionary changes, rather with human behavior.
The three viruses you mention are zoonotic — they can infect different species, including humans.
Increased development of formerly untouched lands is bringing people into contact with animals (and existing, but formerly unknown zoonotic pathogens) in greater numbers.
Humans bring the virus back to concentrated human populations — cities, say — either being infected themselves, or bringing back infected animals for consumption. This increases the opportunities for further spread.
With the help of global leadership that is corrupt, incompetent, or antiscience, the multiplier effect of repeated infections in cities turns a small pool of cases into a pandemic. Rinse and repeat.

The risk of emerging infectious diseases such as COVID-19 from animals is on the rise, in large part because of our environmental footprint and the blurring between the natural and the built environments. Increasingly, humans, livestock and wildlife are interacting in new and unexpected ways, bringing new species – and their resident infections – together with unpredictable results.
Climate change is accelerating the loss of animal habitats and the ways humans change the land. Cutting down old-growth and rain forests, which harbour a rich biodiversity of life, to create agricultural or pastoral land potentially brings people and livestock in closer contact with previously isolated populations of bats, and other animals harbouring previously unencountered disease. In turn, biodiversity loss threatens natural food sources which means animals seek other sources of food found where people live. As climate change causes large disasters like floods and drought, human food sources are also lost, and growing food insecurity pushes people to further encroach on animal habitats, increasing animal contact and contributing to the trade in wildlife.
The speed and magnitude of environmental change has implications for future epidemics and pandemics. The first few cases of COVID-19 have been traced back to a ‘wet market’ that contained wild animals sold for food or medicines. Such markets can be ideal environments for zoonotic spread as the unusual mixing of animals (which is not common in the wild) can provide opportunities for viruses to jump between species, and potentially then to people.

Development isn't just loosing coronavirus — there are other pathogens that have been loosed by encroaching on their natural reservoirs:

We invade tropical forests and other wild landscapes, which harbor so many species of animals and plants — and within those creatures, so many unknown viruses. We cut the trees; we kill the animals or cage them and send them to markets. We disrupt ecosystems, and we shake viruses loose from their natural hosts. When that happens, they need a new host. Often, we are it.
The list of such viruses emerging into humans sounds like a grim drumbeat: Machupo, Bolivia, 1961; Marburg, Germany, 1967; Ebola, Zaire and Sudan, 1976; H.I.V., recognized in New York and California, 1981; a form of Hanta (now known as Sin Nombre), southwestern United States, 1993; Hendra, Australia, 1994; bird flu, Hong Kong, 1997; Nipah, Malaysia, 1998; West Nile, New York, 1999; SARS, China, 2002-3; MERS, Saudi Arabia, 2012; Ebola again, West Africa, 2014. And that’s just a selection. Now we have nCoV-2019, the latest thump on the drum.

The three viruses you mention are serious. MERS and SARS have high fatality rates. The third (SARS-CoV-2) is highly contagious. These attributes disrupt everyday life.
But the aforementioned and other viruses are also serious for similar reasons. Zika, for instance, can cause life-altering birth defects, has been known about for decades, and human-caused climate change has been enabling it to spread to more densely-populated areas.
Evolution — natural selection — takes place over thousands to millions of years. Human behavior has changed the earth only within a few hundred years, much of it in the last century or so.

Thanks for your response. I was definitely thinking that disruptions in the ecosystem such as climate change, deforestation and increased interaction with animals played a role like you said. Maybe my question wasn't clear enough, but I was focused specifically on if there was a reason why outbreaks caused specifically by coronaviruses have been happening in recent history. I appreciate your detailed response.

There are a number of recent outbreaks caused specifically by other types of viruses, as well. But the answer to your question is no, zoonotic viruses are not becoming more prevalent due to evolution.


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Could we restore some animal's muscle structure by it's bone?
Suppose that elephant dies out one day, nothing left to researchers but the fossil. Could fossil infer the existence of large nose?
If there is possibility, how exactly should they perform the deduction?

I think you would be surprised to know that forensic experts use the skull and face bone structure of a dead body to predict how the person might have looked, probably by getting the muscle structure from bone structure. I don't know whether it's true, I heard it in a TV show.


text:
Modeling population growth - Variance
I've been studing population growth models, but there's something I can not find that's fustrating. That's a formula for the variance in population growth. I know that other models can be aplied, but I want to start with the simplest case.
Let's assume a population is growing exponentially as defined by:
$N(t) = N(0)W^{t}$
The parameters $W$(absolute fitness in my definition) tell us that the time for division (if the species reproduces binarally) is given by an exponential distribution with $\lambda = \dfrac{\ln W}{\ln 2}$
So I see a model for $N(t)$ and a random variable associated with this model. What is the pdf, expected value and variance of $N(t)$? The expected value I expect it to be given by the first equation (or the value to be the same) but what about the variance?

The exponential growth without noise is the deterministic approximation. Now knowing that this means that the time for division is given by an exponential distribution, what is the variance in the population size?

My bad, I didn't read the question right. Removing my embarrassing comment.

Basically, you have a Poisson process where the rate doubles whenever there's a (birth) event. The mean grows exponentially, and the variance should be overdispersed since it's a mixture of Poisson...

Not exactly...   Because whenever there's a birth the time for the birth from the individuals that did not divide is the same as before minus the time of birth... But there is also the two new individuals...

By the way, as my final interest is the frequency of this in a larger population, I think diffusion theory, and Kolgomorov forward and backward equations might help... I just don't know enough to use it

Sorry, I meant increased by one, not double. Poisson process where rate grows by one after each event.

Check out Kendall (1949), section 2. He shows that the pdf is a geometric distribution. In your notation, it's $P_n(t) = N(0)W^{-t}\left(1-W^{-t}\right)^{n-1}$, which implies that the mean is indeed $E[N(t)] = N(0)W^t$ and the variance is $\text{Var}[N(t)] = N(0) W^t(W^t-1)$. (Be careful -- his definition of $\lambda$ differs from yours by a factor of $\ln 2$.)

so, my answer isn't incorrect (I'll go ahead and leave it up), but this is the full solution.

yes... I accepted this one but yours already point to the right direction

If $W$ is a parameter, I'd expect (in the simplest case) that $W$ itself is a constant (i.e. it doesn't have a distribution). (By the way, I would normally use $T_{1/2}$ to denote the doubling time, $\ln 2/\ln W$, and would use $\lambda = \ln W$ for the exponential rate, i.e. $W^t= \exp(\ln W)^t = \exp(t \ln W) = \exp(\lambda t)$. I don't normally see people express rates scaled by $\ln 2$.)
In the case of a continuous-time birth-death process (the technical jargon for your model), I believe the analytical answer will be that the standard deviation of the population size at time $t$ will grow at the same exponential rate as the mean population size, and that the variance will grow twice as fast (because it has units of $\textrm{population size}^2$), i.e. $\propto \exp(2 \lambda t)$)
I don't have a derivation/reference handy, will dig around for one. This is fairly basic stochastic-process math, but stochastic-process math also gets pretty hairy-looking (to a biologist) quickly. Bartlett 1960 (Stochastic population models in ecology and epidemiology) is one place to look for basic results, although I'm sure there are many others. This recent PhD thesis gives a thorough introduction to the math of birth-death processes ... although, not to my disappointment, a canned derivation of the variance result I'm too lazy to derive for you.


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Symmetry in animals
Is symmetry in animals due to DNA or natural selection? By symmetry, I mean the left side is an almost (not perfect) reflection of the right half. Is this due to DNA trying to balance the two half or is it due to natural selection where unbalanced organisms die off more frequently and thus reproduces less. Or is it due to some other factor I had not considered?

Your question presents an artificial dichotomy - "Is symmetry in animals due to DNA or natural selection?" Everything about how an organism appears is ultimately programmed in its DNA, (sometimes heavily) influenced by environmental factors as well. Natural selection creates selective pressures that positively or negatively affect the propagation of different DNA sequences. To learn more about natural selection and evolution, I strongly recommend Understanding Evolution from the University of California, Berkeley - it's really great.

Welcome to Biology.SE. As MattDMo said, the question presents a very obvious dichotomy that is wrong and make the impossible to answer. DNA is a molecule while Natural Selection is a process. You should make sure to acquire some very basic understanding of evolutionary biology. I am voting to close as "unclear" as the question contains issues of semantic.

@Remi.b I have a basic understanding of the two concepts. You are saying it is a dichotomy but this is my question and it is not entirely unrelated. DNA is a molecule, but it is the one that holds the blue print to our bodies. To say it's just a molecule is ridiculous. I want to know if there is a trait in DNA that causes symmetry or if symmetry in complex organisms is do to the process of natural selection. Lastly, you say that I should learn about basic evolutionary biology, but how do I do this if people criticized me for making an effort to ask questions. Isn't that the point of this site?

@MattDMo it is not a duplicate of that post. His post is asking why some organs in the body is not symmetrical. I'm wondering what makes us symmetrical at all.

@MakPo you are not being criticized for making an effort to ask questions, and I was simply pointing out an external resource that could help clear up some of your misconceptions about evolution and natural selection. We are just pointing out that you're framing the question the wrong way - it's not DNA vs. natural selection, symmetry (and all other aspects of life) are a result of the processes of natural selection acting on DNA. While DNA is a very important molecule, it is "just a molecule". I would suggest you [edit] your question to focus on the basics - how did symmetry evolve?

@MakPo Sorry if my comments were discouraging. They were not meant to be. You need to get some knowledge (typically through the ressource that MattDMo suggested) in order to be able to understand why a sentence like I want to know if there is a trait in DNA that causes symmetry or if symmetry in complex organisms is do to the process of natural selection. makes no sense.

Before you consider the development of bilatteral symmetry (which is what you are talking about), you need to look at the overall changes relating to animal body plans.
To begin with, sponges (Porifera) completely lack symmetry and came very early in the evolution of animals. Basically, it's a large cluster of growing cells with some differentiation (ie: choanocytes, amoebocytes, etc.). So the lack of of symmetry is simply related to the lack of complexity.
Then, radial symmetry, which has a "top" and "bottom" but no "left/right" came into play with phyla like Cnidaria. An evolutionary jump from assymetry to bilateral, would be astronomical, so we can think of radial symmetry as an intermediate relating to the increasing complexity of body plan development.
On Bilatteral Symmetry, one key thing is the cephalization. Cephalization is where a majority of the nervous tissue and sensory tissue are clustered in one area (a head). In the evolution of animals, Cephalization came with the evolution of Flatworms (Ptalyhelminthes) where sensory tissue such as ocelli (eye spots) were placed in the head. With the head developed, a "sense of direction" can develop where the right/left/dorsal/ventral sides of the body naturally become distinguished.

Some of the information contained in this post requires additional references. Please [edit] to add citations to reliable sources that support the assertions made here. Unsourced material may be disputed or deleted.


text:
Tick Identification
While enjoying the outdoors in mid-Missouri and Northern Iowa, I came across this tick in my belongings. I can't distinguish whether it is a dog tick, a rocky mountain tick or some other species.

The tick you found is a female American dog tick (Dermacentor variabilis) and not a lone-star tick (Amblyomma americanum). Female lone-star ticks do not have white coloration towards the head and only a round dot in the middle of their body. The following PDF document offers a visual comparison of the two species:
https://store.extension.iastate.edu/Product/pm2036-pdf


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What is this - nest, eggs, fungus?
Anyone know what these are? I found them in our local park today attached to a wooden earth-retaining wall.I was thinking some kind of insect nest/egg sac (spider?) They're about the size of a medium egg (hen's egg!)

Welcome to Biology Stack Exchange. It would help if this question had a few more details: where was this photo taken (country / state is probably enough)? What season was it taken in? What was the weather like? What's the vegetation like in the local area?

A Google Image search for "wasp nest" returns a lot of similar looking photos.

It looks like you've opened it up, did you see anything inside it?

@C_Z_ Wasp nests and some similar things already have openings on the bottom or side. Would be safer to keep a distance and watch if anything goes in or out. Or maybe poke it with a long stick and be prepared to run away.

@AL Good point, I was thinking it was probably an egg sac but if there's a possibility that it's a wasp nest you definitely don't want to go poking around in there.

Thanks for all your comments. Some more info: Location is in Oxfordshire, UK - inland, not near any water. Photos taken in a local childrens' play park so lots of grass and some trees etc around. I haven't touched the nests/egg sac! I did notice one looks like it's got a hole in the bottom but on closer inspection it's actually covered over so I'm not sure that anything has left it. Sorry the pictures are a bit blurry - it wouldn't let me upload the originals - files too large.

Updated Answer:
Why it's not the egg sac of Argiope aurantia:
Upon knowing your location to UK, we can rule out quite a few spiders, especially the Argiope aurantia since it is endemic to Northern and Central America.  The spider's egg sacs are also noticeably smaller than "a hen's egg" as this post describes.
Why it's not a gall:
We can rule this out since it appears to be located on a wooden fence post.  Galls require living plant matter to grow.
Why it's not a wasp nest:
There are not wasps that produce threadlike materials. Wasp nests are made from fibers of dead wood and plant stems mixed with saliva of the wasps, and no webbing or threadlike material.  In the picture, we can clearly see some white 'webbing' between the gap of the fence posts directly underneath the mass.
So I really think it is an...
Aethalium of a slime mold:
Given the location, described area, spreading pattern in the picture, and apparent spongy texture of the mass, this looks to be the aethalium (or fruiting body) of a slime mold.  My guess would be in the genus Reticularia or Enteridium, which are typically seen in its reproductive phase as a white 'swelling' on standing dead trees in the spring, or on large pieces of fallen wood.  For example, Enteridium lycoperdon are common throughout the UK and are commonly associated with pine trees, the most common wood used to make fences in the UK.

*This post was edited from my original response.  Please refer to the edit history concerning the previous answer.

There is no web in the photo in the question though, wouldn't that rule out the spider?

There appears to be some webbing directly below the mass (in between the fence posts).

To me that looks more like the building material of the best than it does a spider web.

There are not wasps that produce threadlike materials.  Wasp nests are made from fibers of dead wood and plant stems mixed with saliva of the wasps, and no threadlike material.  My vote still stands as a spider egg sac or a fungi of some sort, such as a puffball.

I agree. This looks lika a slime mold to me


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What is meant by Physarum polycephalum having 720 sexes?
There is currently some media hype about the slime mold Physarum polycephalum, which will soon be exhibited in the Paris zoo. This was my first time hearing about slime molds, but so far so good.
What I don't understand though is this organism supposedly having 720 sexes. This seems strange to me, as to my – admittedly layman's – knowledge, single-celled organisms like this one aren't supposed to have sexes at all, reproducing instead through cell division. It looks to me like pretty much all newspapers reporting on this have no idea either and decided to just keep it because it sounds interesting. On Wikipedia, nothing is said about hundreds of sexes at the time of writing.
What does this actually mean?

It is true that many/most unicellular organisms such as e.g. bacteria or fungi have no need for sex to reproduce, and can divide by simple cell division. However, sex (defined rather broadly) is a universal feature of life. For example see this review article by Rosie Redfield, which examines exactly what we mean by "sex". The broad definition is just recombination of genetic material, which is a universal (or nearly so) feature of organisms.
It's a little hokey to say that Physarum polycephalum has 720 sexes, as "sex", the idea of a specific category of individuals with regard to reproduction, is different from the biological idea of "sex", when we say "yeast have sex".
What Physarum has, like fungi and other similar organisms, is not really sex, but mating type (see here). Mating type really has nothing to do with what kind of sex organs a fungus has, but rather what fungi have sex with. Certain mating types only have sex with certain other mating types. But this isn't really a one-to-one correspondence like male-female. It's much weirder than that.
There are both "heterothallic" (sort of "single-sexed") and "homothallic" ("hermaphrodite") mating types of the protist, and each organism has a mating type. The homothallic ones don't need other individuals to have sex and make offspring. The heterothallic ones do need other individuals. These mating types are defined not by a sex chromosome like in humans, but by a single gene. When they say 720 sexes, what they mean is that we have found 720 different DNA sequences at the mating type gene which have somewhat different mating behaviors.
I think that your evaluation is correct that the journalists are being pretty inexact here. But I think also that it's important to recognize that basically all of biology is sexual, one way or another.


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Is there any way to identify if chromosomes are inherited from the same parent?
I'm a PhD student in bioinformatics working on genomic data, and I was wondering:
If I have access to a person's chromosomes, is there an assay that can determine that two chromosomes come from the same parent, or do I need to sequence their DNA, refer to statistical genomics and infer the ethnic group of each chromosome?

‘Have access to their chromosomes’ - what does this mean? What kind of data do you have?

@user438383 I meant more theoretically - if I had access to samples of a person's DNA. My current dataset it mutations under the form of a vcf file.

Does this answer your question? What can you learn about someone's mother and father by examining their DNA?

@MaximilianPress although your answer to that question does provide some information towards answering mine, I don't think they are duplicates as such. For starters I am looking for quite technical answers, preferrably based on current literature, whereas OP in the linked question was looking for much broader information.

If that is your goal, I would suggest posting instead on bioinformatics.stackexchange.com. Biology SE is more likely to address your question at a higher level with a range of methodologies, such as the linked answer.

@MaximilianPress This could be a bioinformatics question yes, but I feel like it does ride the line between the two. The answer to this could be found in bioinformatics analyses, or it could lie in molecular biology assays.

@Whitehot sure, and that is more or less the answer that was provided at the link, was suggestions of both bioinformatic and wet-lab methods for examining this problem. If those methods are not adequate to answer your question, then it is good to know exactly how your question is not addressed!

There is an implicit assumption in the question that current technology can obtain the correct sequences for each of the two homologous chromosomes (for all chromosome pairs) of a diploid individual.  That is beyond the state of the art today.
In a few special circumstances, the latest methods can begin to approach that goal.  For instance, where the parents of the individual are from highly distinct populations such as subspecies, and the populations have good sequence characterizations, then some have come close to resolving the separate sequences of homologous chromosomes.  See, for example, "Haplotype-resolved genomes provide insights into structural variation and gene content in Angus and Brahman cattle" and "Ultracontinuous Single Haplotype Genome Assemblies for the Domestic Cat (Felis catus) and Asian Leopard Cat (Prionailurus bengalensis)".
Even when the genomes of the individual's two parents are also available (a set called a "trio"), correctly resolving the complete sequences of the individual's homologous chromosomes is difficult.  See for instance, "Accurate haplotype-resolved assembly reveals the origin of structural variants for human trios".

Interesting, I knew that it was a complex task but not that it was that challenging! I am using 1000 Genomes project data, and in this paper https://wellcomeopenresearch.org/articles/4-50 they describe how they created SNP data for both chromosomes in each pair, in the "Phasing and imputation" section. Do you think that this data is unreliable?

I would quibble with this answer: obtaining phased diploid assemblies is an active research area and has been more or less achieved at quite good accuracy, e.g. https://www.nature.com/articles/s41587-020-0711-0. See also https://www.nature.com/articles/s41467-020-20536-y

@Whitehot the phasing/imputation approaches that you mention are reliant on the linkage of alleles in the population- they are likely to be more or less accurate at the level of the population, but not terribly accurate at the level of the individual. Full, reasonably accurate individual-level haplotypes require long reads or in vivo linkage data (e.g. Hi-C), or ideally both. See refs in my other comment.


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Does food grade diatomaceous earth contain mercury
Not sure if this is the right site to ask this question, but since diatomes are or once were biological creatures it seemed to fit this one more than any of the others. I have been supplementing my food, and my cats food occasionally, with food grade diatomaceous earth which is supposed to be healthy and good for bones, teath, skin, hair and cell growth among other things, it is inhert & has no known side effects, its is used regularly as a cattle feed additive & also as a pesticide or anti-parasite treatment to kill worms, fluke and other critters.. I only started doing this as a supplement as i do not generally eat alot of vegtables or fruit & am more of a snacking person.. However I just seen an article that say's beer, wine and many other beverages contain mercury as many of them are filtered using diatomaceous earth (Which pressumably would have to be Food Grade). If there are any minerologist/biologist's is this true? Where does the mercury come from? is it safe? Can the human body filter this out?

That's an earth sciences question or a food forum question. google will research better than we can. first result http://www.vitaletherapeutics.org/deanlsbw.htm

You are more likely to find mercury in natural gas ( before the gas plant filters it out).

Thank you for the reference com.prehensible, thats exactly what i was looking for. if this question is not suited here please can someone migrate it to earth science or similar...


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How can I liquefy egg shell membrane
I want to extract egg shell membrane from the eggs.
And I want to put them together and turn them into fluid so that I can make whatever shape I want.
Is there any method that can make them into fluid?( like using acid or whatever)
+a egg shell membrane consist of collagen.

you need to edit your question,a large part of the membrane in eggs are made of keratin.source: https://www.exploratorium.edu/cooking/eggs/eggcomposition.html

some research is expected before posting.

If egg shell membrane really consists of collagen - here is your answer:
Cook it at 160 degrees Fahrenheit (=about 71 degrees Celsius) over a long period of time until it turns into a gel. I am pretty sure it will harden as soon as it is fully cooled down.
"collagen begins to melt at about 160F and turns to a rich liquid,gelatin"
"Denaturation of the collagen molecule is a kinetic process, and hence a function of both temperature and duration of heating. Cooking at low temperatures require long periods of time to liquify collagen."
Source: https://www.scienceofcooking.com/meat/slow_cooking1.htm


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Bug identification: how to identify this bug?
I found this cast/shed skin from molting in my house:

The house is in the countryside by the beach in Portugal with a temperate and humid climate and mostly pine trees and eucalyptus. Humidity is 84% and temperature around 21ºC indoors. The size is 1-2 cm.
From bugguide.net it looks like a beetle. I also tried InsectIdentification.org but it's limited to US, Canada, and Mexico.
Can anyone identify the cast skin? And does such bug identification require an expert or can an amateur use some resources to do it?

It is not a cast skin, as adults do not molt, and this is an adult beetle. You can tell because it has elytra (forewings), and only adults have them. It reminds me of a Scarab.

I can't see the forewings, but I trust your judgment! Would you like to write an answer? And what resources would you recommend for a newbie to identify bugs?

Trying to identify this specimen much past family (and I agree with @Karl WRT that) might not be possible, as the head appears to be missing; in addition, this appears to be the remains of a spider's meal (there are obvious fibers -- probably silk -- visible in both photographs).


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What is this bug on wood and paper?
I live in a Mediterranean climate and I often find these bugs in wooden furniture and sometimes around books. I would like to find the name and a solution to exterminate them.
The bug is black looks like this on a wooden kitchen utensil:

and the offspring seem white, and look like this on another kitchen utensil:

I squished an adult bug, let it dry, and put it under the microscope. The head looks like this:

The legs look like this:

If needed, I can try to get better microscope images.
I also took a video of them moving: here are the adult bug and the offspring.
I also sometimes hear a sound, like a small bug drilling into wood, but am not sure it belongs to this bug and haven't been able to record it.
What is this bug, and how can I eradicate it?

Very hard to say for sure - possibly a "book louse" or a mite (flour mite?) of some sort.

@bob1 Thanks! They look more like a flour mite than a book louse (it doesn't seem to have wings). I'll measure the size with a caliper next time I find one. Also, I tend to find them around ground condiments like cumin and sage. How can I be sure of the species?

It takes some expertise in ID to do so, you'd need clear pictures of various parts of the anatomy and a relevant reference with binomial key.

I'll see if I can get a better microscope for pictures. Where can I find a relevant reference or the binomial key? Do you suggest a better way to exterminate these insects?

A better picture isn't necessarily due to the microscope, though it does look like you have some chromatic and spherical aberation with that one. Better pictures would require better mounting and different illumination - a high-power dissecting scope would be better. I don't know where to find such a key - try the International Committee on Zoological Nomenclature for references. Best way to exterminate is to keep the whole area clean and dry.


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How does temperature affect photosynthesis?
I am doing a lab for biology and my teacher required me to do this virtual lab. However, it does not make sense when seeing the results of the lab. In 30 second trials, it shows that there are 16 bubbles at 10C, 6 bubbles at 25C and 19 at 40C. This should not happen as 25C is near the optimal temperature (at least in respiration) but it shows the opposite.
Is the site wrong or am I wrong?
Site link: http://www.kscience.co.uk/animations/photolab.htm
Constants: 50 Light intensity, full disolved co2, white light color.

Welcome to SE Biology. I am afraid that questions here have to be self-contained. A link to a reference is OK, but readers cannot be expected to go to another site to  find out what the question is. At present the question is not clear. What is the design of the experiment, what are the bubbles supposed to be, and where is it stated that photosynthesis should be optimal at 25C? You need to clarify your question.

It doesn’t look like the link is working for me on iOS - can you add a bit more information or a screenshot to demonstrate what the lab looks like?

Your experiment should look something like this: The effect of temperature on photosynthetic rate of Elodea (pondweed). I assume you used Elodea canadensis for your test. Maybe the plant is already a bit "exhausted" - try to take a different branch. Or maybe it needs more time to get used to the new temperature.


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What are the teeth of the viperfish composed of?
One of the viperfish's (genus Chauliodus) most unique traits is the transparent, needle-like teeth. Some other abyssopelagic fish (e.g. certain angler fish) have similar teeth. I'm curious as to what these teeth are actually made of. They clearly aren't made of bone, and from what I can tell from various fish skeletons, they decay fairly quickly with the rest of the fish.

They are not unique
The are made of enamel and dentine just like ours, Even the enamel in human teeth is translucent. Note viper fish are tiny so their teeth are likewise very small, so they can look transparent just by being translucent an small. Hydroxyapatite, the mineral enamel and dentine are made of is translucent. the difference is in the crystal structure,(teeth or often porous which leads to more scattering and less transparency similar to why dry paper is white and wet paper is translucent (also true of teeth)). Impurities or more precisely what else is present in the enamel and dentine are present has an effect as well, as teeth are not just hydroxyapatite.
Source for the composition of teeth.
source for the translucency and microstructure of teeth
Source discussing how translucency changes with mineralization in cow teeth.

This answer would be improved if it contained a citation to anything having to do with the viperfish or a discussion of the translucency of enamel in particular crystal alignments. In other words, I fear that providing a citation implies that the information in the rest of your answer is found in that citation, which it is not.

Viperfish are not alone in having transparent teeth is is very common, but something on transparency and crystalography is a good idea.


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Why do some mammals have incomplete orbits?
I've noticed that a lot of carnivorous/omnivorous mammals (most, if not all the members of carnivora and some ancestral cetaceans), as well as some herbivores (marsupials), have incomplete orbits that merge into the temple near the zygomatic arch. I'm wondering what the evolutionary purpose of this is, as well as why we would lack them.

not some, most mammals have incomplete orbits. only a few groups have closed it. It seems to be related to the position of the temporal fossa. https://www.ncbi.nlm.nih.gov/pubmed/15844100 the whole region varies quite a lot in mammals https://www.ncbi.nlm.nih.gov/pubmed/18211281

Some things to think about are the size of the field of view, the protection of the eye, and the normal orientation of the head.


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Are there animals that usually sneeze with their eyes open?
As per title. I believe that most animals tend to sneeze with their eyes closed, but wonder if any normally keep their eyes open.
Is it the case?

Maybe they can!

These marine iguanas seem to:
https://www.youtube.com/watch?v=6G6ZL0fbLHQ
This duck does too:
https://www.youtube.com/watch?v=ZaqeRn6B7sg
Your "most animals" might just be mammals.
This turtle, however, does seem to sneeze with its eyes closed:
https://www.youtube.com/watch?v=rQTJjmfPHdE


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which exact mechanism triggers the first cell differentiation after n divisions?
I would like to understand which mechanism triggers the first cell differentiation after n divisions.
I read previous articles on SE and Wikipedia articles on cellular differentiation and embryogenesis but still fail to understand what exactly makes it so that starting from a given division cells suddenly start to be different.
Wikipedia claims that

In the first hours after fertilization, this cell divides into
  identical cells. In humans, approximately four days after
  fertilization and after several cycles of cell division, these cells
  begin to specialize, forming a hollow sphere of cells, called a
  blastocyst

but do not explain why they begin to specialize.
I could imagine

that a cell has a "counter" on the number of divisions which triggers differentiation after a given amount of divisions
or a chemical substance (either cell-borne or external) forces a change in the division

but why some cells would become "cell A" and some others "cell B"?
I am fairly sure that the biochemical mechanisms which regulate the life of a grown up mechanism can explain cellular differentiation (through hormones for instance) -- I am however interested by this specific moment, this n-th division where identical cells become differentiated.

There are two different questions here. One is how "identical" cells become different types of cells. The other is why do the cells start differentiating when they do.

I am interested in the why more than the how

The why and the how are somewhat inseparable.

The first differentiation in human embryogenesis is from early blastomeres into trophoblast, which forms the outer layer of the blastocyst, and inner cell mass (ICM). It may be unsurprising then that cells on the inside of the 8-16 cell stage morula
differentiate into ICM whereas those on the outside differentiate into trophoblast. However it is currently unclear whether this is a causal relationship (the inside-outside model) or whether blastocyst patterning is set-up earlier in cleavage (such as in the apicobasal polarity model) or if it is some combination of the two.
You were correct in imagining that tissue patterning is determined by chemical substances: a very broad class called morphogens. Cells don't necessarily count how many times they have divided but cell division can certainly affect morphogen concentration and localisation. I suppose in some sense you could describe this as a clock. I wouldn't though, especially because mammalian cleavage is asynchronous.
One line of studies showed that a transcription factor called Tead4 specifies trophoblast$^{ref}$. It was then shown that Tead4 can be regulated by cell-cell contact (mediated by Hippo signalling) $^{ref}$. They hypothesised that the magnitude of cell-cell contact could provide a mechanism by which Tead4 localisation could be controlled in presumptive trophoblast and ICM. This could explain why the cells have different fates because inner cells are completely surrounded (more cell junctions) whereas outer cells are largely exposed to the medium. Note that I only provided that as an example of a possible mechanism. It is not confirmed and, as with any model, the real picture is incredibly more complex and likely involves many factors.
I'm reluctant to go into too much detail on this because you're asking about a complex process that is still under active study and I'm unclear as to how much information you actually want. A book could be written on this subject alone, and many review papers have been published. Here's a recent one:
Development: Do Mouse Embryos Play Dice?
I suggest you read that and then if you have further, more specific questions, we can try and answer them for you.

Thank you for the detailed answer. It looks like a horrendously complicated mechanism (I have a PhD in Physics and the basic ideas can be explained with some hand waving - I was foolishly expecting the same in embryogenesis :)).

I guess the hand wavy explanation would be that tissue patterning is done by chemical signals which can come from a variety of sources. In the case of the first differentiation in human development, the exact mechanism has yet to be fully characterised. It could be that the cells on the inside are in a different environment than the outside cells and so develop differently. Or it could be that the cells that become the inside are already fated for a certain development path.

Also, I sometimes ask basic physics questions and even the hand waving explanations tend to go over my head. For me, hand waving only begs more questions.

Why cells differentiate or specialize is an ephemeral question. I'll make an attempt to answer--the more specialized cells an organism has, the better equipped that organism is to function.
In a given organism, differentiation after n divisions or after t time during development is due to changes that are both intrinsic (genetic) or extrinsic (environmental). For two examples of how intrinsic and extrinsic determinants interact are:
"Unfolding a chordate developmental program, one cell at a time: invariant cell lineages, short-range inductions and evolutionary plasticity in ascidians."
and
"Cell Patterning"
If a cell changes after n divisions at t time, it may be due to its local cellular environment, or in the case of some animals, hormonal regulation that each cell may respond to differently.
As such, why do cell differentiate? Because in organisms, which are large collections of cells, survival is wholly dependent on the segregation of cellular function.

It would be great if you used some references to support your response!

Thanks! I've done that and edited my response accordingly.

Thank you for the answer and the links but I was not really asking why cells differentiate in general but rather what mechanism triggers the first cell differentiation. Possibly in an understandable way (which, per my comment above, seems to be rather difficult)

Richard and Natalie Gordon proposed that there is a mechanically sensitive bistable organelle in the apical ends of cells in cell sheets about to differentiate (competent) and they are under mechanical tension. Depending on where the cell is on the sheet the tension will be resolved by either the apical end contracting or the apical end expanding. This will result in a biomechanical transduction signal from the cytoskeleton that is passed on to the nucleus which then changes gene expression. If the cell has experienced contraction, one signal is sent and it the cell has experienced expansion then another signal is sent. The signal is the determination of cell fate and is done by the cytoskeleton. They have outlined their research and their theory of differentiation waves in detail in their book "Embryogenesis Explained". In your specific example, the first differentiation takes place during mammalian compaction. Cells on the outside expand and become determined to be trophoblast, cells on the inside contract and become determined to be the inner cell mass. All the other stuff, gene expression changes, signalling proteins and the rest are secondary, the result of differentiation after the cytoskeleton determines cell fate with mechanical signals. Note this hypothesis is very detailed and specific, relatively simple overall, and based in mechanics and physics. It is highly testable with no "hand waving". You can read the short version of the theory for free in https://link.springer.com/article/10.1186/s12976-016-0037-2


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Why does female's age of puberty inform on mating system?
Reading from Does increased calorie intake cause increase in libido in humans?, @AlexStone says:

I'm aware that humans have a dual mating strategy - somewhere between pair bond and casual mating. There are a number of physical measures to indicate this - such as sexual dimorphism between male and female, sperm counts and tested size, as well as age of puberty of females.

How does the age of puberty of females can inform us on the mating strategy?
Why does the observed age of puberty of females suggests a "dual mating strategy"?


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Green Film Build up in Glass Water Bottle
So I have this Large Water Jug that I fill only water with.
And this is the 2nd time there has been a layer of green film that builds up at the bottom of the bottle. I don't have any way of getting to the bottom to clean this.
I wanted to know.

What does this green film consist of?
What Chemicals or methods can I use to remove the film without having to manually scrub the bottle?

Thanks
ps. not sure if this was the correct place to ask this question.

a) algae b) if it has formed a scummy biofilm, it might have to be harsh treatment to get it off. kerosene?

@shigeta What about more common household items?

please, remove part on cleaning, as it might be considered as requesting advice concerning personal health. We don't want to be responsible for your/your dog's/your child's chemical poisoning

(but I just leaned my water bottle from that using several washes with 70% ethanol followed by wash with bleach solution. Then rinse with tap water x 5, rinse with distilled water x 5, rinse with MilliQ water x 1)

try diluted bleach - or if you go to the grocery/hardware store you should be able to buy a bottle brush for cheap.

Another way to "scrub" things you can't reach is with a handful or more of sand or tiny pebbles. Bleach and sand swirled around vigorously for a few minutes will remove the majority of it, if not all.

What seems to be forming in reusable water bottles and water coolers is a biofilm. Since it is a complicated system, after maturation biofilm might be very hard to remove without scrubbing. There is a nice article about cleaning water coolers, which might give you some information.
If you look closer on the Google Scholar search results, you'll find that quite a bit of research has been conducted in the area of sanitation of water coolers and study of their flora. For example, consider the following paper from 1996: Analysis of the Virulence Characteristics of Bacteria Isolated from Bottled, Water Cooler, and Tap Water.
There is a very nice list (Table 1) of different bacteria isolated from water. But I would like to point your attention to following table from the paper:

Quote from methods section listing tested antibiotics:

The
  natural and first generation antibiotics included:
  penicillin, ampicillin, erythromycin, kanamycin,
  streptomycin, tetracycline, chloramphenicol, and
  sulphonamide. The synthetic and later generation
  antibiotics included: gentamicin, cefoxitin,
  cefoperazone, oxacillin, piperacillin, imipenem,
  ciprofloxacin, and sulphonamideftrimethoprim

The green slime you observe, I think, is a combination of all those bacteria, plus some that were brought after the water was poured into the container. And it seems that all commercial sources that you didn't purify yourself, will have a variety of microorganisms growing. And around 5% of the total bacterial cell mass is resistant to common antibiotics.


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Long strand of white eggs on balcony cat net - What insect do they belong to?
In the last few weeks we've noticed multiple strands of tiny white eggs appearing on our balcony cat net. It seems that they were always laid after rainfall (we had plenty in the last few days). Old eggs were washed away and new ones appeared soon after.
The way they're arranged, I have a feeling those could be moth eggs. Or is it something else? Should we get rid of it?
p.s.: We live in southern Germany.

Possibly snail eggs. Similar posts: what kind of hot pink eggs are these, what is this agglomeration of pink cells I found attached to a stone, can someone identify these eggs, and what made this is it an egg sac.


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How can co-dominant alleles work in flower petals?
I am studying gene inheritance, and I understand complete dominance/co-dominance and incomplete dominant penetrance in flowers. I know how to recognize each case.
However, how does co-dominance work? If I understand correctly: when a gene is transcribed, both alleles are transcribed. Hence, for flower petals, if I have a "red" allele and "white" allele, and there is incomplete dominant penetrance, I get rose petals. However, if both alleles are co-dominant, why are petals either red or white? Aren't both alleles transcribed? Or perhaps, in the case of co-dominance, heterochromatin is responsible for shutting down one allele in lineage cells?
I hope that I am expressing myself correctly. Thank you very much for your time!

We tend to use "incomplete dominance" to describes situation of haplo-insufficiency.  The white flower petal has two broken alleles for making pigment, and one working copy doesn't yield enough pigment to make the flower look as red as it would if it had two working red pigment alleles.
"Co-dominance" is for two functioning alleles when the effect is that you can see them each, and the result is not an intermediate blend.  Like having a working A antigen and a working B antigen. A blood will not clot when mixed with A blood.  AB blood doesn't halfway clot, it also won't clot at all, just like A blood.


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Can we make a rough estimate of the number of generations since the origin of life?
According to what we've learnt :

we can approximate the number of generations since the first human pretty much like us (depending what / who we talk about).
we have an idea of the series of life forms we come from.

So is it possible to give it a very rough number ? Or it's not, because of some issues - but which ones ? (I only think about the many, short generations of the first forms, which moreover we don't really know about, as a limit to counting)
What if we stop counting at "unicellular" (or else) ?

Interesting question. Using the tree of life, we could get back as far as the last universal common ancestor (LUCA). I don't know if we can estimate generation times for early prokaryotes within an order of magnitude, though. Things get even harder before LUCA, because we don't know what life was like then. For example, how long did a generation last in the RNA world (if there was one)? Is the concept of a generation even meaningful in that world?

Perhaps we stick to an organism, that has been around a while, get its generation time, and calculate back from that. But as Corvus said, the more back you go, the more inaccurate you get.

shouldn't be too hard. see this http://biology.stackexchange.com/a/19569/8290

If you're willing to accept many orders of magnitude and define life as the Last Universal Common Ancestor.
For the rest of this answer, life begins 3.5 Gya with cyanobacterial mats and stromatolites and so on. Genetically the LUCA is dated to around this time, which matches the fossil record and everything's great. The LUCA can't have sprung from nothingness, so there may(will) have been (many)generations before the LUCA of things we would recognize as life, but I'm ignoring them. If they wanted to be considered they should have left descendants.
The fastest doubling times for modern bacteria are about 7-9 minutes but most are longer. E. coli takes about 20 minutes, and yeast takes hours. Given the 3.5 billion year clock, that gives an upper bound of about 1x10^14 generations. (Green sea turtles take 20-30 years to reach sexual maturity, or 1.1x10^9 generations). Something a bit representative is probably Pelagobacter ubique, which is vastly successful and takes about 29 hours to divide. Averaging out ice ages and so on and skipping the slowing of generations multicellularity probably implies(the Cambrian explosion is 82% of the way to the present day, being only 543 million years ago. We could account for it, but our guesses on generation time are way more inaccurate than any possible effect that could have) would estimate about 1x10^12 generations.

If they wanted to be considered they should have left descendants :-)

Averaging out ice ages and so on and skipping the slowing of generations Is it just hand-waving (I say that respectfully)? If not, I would be interested in math behind these statements

Nope, it's hand-waving. :( It would be nice to take into account but the largest source of error is the average generation time pre-cambrian explosion. Estimates of that need to be within 15% or so to outweigh the error introduced by assuming there has been one generation since the Cambrian explosion, and even tighter to justify accounting for a yearly spawn(starting in the devonian, maybe? I'd have to review the evolution of land animals) instead of just random growth. It's basically a significant figures issue.

This question has actually been covered (although not to the complete extent of evolutionary history) by Richard Dawkins in his book The Ancestor's Tale.
He gives the following estimates of LUCA time and generations:
Monkeys and apes: 40MY(3M)
Mammals: 180MY(120M)
Reptiles: 310MY(170M)
Ray finned fish: 440MY(195M)
Sharks, hagfish and lampreys: 530MY(240M)
Lancelets and all chordates: 560MY(270M)
However, he ceases to provide any generation estimates from here onwards, due to the error and general uncertainties being too large for a meaningful answer.

I like that this answer and my answer are both answers to the question but consider exclusively different creatures.


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Question on protonation/deprotonation of amino acid side chains
I understand that actual pKa of amino acid side chains is greatly influenced by the surrounding environment. I am trying to deeply understand the equilibrium between protonated and deprotonated form of amino acid side chain by taking Lys as an example. Lets imagine a protein having solvent exposed Lys residue. At physiological pH, theoretically this Lys residue on every protein is in largely protonated form (ofcourse some are deprotonated). Now say with some reagent I modify few of this particular Lys residue (using NHS ester etc.). Now does the remaining unmodified Lys residues undergo protonation/deprotonation to nullify the effect caused by the chemical modification and maintain the state of such equilibrium? Also, I am curious is it always impossible to achieve 100 % modification of this particular Lys residue due to the existence of equilibrium state?

I want you to imagine the protons pressing on the radicals. When you increase the protons in solution, the pressure becomes greater. Some radicals will pick up protons before others can. Water also comes into play pulling the protons from the radicals so you have this sort of back and forth at the very small scale. Equilibrium is when these effects basically cancel out, the radicals lose some protons to water which they gain back the next moment. The system sensibly tends towards equilibrium if you think about it. Now try thinking about what happens if I decrease the amount of protons.


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Preparing sample for SDS PAGE
I have more than 10 cell lysate samples (70 µL each) whose concentration varies from 1.9 mg/mL to 4.8 mg/mL. I have 5X and 2X SDS sample buffers. I would like to prepare SDS PAGE samples in such a way that the final concentration of all the protein samples would be equal. I am struggling to deal with it.
What I know is while using 5X buffer, for 4 parts of sample we use 1 part of buffer to make it finally 1X. Similarly, for 2X buffer, we use equal amounts of buffer and sample to make 1X. Also, I would like to know will it be a problem if I make it more than 1X? Why we need 1X?

Usually you would want to keep the amount same, not the concentration. However, if you still want the concentration to be the same then you can add suitable amounts of PBS or your lysis buffer.
For e.g. if you have two samples with 1mg/ml and 4mg/ml concentrations and you want to load 20μg of total protein, then you can take 20μl of first sample and add 5μl of 5x loading buffer. For the second sample, you would take 5μl of the sample, 5μl of 5x loading buffer and 15μl PBS.

Why 1x?

Because researchers before us found this composition to be optimal (or just simply stuck to it as a matter of practice).

Would it be a problem if the final concentration of the loading buffer is more than 1x?

Apparently not, in my experience if it is up to 1.5x. Never checked higher concentrations.

Thanks for your answer. I want same concentration in order to load equal volume to the gel. I know it's the amount to be the same not the volume/concentration. But as I have many samples (10+) it's more convenient to pipette out equal volume & less error prone.

@Science123 Then you can use PBS to make up that volume. Usually, I do the concentration calculations on Excel. It is also convenient to calculate how much extra PBS to add, in Excel.

Yes. Exactly I used Excel because it is very convenient when we have multiple samples.

Your buffers come concentrated so that smaller volumes can be packaged, shipped and stored. They're intended for use at a 1X concentration, unless otherwise noted. So for example, if you get a 5X buffer then you should use an appropriate diluent to obtain a 1X concentration in the volume you need. This might be 5 mL (1 part) of 5X buffer into 20 mL (4 parts) of diluent to get 25mL of 1X buffer.
You would have to study the effect of using a more concentrated buffer in your process, but it can may affect your results, and it would certainly cost you more money.
A good question to pose yourself would be: If I use a more concentrated buffer for my SDS-PAGE, and there is variability in the results, how would I be able to tell if the variability came from the buffer concentration or not?
Instead, you can try bringing your protein samples up to the same concentrations first, and then dilute into your buffers as needed.


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Can denatured GFP show fluorescence?
GFP ( green fluorescent protein) can show green fluorescence. And its fluorescence is due to the tri peptide chromophore which is given in below I was wondering, can we observe fluorescence, if we denature it by boiling at 95 degree celsius? Say can we observe fluorescence band in SDS-PAGE?
I assume it can show some fluorescence as it is not due to any cofactors etc.

According to PDB (protein data bank — a repository for protein structures) the chromophore must be protected from interaction with water molecules to fluoresce.

The chromophore is found right in the middle of the [protein], totally shielded from the surrounding environment. This shielding is essential for the fluorescence. The jostling water molecules would normally rob the chromophore of its energy once it absorbs a photon. But inside the protein, it is protected, releasing the energy instead as a slightly less energetic photon of light.

This means that denaturing the protein will result in quenching of the fluorescence1, so you are unlikely to see significant signal on a denaturing gel.  In fact, as WYSIWYG has pointed out, fluorescence has been used as a marker of renaturation of GFP1.
Reference:
1: R.Y. Tsien (1998) The green fluorescent protein. Annual Review of Biochemistry 67, 509-544.

Additionally, there are biophysical studies on gfp folding in which increased fluorescence corresponds to folded state.

@WYSIWYG any reference if you give it would be appreciated

I wonder what would happen if you exchange the water in the gel with methanol or ethanol. Will these quench the fluorescence?

@Science123 check this out: https://www.pnas.org/content/109/44/17832


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Are there any DNA base sequences that are shared by every living being that we know of? And if yes, are some of those sequences "silent"?
In "every living being" I am not including viruses as another question already answered that.
I have read that some part of the DNA sequences of humans and other animals/plants are "silent" as in not affecting the phenotype of a species.
I was wondering if there was some part of those silent sequences that are also common to all living being.

What is your length cut-off? Any arbitrary sequence of 10 base pairs is likely to be found in a 1 Mb pair genome, if you are talking about exact matches. And where exactly did you read this? We need to be able to check and assess your source.

I see, sorry about that it's my first time here. My source about the non-coding bit is on the french Wikipedia I'm afraid but here it is: link The paragraph titled "Régions non-codantes" talks about the region of the DNA that are not coding. About the size of the sequence, I don't really know but I would say any length that seems to be long enough for not being just a probable occurrence but something a bit more "meaningful". I understand that this is probably way too vague.

It’s ok. I can read French. I’ll have a look at it when I have a moment. Can you give me the exact French text (just the start will do) so I can locate the section you mention. (For the benefit of everyone, I’ll answer in English.)

Yes, so the paragraph talking about non-coding sequences is titled "Régions non-codantes" and more specifically the paragraph starting with "En plus des gènes, les génomes contiennent en effet souvent des pseudogènes. Ce sont des séquences qui ont de nombreuses caractéristiques des gènes (séquences codantes, séquence promoteur, signaux d'épissage…), mais qui ne sont pas fonctionnelles et ne conduisent donc pas à la production d'une protéine." is the one that specifically talks about the parts of the DNA that cannot produce a protein.

OK. I'll can address that when I get a moment. But where does it mention "sequences shared by every living being"?

Oh it doesn't mention that, this article is only about some sequences being silent. Sorry if that was unclear but that was the point of my question: Are there any silent sequences that are shared by everything alive?

The answer to that is No. I'll write you an explanatory answer but I need to see what parts of it have been covered in previous questions. It may be the weekend before I have time to do it, though.

No worries at all, thanks for taking the time to consider my question!


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Identification of this bug or insect
I found this bug dead in my house in Mississauga, ON, Canada.
I didn't have a ruler around so a regular toothpick was used to show the size.
I'm thinking it's a pill bug but I want to make sure.

Yes, that is a pillbug, or "roly-poly", Subphylum, Crustacea, class Malacostraca, family Armadillidiidae.  https://en.wikipedia.org/wiki/Armadillidiidae


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Which organelle synthesizes glycogen phosphorylase and why?
I know that glycogen phosphorylase is not synthesized in the rough endoplasmic reticulum of liver cells, unlike many other proteins such as insulin receptor, lysosomal enzyme and serum albumin. I would like to know the organelle where glycogen phosphorylase is made and why it is made there.

Protein translation occurs via ribosomes bound to strands of messenger RNA in the cytoplasm; these structures are called polysomes but don't have a membrane surrounding them so you might not want to call them organelles. Polysomes making proteins destined for secretion, for the plasma membrane, or for some organelles (like your examples) are directed to the endoplasmic reticulum via a signal peptide typically near the beginning of the translated sequence. The combination of polysomes and endoplasmic reticulum is what is called rough endoplasmic reticulum. See this Wikipedia page for a more complete explanation of how particular proteins are targeted to their correct locations.


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Do animals get sick with hemorrhoids?
Do animals get sick with hemorrhoids ?
And why Humans are most affected of it ?
Is it because the gravity center of Humans is sittuated in the anal ?

Why are haemorrhoids more common in humans than in animals?
This is due to the majority of animals, including apes, are on all fours. Only the human species stands and walks straight up with two feet. Therefore, the blood in the body has enhanced arduousness in circulating and travelling back to the heart. A justification for the commonness of hemorrhoids in humans, is there is a higher frequency of blood congestion which then further leads to hemorrhoids.
There are animals which can get haemorrhoids

Cats
Dogs
Apes
Horses

The reasons and causes why animals can also get hemorrhoids is similar to humans, besides the structural reasons. This may include:
In Horses

The horse may strain while delivering young ones

When the bowel movements are disturbed, as in constipation, it leads to an increase in pressure applied to the rectum region. Unlike humans, the increased pressure from constipation does not come from straining to get the excrements out, but from the impaction of the excrements within the horse and the resultant pressure that causes.  This in turn leads to expansion of the blood vessels around the anus and this may cause hemorrhoids and eventually bleeding.

In cats

One of the main reasons behind the occurrence of cat hemorrhoids is heredity, which plays a major role in deciding who would and who would not get afflicted with this condition.
Diets low in fiber and liquid content are the main cause of constipation, which in turn leads to excess pressure being applied during defecation and straining when bowels are passed. Too much pressure in the rectum and lower abdomen causes blood vessels in this region to expand, thus leading to the creation of lumps called hemorrhoids.

There have also been some investigations in which haemorrhoids were induced by ligation of the inferior haemorrhoidal vein into apes. The outcome of this was that after a certain amount of days, there were hemorrhoidal piles in the anus in fifty percent of the animals. The outcome was unremarkable. There was no bleeding and all animals showed no signs of pain or suffering.
References:

"Horse Haemorrhoids, Horse Hemorrhoids, Horse Haemorrhoids, Horse Piles - Web. 01 Mar. 2016.
"Result Filters." National Center for Biotechnology Information. U.S. National Library of Medicine, Sept.-Oct. 2006. Web. 01 Mar. 2016.


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Limited space for animals - how is that bad?
I am writing an English paper wherein I have to appeal for change in the way humans treat wildlife. I was initially given a situation wherein I took a ferry in a certain area and saw a dead baby dolphin.
Along the way, I (it is written in second person) apparently notice how little water is now available for the dolphins (due to some bridge being constructed).
What exactly is bad for dolphins (or animals in general) when they have limited space to roam around?
So far I thought of dolphins hitting boats due to the crowded state of the area in question.

I would consider food supplies too. If you trap a population of dolphins in a small area, and they eat all the available food there, they will begin to starve if they cannot leave to get more food.

The building of a bridge on a river seems like an example of habitat fragmentation. There are a number of reasons why this may be detrimental to the animals.

Reduced resources available. I'm not too familiar with dolphins, but all animals need food, shelter and a place to raise their young. A smaller habitat can't support as many animals due to limited resources.
Isolation from other habitats. The bridge may cut off the dolphins on one side of the bridge from the other side, meaning they can't mate with dolphins on the other side or migrate. The fact that dolphins on one side of the bridge can only mate with the other dolphins that share that size causes a decrease in the genetic variability on both sides of the bridge. Decreased genetic variability means an increase in inbreeding depression and reduced ability to adapt to disease and environmental changes.
The edge effect. This means that areas next to the edge of the habitat (i.e. next to the bridge) will be even less suitable than they were before

Could also be good to mention the psychological effects, especially on more social creatures like dolphins, of being in a confined area.


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What is the convention for log notation in biology?
I'm reading through some oldish (1980s) papers on length-weight relationships in fish and crustaceans. Many report log-log relationships without specifying whether this is natural log, base 10, etc. In mathematics log is typically assumed to mean natural log, but the results reported in these papers make more sense if you assume "log" means "log base 10".
Is there a convention in biology that I should be aware of?

Welcome to Biology S.E.! If you need any assistance with the site, please visit The Help Center.

I typically use log10 for doing things like dose-response curves, but something like fold-induction of genes may be better expressed by log2. It would probably be safe to assume log10 if they don't specify, but for your own work you should definitely specify which base you're using. I can't recall ever seeing the natural log (base e) in biological papers, but that may just be my fields of interest, which aren't terribly mathematically-heavy.

There is a reason for prevalent usage of log2 and log10 compared to loge in biology and other experimental sciences. Usually while doing measurements we are generally interested in fold changes and we generally talk in the sense of two-fold (or multiples of two) or ten-fold.
Doubling is a common phenomenon at least in case of growth and so a two-fold change would represent an event of doubling. log2 gives you the extent of "doubling". Even in computer systems memory is always in the exponents of two (because of binary); so even there log2 would make sense.
In biology you would generally not see a ten-fold change but in physics it is relatively common. Most values are represented in scientific notation which basically uses an exponent of 10. Also the metric units are in multiples of 10. Here log10 would be more suitable.
loge has a special mathematical importance i.e. it can be denoted as a series. The euler's number has other important properties too. Therefore in most theoretical studies, both in biology and physics, loge is preferred because it makes more mathematical sense.
To sum up, experimentalists prefer log2 or log10 because they are better for representing measurements whereas theoreticians prefer loge because of its mathematical importance.
W.r.t the old paper that reports log-log relationships, the base of the logarithm wouldn't make any difference to the slope. But most likely it must be log10 (I think back then log10 was the default log; log2 would be much more suitable for lengths and weights of organisms compared to log10 because these measures would not vary in multiples of 10).

i'd say that there is no special "mathematical importance" in $log_e=ln$, it is just cleaner. If $x=e^t$, then $ln(x)=t$, without any hanging constants of conversion $log_e\rightarrow log_{10}$. In experiment it makes more sense to measure change in 2 or 10 times, than 2.71

@aandreev well it is easy when you are writing functions to describe a system. you can always convert the scales but when you are writing equations then ln is a direct result of some equations such as $\int \frac{dx}{x}$


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Which birds are capable of flying both forward and backwards?
Very random question - but it's often said that the hummingbird is the only bird that can fly backwards (for example, https://www.worldatlas.com/articles/which-is-the-only-bird-that-can-fly-backward.html).
Is this true? Aren't there any other birds that can fly both forward and backwards? Is it some kind of bird category of its own?

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you might still have (ideally with references to reliable sources). For this question you should also carefully define what you mean by flying backwards (many birds flying into the wind can move backwards)! ——— Please also take the time to take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!


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How many water molecules will be produced starting from acetyl-CoA in citric acid cycle
I am puzzeled by the answer. Acetyl-CoA when enter citric acid cycle, it produces 3NADH, 1FADH2, total 4 reducing equivalents. If each one makes 1H2O, then 1acetyl-CoA should make 4H2O. Why some textbooks make it 2H2O. In addition, almost like all (or many) do not balance oxygen; they say entering 16O2 and making 16H2O, so how?
Thank you.

Acetyl-CoA has three carbon-hydrogen and one carbon-carbon bond, and it is electrons 'held' in these bonds that are available for biological oxidation.  Thus we say that acetyl-CoA contributes four reducing equivalents. In the TCA cycle, these are transiently passed to NAD+ (to give NADH) and to FAD (to give FADH2): the cofactors may be considered intermediate electron carriers.
It takes 4 electrons (2 reducing equivalents) to make 2 water molecules from 1 O2 (or 4 electrons to reduce 1 oxygen 'atom' to 1 water molecule), but this takes place in the cytochrome oxidase reaction of the respiratory redox chain (with reduced cytochrome C as electron donor), not in the TCA cycle.
It is important to realize that water contributes no reducing equivalents to cellular respiration, and that hydration reactions are neither oxidation or reductions. For water to contribute reducing equivalents, it would have to be 'split', as it is in photosynthesis.
In addition, oxygen is not consumed or produced in the TCA cycle.
The assertion that water can pass electrons to NAD+ in the TCA cycle is an infamous 'textbook error', notably advocated by Efraim Racker in A New Look at Mechanisms of Bioenergetics, and my opinion on this (for what it is worth) is given in this SE answer.
For the role of water in the TCA cycle and the controversies surrounding it, I would recommend the letters by (i) D.E. Atkinson and (ii) Herreros & Garcia-Sancho on TCA cycle confusion published in TIBS and kindly made available by David.  (These references are not indexed by Pubmed and are apparently not available from the TIBS website)

Many thanks user1136. When you say:(or 4 electrons to reduce 1 oxygen 'atom' to 1 water molecule), do you mean 4 electrons or 2 electrons. My main concern is the number of electrons. In Lehninger, the  chapter for oxidative phosphorylation and the figure for path of electrons in complex IV (cytochrome c oxidase), he draw 4 electrons coming from cytochrome c and then to make 1 H2O. I think it is an error. 4 electrons means 2H2O not one (because we breath O2 not single oxygen atom).


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How do cis-regulatory elements and trans-regulatory elements behave differently?
Suppose you are working with an operon in a diploid organism.
I'm looking for either a biochemical or genetic explanation.
What I'm having trouble with mainly is understanding how something would only be able to regulate a gene on one chromosome but not the other. I was thinking cis would be favored because the gene is close by, but everything is just floating around randomly in the cell so it should favor cis either way and level out if you waited long enough.

Aside from "just floating around randomly", molecules also change the conformation of DNA and can move along the DNA. Such effects will propagate along the DNA and thus act in cis but not trans.

I was thinking cis would be favored because the gene is close by

Your intuition is correct.  Cis-regulatory elements like enhancers are more efficient at enhancing transcription of genes in cis than genes in trans, but trans interactions of cis-regulatory elements do occur.  Take a look at figure 2B of this paper and the accompanying text:

... quantitative RT-PCR showed that relative levels of GFP transcripts from constructs inserted at 37B were similar to those from transgenes at 53F, with 1.7% [95% C.I., 1.6–1.8%] of total GFP transcript in eye discs where GMR acts in trans relative to those where activation is in cis ...

The interaction of alleles between homologous chromosomes is called transvection, and this can be realized as binding of the enhancer associated with one allele to the promoter of the other allele.  Figure 9 of this paper is a good explanatory graphic.