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The death of Earthworm
In rainy season when children sprinkle salt on earthworm ,it dies.But salt is not dangerous.We use it daily.Then why earthworm dies?

Welcome to Biology.SE! What research have you done before asking it here?

"salt is not dangerous" - Citation needed.

We use salt daily and ofcourse children don't take it off from mines just to sprinkle it on earthworms.I'm talking of table salt.Any more citation?

Ever heard of what happens when you drink salt water? Alle Dinge sind Gift, und nichts ist ohne Gift, allein die Dosis macht dass ein Ding kein Gift ist: the dose makes the poison.

Re "salt is not dangerous", you might consider why low-salt diets are recommented for people with high blood pressure or some kinds of heart disease, or why rubbing salt into wounds has become a common saying.

Well it is dangerous but it is not poisonous.

@Sara Asfar: Salt certainly is poisonous, it's just that it takes a fairly large amount to kill you.  Per Google, the LD50 of sodium chloride is about 3000 mg/kg, so eating about half a pound would likely be fatal.  Note that it's fairly common for things to be harmless or even necessary for health in small quantities, but harmful or fatal in larger amounts.

It's because on the earth worm skin's special mucous. Acording to this article: Why do earthworms die when salt is sprinkled on them? the mucous makes moist to the worm's skin, which is  vital for their survival. Moreover, the worms don't have a respiratory organs, like lungs, gills, etc. This means that Carbon Dioxide and other characterized as "dump" gases can not be exchanged with the Oxygen. But worms breath through their skin, with the help of these special mucous that are developed on its skin. If their skin dries out the result will be death, because the gas exchange will not last without the mucous help. Similarly, the circulatory system won't function, because its main role is to trade gasses with the cells via red blood cells.
What about salinity?
Salinity is a very important factor for the earthworms health, because high salinity destroy their valunable and sensitive skin and kills the mucous that in fact help the worm to "breathe". Low salt concentrations are very beneficial for the worm, because not only their mortarity level is increaced, there are size changes to the worm's body (noticeable bigger size).
Here are and some photos of a worm that its enviroment has low salinity and high salinity:
High salinity:

Low-to-medium salinity

Source: Why do earthworms die when salt is sprinkled on them?.

When quoting an article, the quotes should be clearly marked, otherwise it's considered a form of plagiarism.

Either it is plagiarism or not but it really gave me answer to my question.Why the people like you seem to proof read other's post just for criticizing them or down vote them@anongoodnurse

@SaraAsfar plagiarism is quite a serious problem. It's not just about getting your answer, the answerer should write a proper answer for this whole community, acknowledging all its conventions and restrictions.

@OP - plagiarism is considered serious malpractice. Please convert your answer into your own words, or explicitly mention where the citations were obtained from at the appropriate places in your answer.

@AliceD Okay I am making it community wiki.

@The_Mad_Fish and why would that make things better?

@AliceD Please check my new anwer that it is based on the article and doesn't show any plagiarism. Thanks.

Also, edits are welcome :)


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Do exon deletions in C.elegans mutants necessarily result in nonsense mediated decay of the transcript?
I am trying to write out my research proposal about a project in C.elegans. There are multiple mutants of the factor that I want to study, each with different mutations. I know that a mutation that abolishes the promoter and transcription start site of the gene will most likely be a null mutant. But what about strains that have internal deletions? For example, if I were to generate mutants missing specific exons such that there was a predicted ORF for the gene product, is this transcript automatically targeted for nonsense mediated decay? I was told that this was a C.elegans specific process (deletion mutants are often protein null?), but I am having trouble finding this information.

I would assume that it may depend on the target in question. If the exon you remove causes errors in splicing of the surrounding introns, degradation will be the likely fate for the transcribed RNA. If the introns are correctly spliced, I would assume that you may end up with a deletion variant of a protein. Whether the deletion variant is functional or not will likely depend on which exon you remove.

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What is the energy cost of an action potential?
As I understand it, ions flow down their electrochemical potentials through ion channels during a neuron's action potential. Otherwise, ion pumps work to restore and maintain the resting membrane potential. What is the energy cost of a neuron's action potential? That is, how much work must the ion pumps perform to restore the resting membrane potential after an action potential occurs?

There is a misconception in your question that comes up a lot, most recently here: https://biology.stackexchange.com/questions/62752/purpose-of-k-channels-in-action-potential/62755#62755 The Na/K pump is not necessary for restoring membrane potential after an action potential, it is necessary for maintaining the concentration gradient of sodium and potassium ions over the long term.

Thanks for the clarification. Is it then correct to say that running the Na/K pumps to maintain the concentration gradient are the primary energetic costs of neuron action potential signaling?

Yes, that's correct. The pumps will also have to operate even if there are no action potentials, though action potentials do increase the demand on the pumps. However, so does subthreshold activity: both EPSCs and IPSCs result in ion flow down concentration gradients as well.

There's a few [1, 2, 3] sources that claim it's on the order of $10^8$ ATPs per action potential. The first paper (which is a review that cites the second paper) also has some equations for converting from ATPs to free energy, although that's going to be very context dependent.
If you can't access the third paper, someone has helpfully entered the relevant figures into the bionumbers site.

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Identifying a lone bone found newar Rowena Crest, Oregon (USA)
I was wondering whether anyone knows how to identify what animal the following bone belongs to.  I assume it a femur, but it seems rather short and squat.  The following photos show two views of this bone and I've placed a 15cm ruler in the frame with the bone.

Can't be sure about the species, but I agree with @kmm's answer that this is a humerus. The condyles (i.e., the "trochlea" and "capitulum" in the case of the humerus) are clear giveaways on the left side of the picture.

www.boneid.net provides a great searchable database of identified bones

Did you ever figure out what animal that belonged to? We found the exact same bone (just the other side) in the Adirondacks of upstate NY

My guess is that it's a relatively young cow humerus. The strongly grooved trochleas are more characteristic of a humerus than a femur, which usually just has two condyles. The deep pit is where the olecranon process (your bony elbow) goes. The proximal end is missing, which indicates that the growth plate was not fused, suggesting juvenile.
And I guess cow because cows are very common and have robust bones compared to other artiodactyls.
Here's an image pulled from the web:

It is not necessarily young, it looks like it has been out in the weather a while, the end could have been gnawed or weathered. Just based on size and the shape of the condyle it is either bison or cattle, and cattle is far more likely.

@John Young means the animal was of earlier than full-grown age when it died (based on the size), has nothing to do with how long it's been outside. Limb bones of cattle are sold for people to give their dogs, by the way.

@BryanKrause based on size I could see it, although cattle can vary quite a bit by breed no it is not a great metric to go by.

I'm not sure why (or how) the bone of a cow/buffalo would get where I found it.  There are certainly no cattle that graze any where near there.   Also, there are no gnaw marks on the bone either, so it doesn't seem like the sort of thing that had been given to a dog.  Could it be something more likely to live in the area like a wolverine or bear?  Though, still the size just doesn't seem right for those suggestions.

There are cows everywhere in the US, and they escape and get everywhere else. There is no state in the US where you cannot find cattle. And no, it does not look anything like a bear or wolverine bone.

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Thyroid transplanted to the abdomen
This question was posed in our endocrinology class, however I have no idea how to answer it:

The thyroid gland of a 5-year old boy is transplanted from its normal position in the neck to the abdomen (between the kidneys). Assume that the gland develops a good blood supply in its new position and that it remains alive.
List the abnormalities that will develop in this child:

after two months.

after 10 years.

Any help will be appreciated.

We expect people to do their own research prior to asking and to present it with the question. Otherwise the question might be downvoted and/or closed due to no effort. So, what have you found out?

do you haver any ideas what would happen? what class is this for - a college level or graduate level course?

It's for a college level course. I haven't found anything that would suggest that this is a common, or even at all possible procedure. It seems to be purely theoretical.

I know removing the thyroid would affect the child's metabolism, but whether the gland would be at all viable elsewhere in the body I guess is the question. Presumably it would still function as a endocrine gland due to the blood supply, but would it receive the relevant tropic signals from the hypothalamus and AP?

so what do you think will happen? add that to your answer and it will give us an idea that you've tried to do a little thinking in your own...

You have the answer. Just back it up.

Thyroid gland is known to absorb iodine from food.It will not be able to absorb between the kidneys.


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Why does V. cholerae produce a human specific choleragen?
V. cholerae secrete choleragen to grow and escape human intestines, however choleragen does not work on other mammals, why so? Why didn't it evolve a general mammal affecting choleragen? This question is a continuation of the last comment on the only answer for my previous question, How does Vibrio cholerae benefit from infecting its host? Kindly refer to the answer and comments in that question as well.

Vibrio cholerae originated in the Sundarbans, a very large wetland at the mouth of the Bay of Bengal. Although it can exist as free living, it is much more fecund when associated with tiny crustaceans called copepods. In 1760, the East India Company settled and sprawled, hewing the mangroves and planting rice. So, that was the first opportunity of note introducing V. cholerae to a major species of land animal, humans. The frequent contact with a sizable population of humans, plus time, allowed V. cholerae to evolve the traits to become a parasite.
For example, a hair-like filament evolved which allowed the cells to clump together forming colonies that could stick to the gut. At that point, perhaps with additional traits, V. cholerae became a zoonosis. That is, a disease we acquire from animals, copepods in this case, but not directly from other humans. Further evolution over time gave it the traits to spread directly between humans making it a true human pathogen.
So, humans were the species that became available and V. cholerae evolved to take advantage.
This is a minute fraction of the whole story as related in the 2016 book Pandemic by Sonia Shah. She is a science writer, the book is extremely well referenced. Since this is your second question on this, I suspect you may well be interested in the book.


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Why do animals excrete excess nitrogen instead of recycling it?
I am aware of the different ways animals excrete excess nitrogen (mainly ammonium, urea, uric acid). My question is: why do we excrete excess nitrogen instead of recycling it? How can we explain that there has been no selection for more nitrogen recycling in animals, as this would probably constitue a selective advantage?
I have read here that "In the quest for sufficient food energy to meet caloric requirements, animals ingest more nitrogen, largely as amino acids, than they require. Accordingly, the excess nitrogen ingested must be excreted in some form.". This is exemplified by this paper: a low protein diet comes with lower urea levels.

Herbivores and carnivores have vastly different nitrogen intakes, so it depends how much excess or paucity there is in the diet, i.e. ruminants recycle nitrogen more than carnivores. https://www.google.com/search?q=nitrogen+metabolism+in+mammals&oq=nitrogen+metabolism+in+mammals&aqs=chrome..69i57j0i22i30j0i390i650l3.7608j0j4&sourceid=chrome&ie=UTF-8 I would say they excrete it if they have a major excess, especially given the pH considerations of nitrogen, urea and ammonia.

An analogy with human recycling may be helpful: For millenia we've been tossing our garbage because it's easier than saving and recycling it. Recycling is hard, and we've only recently started recycling because we've been using some resources faster than we can replace them, and the environmental impact of tossing garbage has gotten exorbitant.

Helpful answer: https://biology.stackexchange.com/questions/111475/why-do-cartilaginous-fishes-not-excrete-ammonia/111477#111477

Recently asked: https://biology.stackexchange.com/q/111880/16927

I think your quote more or less explains it: what advantage is there is recycling nitrogen when you're ingesting more than required?
Additionally, we recycle nitrogen all the time, especially in amino acid form. Proteins are constantly broken down into their amino acid constituents and recycled into new proteins.
When you talk about waste nitrogen, that involves the excess (no need to recycle an excess - excess means there's already too much).
Further recycling may make some sense in conditions where nitrogen intake is not in excess, such as hibernation.

Since liver converts excess amino acids into glucose and subsequently glycogen. Won't it be better to store proteins as a reserve food material in form of muscles and other structures etc. ? That should be better than storing it up as fats which beyond a limit cause hundreds of health problems

@Aurelius Fat is more energy-dense than protein, and it costs energy to move that stored stuff around. Negative health impacts from fats are coming from over-storage that's only made possible by our extensive technological advancements over incredibly rapid time evolutionarily. And, in any case, storing nitrogenous materials as energy would hardly make a dent in the excess nitrogen in an adult human with a protein-rich diet.

I would add to the points made by @BryanKrause by stressing that the poster is misusing the word ‘recycling’. In metabolism you can only recycle something that was previously present, such as protein (as in turnover) or nucleic acid bases (for which there are salvage pathways).
The alternatives for dealing with dietary excess of a metabolite are either to reject (excrete) it or to store it for use in future conditions of deprivation. Presumably because the demands for energy are greater, more immediate and more crucial for life than that for protein precursors, animals have evolved to prioritize the storage of the carbohydrate portion of amino acids (as fat predominantly), rather than store both carbon and nitrogen as protein.
Indeed, when muscle protein ‘wastes’ in extreme starvation, this is to provide energy — and particularly glucose and ketone bodies for nervous tissue. The nitrogen portion cannot be utilized too, so that it also excreted under these conditions.
As with many questions of evolutionary rationale, the simplistic “this would probably constitute a selective advantage” is unsupported by actual evidence. In this case it is negated by a consideration of actual human starvation and the chemistry of the molecules involved.

Body builders have to take up a high protein diet. Because of exercise the excess nitrogen is used up in muscle making. Won't it be advantageous if it was done without exercising considering our body would rather die of obesity than excrete carbs or fats.?

While we are at it, why is the body so crazy about carbs and fat storage? Why does it store more fat than would be required to survive without food for months? And when it has all that extra fat why make us hungry for more.

@Aurelius my answer is to a specific question. The way that SE works is that if you have a different question or questions — which you clearly have — you should post it as an independent question (after careful preparation to provide clarity and context). This will enable others — who may know more than me about the topic — to contribute, and, above all, allow indexed access to those who share your concerns.

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Why does heating kidney beans at a low temperature potentiate the toxicity of phytohaemagglutinin?
I recently found out that red kidney beans contain a relatively high amount of the toxic lectin, phytohaemagglutinin.
An article on phytohaemagglutinin on the FDA website states:

Several outbreaks have been associated with "slow cookers" or crock pots, or in casseroles which had not reached a high enough internal temperature to destroy the glycoprotein lectin.
It has been shown that heating to 80°C may potentiate the toxicity five-fold, so that these beans are more toxic than if eaten raw.

What I do not understand is how the toxicity could increase if the beans are cooked at lower temperatures in a crock pot. I would understand if the toxicity remained the same (that is, not be deactivated), but I thought a toxin is nonliving (i.e., unable to grow and reproduce) since it is not a bacteria?
I know nothing about biology, so I am utterly confused.

The source quoted is the first edition (2009) of the FDA's Bad Bug Book.  The second edition (2012), no longer asserts that the toxicity increases over the raw state when heating to 80°C, nor does it contain the assertion that "Undercooked beans may be more toxic than raw beans."

@mgkrebbs Nice find. I am still curious about how this would be possible.

I am a Snr lecturer and a PhD candidate. Currently, I am putting my theses together. My research area involve in part the kinetic degradation of lectins in neglected and underutilized legumes. I  also looked at the possibility of using irradiation to produce complexed degraded starches  to inactivate lectins during low temperature extruder cooking.I observed in some of the extruded samples that lectins have actually potentiated up to about 50%. I was confused. I know lectins are proteins so they are supposed to denature when heated. I was looking around to see whether someone has made similar observation and I saw that indeed somebody has reported similar observation. I was so over joyed but it was short lived-no explanations were offered.  I now offer a possible explanation. Yes, lectins are proteins(or glycoproteins) and like most proteins their tertiary and quaternary structures are 3D. So the 3D forms have a couple of smaller subunits, woven together into the giant super structure(lectin). In the 3D form, most of the binding sites are "buried" or not fully exposed. It is possible that these smaller units have binding sites for carbs and are best positioned to present their ligands for  exposure and maximal binding when the 3D structure begins to "melt down". This melt down occurs at low temperature when denaturation has actually started.  Thus, the greater the exposure  number of subunits bearing the binding sites, the greater the potentiation. My work used low temperature extrusion cooking and the observation occurred in the extrusion cooking.
I just hope this suggestion is adequate. That is indeed the explanation I am going to offer for my observation anyway. Wish me best of luck!
Bye!

Welcome to Bio. On this site we encourage the use of references,  links to websites etc. to back our answers up and to allow other users to do background reading on your answer.

Additionally: Can you please remove all content about your PhD and so on which is not important to answer the question?


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Synapse formation
I am trying to learn about neuronal synapse formation, but the literature is intimidating to someone with little background knowledge.  I am interested in synapse formation in both human adults as well as during human development.  Could someone point me to a good paper or review that provides the necessary introductory information?  I am a highly technical individual, but have little more than a 1 year introductory neuroscience course at the undergraduate level.
EDIT:
I'm interested in the formation of structure in small-scale systems (100's to 1000's of cells) of neurons, so I imagine that would require a combination of cell-based and neurophysiological knowledge.

Welcome to Bio. What do you wish to know, I mean what is the area of expertise? Molecular Bio (Cell signalling), morphology (cellular level) or neurophysiology (communication)? There is a lot of stuff out there. Finding literature mainly means knowing what you don't need.

Alright, to be honest this question is definitely too broad to answer. Even the formation of small structures is a HUGE (and I mean huge) field of study that doesn't just span neurons. I will tell you how you can find such papers and the ones you are looking for are specifically called "Reviews". A review article basically rounds up (usually a hundred or so) articles to form a consensus about what the prevailing thoughts on a specific topic are when looking at the research done by the scientific community of course. If you want to learn about neuron development I suggest you use a scholarly se


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Interspecies competition and pathogen
Following my answer to this question, a debate ensued on whether the loss in population of one species (namely red squirrels) due to its lesser resistance to a pathogen brought by a competing species (namely squirrel parapoxvirus and grey squirrel) should be labelled as a result of interspecies competition or not. Here I will try to state it as a question with in a more general setting. I'll give my own answer to it, and would welcome other views on the issue.
Assume the following: Species $A$ lives in a closed ecosytem and has reached carrying capacity $A=M_A$. At time $0$, a new species $B$ is introduced which is in competition with $A$, and additionally bears a pathogen to which it is resistant but which causes a high lethality rate in $A$.
It is observed that $A$ dimishes while $B$ thrives. Can we necessarily ascribe it to interspecific competition?

If you are specifically thinking about longer-term, evolutionary effects (see tag) I think that you should make that more clear in the actual question. As it is written now, I don't really see why [tag:evolution] is relevant.

No, you cannot for certain ascribe it to competition, without further information. The mediation by a pathogen is similar to the effects on prey species that are indirectly caused by shared predators (e.g. Prey B increase -> Predator X increase -> more predation on Prey A). Such effects, which can be tricky to separate from direct competition, are usually called apparent competition (see e.g. the classic paper Holt. 1977. Predation, apparent competition, and the structure of prey communities. Theor Popul Biol 12).
However, to some extent, the terminology used may depend on what you view as "the environmental background". All species have lots of adaptations to certain aspects of their living environment, and these naturally differ between species. Some might be more resistant to a certain pathogen (of to drought or other abiotic factors), but this might trade-off against other traits. I that respect, you might view species B as outcompeting species A in a certain environment (e.g. in the presence of the pathogen). However, since you specifically know about the pathogen (which is the focal point of the question), and that species B will probably function as a host/source population of the pathogen, I think it is more useful and informative to label the effect as apparent competition. To partition the direct and indirect effects you will however need moe information.

There are two possible effects on the evolution of A:
(i) interspecies competition with B which effectively reduces the carrying capacity, which can be modelled by writing $M_A^{\textrm{i}}(B)=M_A \frac{A}{A-\alpha B}$ (Lotka-Volterra model), and
(ii) infectivity with an infection rate $k_I A B$ which can be treated as direct mortality if pathogen is 100% lethal for A (which is a good approximation for red squirrels it seems, here we've even supposed A once infected didn't live long enough to pass disease).
The question is: can we have a population reduction even if there is no interspecies competition, i.e. $\alpha=0$? The answer is yes, since as long as $B>0$, there'll be a decay of $A$ to a fraction of $M$ (with a simple logistic model, this would be $\frac{r}{r+k_I M B} M$ where $r$ is the rate of natural increase)
This matches with the interpretations of Tompkins et al transcribed in National Geographic

You should give your suggested answer with the question. I edited your question accordingly, feel free to edit further. I also tried to make it a bit clearer as I did not understand some of your phrases. Please also check for misconceptions I introduced. I will try to suggest an answer to your question in the following days (little time these days ...).

I'm not sure why I should put the answer in the question-- it's a possibility offered by SE to provide your own answer to your questions, and allow SE process to discuss and improve them independently of question. Thanks for your other edits anyway, I'm incorporating them.

@AlexDeLarge self-answering questions is not only allowed, it's encouraged.

@MattDMo I know. But I just felt it would fit the question better than as a self-standing answer and therefore suggested an alternative. I have no problems with it being the way it is, though. :)


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Is erythropoietin released when breaking down RBCs
I came across the MCQ in my physiology book, it says:

Erythropoietin.....
i) may decrease the life span of RBCs.
ii) is not released on breakdown of RBCs.
iii) may stimulate the stem cells.
iv) is formed mainly in liver.
v) is lipid in nature

I think ii) and iii) are correct answers, as when breaking down RBCs we don't get erythropoietin, and erythropoeitin stimulated stem cells to produce RBCs, am I right?
Because the book says that only one choice is correct. Help me please! Is there something I don't understand?

To simplify only a bit, EPO production is controlled by the level of oxygen in the blood. You can argue that RBC destruction causes hypoxia, but in truth, if RBC destruction does not cause hypoxia, there is no stimulus for EPO production. Like every hormone, there is more to it and more to discover. But the obvious answer is iii, and anything more is overreading.


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Do ants use something similar to the honey bee "waggle dance" to instruct the rest of the colony where to find a food source?
In the 20 years since we built our home, we've just recently had our first ant infestation.
I'm familiar with the fact that ants leave scent trails to find their way back and forth between the colony and a food source.  So in my limited experience with ant eradication, I assumed that by taking away the empty ice cream bowl and scrubbing the scent trail which lead to it off the kitchen counter (multiple times with different household cleaning products) the ants would quickly give up their search.
My assumption was that the oncoming foragers would be confused by the abrupt end of the scent trail and wander aimlessly in the gap between where the trail had been scrubbed away and the former location of food.
However, what I’ve observed again and again is ants continuing to move across the scrubbed counter to the exact location of where the food used to be -- as if they didn't need the scent trail.  Their only confusion seems to be the lack of food at that spot.  This behavior will continue for several hours after the removal of whatever food had been there, despite multiple eradications and vigorous scrubbings of where the original trail had been.
Ants follow odor plumes to food sources according an answer in another Biology Stack Exchange post.
(Can ants sense food from a long distance?)
And from a link in the same Biology Stack Exchange post “If they [patroller ants] didn’t return to the nest, departing foragers would know it wasn’t safe to go search for food.” and “The ants can take advantage of sudden windfalls of food, but they don’t waste energy and resources if there’s nothing there.”
(https://wikkorg.wordpress.com/2015/04/23/ants-swarm-like-brains-think/)
Here are my questions:
Are ant scent trails strong enough to withstand multiple washings with soaps, detergents and disinfectants?
Can ants detect airborne food molecules in very small parts per million, even after the food and its odor plume have been removed?  If not, do ants use something similar to the honey bee "waggle dance" to instruct the rest of the colony where to find a food source?  Or both?
Why and how do they keep coming back to a place where there is no food, especially if (eradicated) members of the colony are not returning?

I know that some other Hymenoptera, including ants, have primitive waggle dance-like behaviours that are used for recruitment of workers to food sources. I don't know if they can convey spatial information though, but will try to find out more. The book The Ants by Hölldobler and Wilson is probably a good bet for more information.

I can only help you on one question about if ants perform a similar communication such as the "waggle-dance" to tell other ants if there is food elsewhere?
Ants will send out scout ants or forages, which will go out in search for food. The ants will lay a pheromone trail, by tapping their abdomen on the ground, like breadcrumbs. If the ant has found a food source, they will taste the food and take part of the food and store it in their crop. The ant will take the food sample and re-trace her trail, making it more detectable when returning to the food source. Once the ant reached the nest and finds another ant, she will regurgitate the food from her crop and position it between her mandibles. She will go towards another ant and exchange the food and pass it on to the ant in a "kissing" motion. This is called trophallaxis, where there is a donor, the scout or forager ant, and a recipient, the ant back at the nest. The ants will then follow the trail the scout first put down and will eventually create a motoway of food going to the nest.
Look up people like Nigel Franks and John Sudd - The behavioural ecology of ants.
The lives of ants - Laurent Keller and Elisabeth Gordon
The Earth dwellers - Erich Hoyt
sciencedirect.com/science/article/pii/0003347295801405 about trophallaxis in solenopsis ants sciencedirect.com/science/article/pii/037663578290050X about trophallaxis in Myrmica ruba
Hope that helps.

can you add some links to references or the sources that you indicate? interesting answer...


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Why are most mutations recessive?
Why are most of deleterious mutations recessive in nature? I understood that if it's recessive then one reason may be that the mutant gene doesn't code for a functional protein and so there is no  phenotype to express.  But why is it recessive in the first place?

It is a bit ironic that you phrase your question with 'in the first place'. There is a parsimonious explanation for the effect: Dominant deleterious variants are quickly removed by purifying selection whereas recessive deleterious variants can "hide" in individuals that carry a dominant neutral/advantageous variant.
You can think about it this way: In heterozygous carriers (in which the other variant has a neutral or positive fitness effect), a recessive deleterious variant has no (strong, depending on the dominance coefficient) negative effect on fitness and therefore, in those heterozygotes, purifying selection will not remove the variant (efficiently, again depending on the degree of dominance) - it can only act on homozygous carriers of the recessive variant. A consequence of that is that the recessive deleterious allele usually segregates at low frequency with most carriers being heterozygous.
In short: This probably has little to do with there being more recessive deleterious variants per se (even though that might also be the case due to the mechanisms you described in your question). In the snapshot we are looking at when we investigate genetic data, the likelihood of finding dominant deleterious alleles is way lower than finding recessive deleterious alleles as the latter usually just persist for a way longer period of time.

@JewelJohnson: You are welcome. If the post answers your question, I'd be glad if you'd accept it. ;) Cheers!

How do I accept it?


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How to predict future generations from heritability
The heritability of human intelligence is estimated to be around 0.5. There are of course various estimates, some lower, some higher. But let's work with this value of 0.5 for the moment.
I wanted to know how this relates to the trait value of future generations and read a bit about it. For example, in some related posts:
how should one interpret heritability is it related to r2
why is a heritability coefficient not an index of how genetic something is
how to interpret the breeders equation
Turns out the breeders equation gives us an idea about that. But we need a second variable: Selection.  I read that selection is based on the reproductive success of individuals with a certain trait value.  But how would I calculate this value?  Let's assume that the reproductive success is higher, for humans with higher intelligence. Let's simplify and say, the fertiliy rate of above average indivdiduals is 2.10 and the same value for below average individuals is 1.90. How would I plug those numbers into the breeders equation?
I tried the other way around. We know that intelligence is increasing over generations in western civilizations (see Flynn effect). Again, estimates vary (and can actually be negative) but we can work with an increase of 2 IQ points per decade. So lets say 5 IQ points increase from one generation to the next in a western civilization population. That would mean:
S = R/h²
S = 5/0.5 = 10
What would this value of 10 mean? How does this boil down to the reproductive success of individuals with certain trait values?

It might eventually help to also read the post How does Natural Selection shape Genetic Variation?. I tried to answer but have failed so far! I might try again tomorrow with a book in hands. +1

"How would I plug those numbers into the breeders equation?"  You would use those fertility rates in calculating the selection differential (S), which would essentially be a weighted intelligence average of the reproducers minus the population average (reproducers+non-reproducers).  So, if the population starts wih 100 IQ and those with 125 IQ produce 2.1 and those with 75 IQ produce 1.9 and those two groups are equally populated, the weighted intelligence avg of reproducers becomes (125*2.1+75*1.9)/4=101.25.  The selection differential is then 101.25-100=1.25.  Response is 1.25*.5=.625.  IQ moves to 100.625.  In your example, S=10.  That is, (x*2.1+y*1.9)/4-100=10, where x is the avg IQ of the above average group and y is the avg IQ of the below average group, assuming the two groups are equally populated.

Thanks. I got a slightly different result.  $$S=\frac{1}{\bar w}\sum_{i=1}^{\text{nb inds}}m_iw_i - \bar m$$ $$m_i = 125 \quad  w_i = 2.1 \quad   | i=1$$  $$m_i = 75 \quad w_i = 1.9 \quad | i = 2$$ $${\bar w} = 2$$ $${\bar m} = 100$$ $$S=\frac{1}{2}((1252.1-100)+(751.9-100)) = 102.5$$

I just realized that this might be due to the calculation taking $w_i$ as the value for couples. So for individuals we would divide by two. But then we would also have to divide ${\bar w}$ by two, and we get the same result. Maybe I got the formula wrong or am I misinterpreting something?

Is the top equation that begins with "S=..." yours or did it come from a text?  Our results are the same except you divided by 2.  I divided by 4 in order to get the average progenitor IQ weighted by the quantity of offspring produced (2.1+1.9=4 was the total quantity of offspring produced).

I got it from another post here (http://biology.stackexchange.com/a/16807/27686). Might be wrong. Your calculation seems logical anyways.

Meanwhile, I also found a paper here (http://www.sciencedirect.com/science/article/pii/S016028961000005X) and there is the following equation $$ S=\frac{1}{N}\sum_{i=1}^{N}(IQ_i - \overline {IQ})*\frac{CH_i}{\overline {CH}} $$ Where $CH_i$ is "Children of individual" and $\overline {CH}$ is "Average children in sample". But I do not really understand why we do not simply weigh with the number of offspring per individual as you did.

Can I ask what software you used to write these equations?

It's not a software, more like a code. It's called MathJax:  https://math.meta.stackexchange.com/questions/5020/mathjax-basic-tutorial-and-quick-reference


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Why aren't there any transitional animals today?
You have probably heard this question before and in different formats. Usually, it is used as a "proof" to disprove the theory of evolution.

I understand that the apes we descended from are not the same apes we see today. However, I can't understand why there aren't any human-ape creatures anymore.
In the world of today, wouldn't an intermediate species (between apes and humans) "win" over both because it has the "feature" of the two.
A creature that can both climb trees and walk on two legs would be more suitable to live in forests than the current forest inhabitants. (apes and humans)

Every species on the planet is "transitional" - this is because there is no ultimate or final species. Species branch out from one another, sometimes species go extinct, leaving gaps between the extant branches.

Possible duplicate of Examples of extant animals in a submature morphologically unstable evolutionary state?

@C_Z_ I'm specifically interested in the human-ape thing.

"In the world of today, wouldn't an intermediate species (between apes and humans) "win" over both because it has the "feature" of the two." - ever heard the expression "Jack of all trades, master of none"? An intermediate might do ok in the adaptive landscape of either species flanked by it, but it won't be able to outcompete within them

@Mhmd I strongly recommend reading through the introductory course Understanding Evolution from the University of California, Berkeley. It will address a lot of the misconceptions you have.

Related (but closed): Where are the evolutionary “inbetweeners”?

Our closest relative are Chimps and Bonobos. Our lineages split from a common ancestor several million years ago. Since then every other species in the human lineage other than sapien went extinct (neanderthal genes not withstanding) and we have the fossil record to prove it. It isn't that surprising that the rest of what came to be the human lineage went extinct, just as most all of the ancestors of the chimpanzee lineage went extinct after the split. That there are chimps and bonobos just means they were well adapted to their niche ranges and survive today. Same with birds and dinosaurs.

But,if true,there should be billions of transitionals,like when you look at a good set of artist's paints....each colour changeing 1 tube at a time to the next colour.Where are they in the fossils?

Every species on the planet is "transitional" - this is because there is no ultimate or final species. Species branch out from one another, sometimes species go extinct, leaving gaps between the extant branches. But it also comes down to how you look at it; if you were comparing blue whales and humans, then chimpanzees (and many other species) would be "transitional", so some "transitional" species are extant, others are extinct. In fact, it is estimated that 1% of species that have ever existed are extant, the remaining 99% are extinct.
It's very hard to say why the "transitional" species of chimpanzees and humans went extinct. There's a lot of (sub-)species that would fall in that bracket, thus to answer that specifically would be too broad and speculative for this site.

Some concepts and key points

Speciation is a gradual process with species forming over time out of one in to two (or more).
Species is a hard concept to pin down because it applies binary/categorical classification to a very much continuous distribution
Evolution is a process of change, and in all likelihood it will be an unceasing process because at least one of the mechanisms will likely be affecting every species in some way. This means that every species is "transitional" because no species represents an end point.

This is just going to be a quick answer, as it's too long for a comment (I'll leave it to others to fill in the gaps if they wish). The image you present in your question is based on a false premise. Humans did not evolve from apes. Humans and apes evolved from a common ancestor, which was neither human nor ape. So, the arrow on the left of the image, saying There are millions of these, is incorrect. Our common ancestor is now extinct, as are all of the so-called "transitional species", another term which is incorrect because, as rg255 points out, all species on Earth are "transitional", because we are all evolving (at varying rates, to be sure). In between our last common ancestor (LCA) and modern Homo sapiens there were many species that existed for various amounts of time, then died out for various reasons, in some cases because of direct competition from more recently-evolved and better-adapted species.


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Radiation dangerous or not?
I've always been told that most electronic devices such as WiFi/phones/laptops and such emit a non-ionizing radiation which is completely fine as it does not damage human DNA. I've been googling and i see people arguing about it but there seems to be no evidence to back up the fact that it's not damaging. I'm just curious is what I'm saying correct? or can it damage the human body as i see people mention it can lead to pretty serious health problems.

WIfi and phones emit radio waves, you you might want to ask about that specifically, all non-ionizing radiation is too big a spectrum to cover in a meaningful answer.


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Light signals in the courtship and mating
I am investigating on the emission of signals in the courtship and mating in the animals.
I know that the fireflies emit light signals as a courtship ritual.
Are there other animals that use this phenomenon of luminescence?

Many Ostracods (esp. the Cyprididae) use bioluminescence to attract mates. The Bermuda fireworm (a polychete worm) also uses bioluminescence to attract mates.
If you have not yet, you should definitely have a look at wikipedia > Bioluminescence


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Mutated cell proliferation
Reading Jennifer Doudna's fascinating book on CRISPR. So she describes rare cases where a mutation in a single cell removes the gene responsible for a genetic disease. The cell proliferates and the disease is cured. What I don't understand is--aren't all the aberrant cells also still dividing and passing on the harmful mutation to their progeny? How does the single healthy cell edge out all the other cells to "cure" the patient.

There are some diseases in which a minority population of normal cells can rescue the organism, even in the presence of a majority of mutant cells.  Sort of like a group vacation to Kazakhstan with one friend who can speak Kazakh.  Very different experience from a vacation where none of you speak Kazakh.
Take for example hemophilia A.  Cells have a mutant gene for factor 8.  Without factor 8 blood does not clot properly and people have bleeding trouble.  You do not need much factor 8.  Just a little bit can prevent spontaneous bleeds.  People who are heterozygotes for hemophilia A (carriers) are fine at 50% normal.  So if you edited mutant liver cells such that they could produce factor 8, even if they were only 10% of the total cell population of the liver, having some factor 8 would sidestep the full hemophilia phenotype.
Likewise metabolic mutants - some children are born unable to handle certain substances.  Phenylketonuria is the one you read about every time you drink a diet coke.  If a minority population of cells could be produced that were able to handle phenylalanine, those would rescue these kids even if most of the cells still could not.

Are you talking about people?
Because in bacteria, a mutated bacterium with a beneficial mutation will definitely edge out the competition, or if it is in a "good mood" (cell humor lol) it will share its DNA with the other bacteria.
You're absolutely right about people, though. One cured cell won't cure the patient.


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Is oxygen a respiratory substrate
I know that carbohydrates such as glucose are respiratory substrates for cellular respiration, but in this process, oxygen is also used to produce ATP so is it also a respiratory substrate?

I don't know if I've ever heard the term "respiratory substrate" before. But, I've said it many times on stackexchange, so I guess I'll say it once more.. I hate semantics. And, I really do not see the importance in being able to define something by some arbitrary human idea. So, what is important?.. What is important is that you know what everything, as a single entity, does on its own. Can you tell me what the function of oxygen is in the body? What happens to it? Where does it go?

By the way.. Welcome to stack exchange! Here's a link to a nice overview of what we're all about

You must explain what you understand the term "respiratory substrate" to mean if you know glucose is one. Also respiratory, in a biochemical sense. Then we can answer your question, but by that time you should be able to answer it yourself.


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phosphorylation of Glyceraldehyde 3-phosphate
This question is related to something that happens when 3-phosphoglyceraldehyde is converted to 1,3-bisphosphoglycerate during glycolysis.
As I understand it, 3-phosphoglyceraldehyde is deprotonated by NAD+ and phosphorylated by a Pi group, which results in NADH + H. The extra H apparently comes from the Pi group (which I believe is called orthophosphate [1]).
Now, where does the Pi come from? is it just sitting in the cytosol?, does all Pi have a hydrogen? can someone clarify what an orthophosphate is, I never heard of that term.

You can google orthophosphoric acid. Pi is the acronym of inorganic phosphate.

Yes, the cytosol contains a high concentration of orthophosphate (in yeast, between 10--75 mM) so it is readily available for this reaction. The notation P$_i$ is commonly used because the orthophosphate ion can exist in multiple forms in water solution:
H$_3$PO$_4$ $\leftrightarrow$ H$_2$PO$_4^{-}$ + H$^+$ $\leftrightarrow$ HPO$_4^{2-}$ + 2H$^+$$\leftrightarrow$ PO$_4^{3-}$ + 3H$^+$
When we don't need to specify an exact form, P$_i$ is convenient as a shorthand for "some phosphate ion".
At the cytosolic pH (about 7.2), almost all orthophosphate is in the H$_2$PO$_4^{-}$ and HPO$_4^{2-}$ forms, which are roughly equally abundant. So yes, there is (at least) one hydrogen on orthophosphate available for the enzymatic reaction.
The term "orthophosphate" rather than just "phosphate" is common in biochemistry because phosphate also exists as polymers, including the di- and triphophates (in nucleotides, for example) as well as longer polyphosphate chains. These form are all referred to as "phosphates", while "orthophophate" specifically means the "monomer" P$_i$.


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Energy transfer from P680 to oxygen-evolving complex
This topic is confusing me.
As I understand it, in the PS2, photons are used to split water into molecular oxygen + protons and electrons in the oxygen-evolving complex. To do this, a photon is used to excite an electron in the P680, this electron is then released to go through the electron transport chain and somehow the oxygen-evolving complex gets energy from it to make water endure a "photochemical reaction" as described in my biology book.
But how the electron can transfer its energy to the oxygen-evolving complex if it went directly to the electron transport chain? how the energy produced in the P680 transported to the Oxygen-evolving complex?
I would appreciate simple terms as I'm still a college student.


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Why do bulls-eye rashes look like they do?
People infected with Lyme Disease often present with an erythema migrans ("migrating redness") rash. Most often, these rashes are in the shape of a bulls-eye.
Rash image.
Presumably, this is a reaction that many of our bodies have to the Borrelia burgdorferi pathogen.
Lyme disease also sometimes presents with different-looking rashes, and other pathogens also sometimes produce a bulls-eye-looking rash. CDC Link on Lyme Disease Rashes and Look-alikes.
What causes the bulls-eye shape of these rashes?
Thought process: A gradient of redness from the site of the tick bite makes sense--an immune response might be strongest at the bite site--but I'm still stumped on why there would be a spot of redness surrounded by a no-rash-ring surrounded by a rash-ring.

Note: If I remember correctly, external links to images are usually frowned upon. Although the images linked in this post aren't super graphic, I decided to make them external links for the sake of anyone who is sensitive to medical images.

The spreading of the rash is caused by dissemination (migration) of the Lyme spirochetes (Borrelia) through the skin out from the initial site of infection.
The spirochetes trigger a immune reaction that involves macrophages entering the skin and releasing pro-inflammatory factors.
The clear areas (when present) apparently represent areas where macrophages have been cleared from the skin and thus are no longer triggering a inflammatory response.
The different patterns associated with the rashes can be explained by differences in how fast macrophages are cleared from the skin.
Reference:
Vig, D. K., & Wolgemuth, C. W. (2014). Spatiotemporal evolution of erythema migrans, the hallmark rash of Lyme disease. Biophysical journal, 106(3), 763-768.


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Cross-species infections
I’ve heard that HIV developed from SIV, etc.
I’ve also heard that most species (including most monkeys) can’t get a common cold like humans.
So then what causes infections to be able to travel across species, or vice-versa?
For the sake of the question, I’ll narrow the scope. Let’s say we have a virus that can infect humans but not infect close human relatives, like Chimpanzees. What about that virus biology or animal biology causes that difference?
I know with some animals it’s about body temperature or skin composition, etc. But humans and chimps are physically pretty similar. Is it all about the immune differences?

Viruses evolve alongside their hosts. If you swapped a human chromosome into a chimp cell for the matching chimp chromosome, there would be a lot of genetic similarities but you would also surface a bunch of incompatibilities because the genes on each chromosome have been evolving independently from the rest of the genome.
Viruses interact with their host genome at many stages. First, they need a way to identify their target hosts (cells) in the environment and gain access to the cells. They do this by recognizing markers on the cell surface. For something like HIV, this identification is far more specific than identifying just humans even: they are identifying particular immune cells.
Once inside, viruses interact with the host to express viral genes, produce and assemble new virions, and get transmitted to subsequent hosts. If an incompatibility occurs at any of these stages, the virus won't be able to replicate.
However, because there is a lot of homology across related species, it is feasible for a virus to infect more than one host. If a virus evolves in a context where it commonly infects multiple hosts, there can be selective pressures for it to maintain those abilities across all the hosts. Alternatively, selective pressures might cause the virus to evolve into separate lineages, one infecting ducks and another infecting sparrows, for example.
For a virus that is specific to a certain host (or range of hosts), it is likely that it will have difficulty in another host outside the context in which it evolved. However, there is also variability in viral genomes, and if many viral copies are exposed to a novel host, there is chance that some of them can survive in that host. This will select for those particular viral genes, and subsequent viral generations will be further selected for traits that help replicate in that host.
Immune reactions could also play a role, but in most cases it is the specialization of the viruses themselves that hold the key to host specificity.

Ahlquist, P., Noueiry, A. O., Lee, W. M., Kushner, D. B., & Dye, B. T. (2003). Host factors in positive-strand RNA virus genome replication. Journal of virology, 77(15), 8181-8186.
Hao, L., Sakurai, A., Watanabe, T., Sorensen, E., Nidom, C. A., Newton, M. A., ... & Kawaoka, Y. (2008). Drosophila RNAi screen identifies host genes important for influenza virus replication. Nature, 454(7206), 890.
Schild, G. C., Oxford, J. S., De Jong, J. C., & Webster, R. G. (1983). Evidence for host-cell selection of influenza virus antigenic variants. Nature, 303(5919), 706.

Great answer and concise, thank you!! One question I have that I may address if I have time (or if you/someone else wants): so your answer says that one possible reason why rhinovirus doesn’t infect mice is that the receptors are different. So (1) what are the receptors that rhinovirus binds to in humans and (2) can we do an alignment between those receptors in mice and humans? Do we know which misaligned residues/change in structure leads to the mismatch?

@CalendarJ That would be an excellent separate question. Not my area of expertise but I am almost certain that rhinovirus cell specificity has been studied, though I'm less certain that specific residues involved in human/mouse differences would be understood. In any case it's a good question that should produce a well-referenced answer.

The biggest key to understanding viruses and their hosts (more specifically, host cells) is external (membrane and ECM) protein structure.
As a general rule of thumb, viruses need to latch on to their host cells. Some viruses abuse transport mechanisms to trick host cells into "eating them" and running their contents. Other types of viruses have nasty-looking clamps (most prominent example that comes to mind are bacteriophages) that grab specific structures on host cells while the central piece of the virus punches a hole in the host cell's membrane to feed it malicious DNA/RNA and enzymes.
Cross-species infections usually abuse structures common to many species. For example, sialic acid receptors are commonly abused as viral entry points (see https://www.ncbi.nlm.nih.gov/pubmed/23873408). If humans had genomic support just like computer operating systems receive updates for vulnerable components, sialic acid receptors would have been labeled a critical risk millennia ago and patched.
Obviously there are other factors that can thwart cross-species infection. A successful cross-species virus needs to use a minimum supported operation subset of cell functions common to its hosts. If a potential (by external structure match) host cell is unable to make a piece required for viral replication, it fails. If a potential host cell (or the host itself, in the case of multi-celled life forms) is built with some oddball anti-infection measures (for example: tamper-detection, integrity check before producing protein from RNA, or unexpectedly robust immunity), then the infection could fail anyway.


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How pricey does the media need to be for a typical bacterial culture experiment?
I'm considering various lab supplies for a protocol we're going to be running, and have been struck by the remarkable difference in price for different quality levels of the same basic substance.
Sigma will sell you water, for example, for anything from \$15/L to \$500/L and even over \$10,000/L, depending on what level of purity is guaranteed. Obviously, one doesn't want to use inferior tools and guaranteed unreliable results, but also it would be foolish to use a reagent that's far pricer than one's actual tolerances.
Most of the actual protocols that I encounter, however, don't seem to actually specify what grade of purity they need, and I'm trying to figure out how to navigate the problem. Trial and error is definitely not a good option, since (a) it can waste a lot of time, and (b) good and bad results in a trial don't actually tell you what you need (a good result could be an unusually good batch of poor reagent; a bad result could be from an entirely different problem). Asking the authors is also not a great solution, for a number of similar reasons.
To make this concrete, let's consider a very simple and typical case that I am currently encountering. The protocol I'm setting up for right now cultures E. coli in LB media. Sigma will sell me LB media powder as "quality 100" L3152 for \$139/kg and "quality 200" L3522 for \$182/kg. Both say they are "good for E. coli".
Is there any reason not to pick the cheaper media? How should one decide how much quality their media needs to have for a typical bacterial culture experiment?

It looks like Merck have different levels of quality control for their products. MQ 100 being the lowest up to MQ 600 being the highest. From what I can see the MQ200 product here has defined composition (of salt, tryptone and yeast extract in g/L) whereas the cheaper MQ100 product does not appear to have its composition ensured.
I am sure your cultures will grow in cheaper media but perhaps you would theoretically lose out on some replicability and perhaps if you were doing metabolically focussed experiments you would want to be certain of your media composition.
As for water, I have always used distilled water which is then autoclaved after you add the media with no problems.

What quality level do you tend to use in your own experiments?

@jakebeal I am fairly sure the composition is ensured - I think it would perhaps be best practise. But again, definitely not required for microbial growth or is really likely to have a meaningful effect on your results - I guess scientists can be quite pernickety about these things though!

The answer depends on the application and level of oversight/compliance you require. Most research labs I've seen use de-ionized or even reverse-osmosis water (from a tap) for most culture media applications. But when I was doing trace-metal analysis, I had to use higher grade water for almost all steps in my experiment. Mostly, we needed a certification with each batch that our specific analytes were below acceptable levels (usually around 1 part per billion). But even "trace-metal" grade reagents often contained iron in the part per million levels, so we had to order even higher grade (pricier) water when we wanted to look at trace-level changes in iron metabolism.
One challenge is that there are few industry-wide quality grading systems. Most of them are specific to a given manufacturer, so it takes a bit of homework to understand what the mean, specifically. For example, it seems like the M-Clarity system used to define "quality" in the link you shared is a Sigma-Millipore specific program designed to help customers with product selection for regulatory compliance. The MQ 100 - MQ 400 levels all appear to follow the same industry manufacturing standards (ISO 9001), and only vary in the level of product analysis and change-notification offered to customers.
If your lab were performing quality control or assurance in a regulated industry, you'd need to ensure that all of your reagents (and laboratory practices) are in compliance with such regulations. If you're in a research lab, these extra features may or may not add any value to your work, depending on the specific applications you have in mind. For most experimental applications, there's not likely much added value in being notified every time a manufacturer gets a different raw materials supplier since most LB ingredients like tryptone and yeast-extract are already complex (undefined) substances. Then again, if your research aim is to optimize growth for industrial fermentation reactors, that information might come in handy.

This answer only concerns Streptococcus pneumoniae.
The lab I worked in used  cheap ingredients, the same as everyone else claimed to in this field.
The only shocking thing I found was that the sterile media (already prepared) that I was given to use  for DNA extraction did not work (DNA would be fragmented). It turned out the media had been waiting in the incubator for a year. Made fresh media and all was well.
Todd-Hewitt Broth (THB) with 0.5% Yeast Extract (YE)
3.0 % (w/v)  of Bacto™ Todd Hewitt broth powder (Difco cat# 249240)
0.5 % (w/v) of Bacto™ yeast extract (Difco cat# 288620)


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How large an expression boost is typical from codon optimization?
There are lots of different codon optimization approaches out there, and a lot of different qualitative reasons to want optimization (e.g., organism codon bias, GC content, avoiding secondary structure).
One may also want to avoid optimization, however, in order to increase reusability of a component, comparability with prior results, or opportunities for error.
I'd like to know how much I'm likely giving up if I decide not to codon optimize. For example, in my typical work giving up 10% is likely to be lost in the noise, but giving up 2x is worth thinking carefully about, and giving up 10x means it's a must-have.
I know "it depends", and there's a lot of qualitative information out there, but is there any way to get a good rough-order-of-magnitude estimate of the typical expression boost from codon optimization?

The "it depends" might hint toward a nice opportunity for a bioinformatics tool as prior data should allow to make an informed prediction. Maybe biostars.org or https://bioinformatics.stackexchange.com would be able to help on a related question, whether there already is a tool to predict boost based on custom sequences and/or expression host.

I think that there is a problem with how well current codon optimization algorithms actually "optimize" protein expression. I am not aware of any algorithms that work beyond a heuristic level and so for an arbitrary protein, one cannot predict the expression boost that optimization will provide - sometimes yield is significantly decreased. This review covers some of the complexities of optimization really nicely https://doi.org/10.1016/j.molcel.2020.09.014.


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How standardized is lab-grade skim milk?
I was surprised to learn in the answers to this question that in many cases the preferred cryoprotectant for many organisms is skim milk, rather than something more simple and well-defined like glycerol. And indeed, Sigma will happily sell you lab-grade dried non-fat cow's milk for lab-grade prices.
It seems to me that this could potentially cause significant variability and reproducibility issues. Milk is pretty sensitive to the condition of the producing animal, and when dealing with a cow we're talking about a very large and complex source that's not hyper-standardized like lab-grade rodents.
I don't seem to be able to find anything much about specification on Sigma's site, however (the spec sheet for milk has only the obvious like "opaque white fluid").
Does anybody know to what degree lab-grade milk is actually standardized, and if this should be a concern for protocols like cryoprotection?

There is a degree of variability in milk, and in some cases this cause problems in protein work. Despite being a standard for ELISAs, it's not known to be the most reliable blocking buffer. As far as cryoprotection goes, variability doesn't seem to be a major concern.
Standardization varies depending on manufacturer. The Sigma link you included reports a quality level of MQ 200. The MQ level is something Sigma created in an attempt to increase clarity about quality controls. Products rated MQ 200 are for non-regulated applications. For this level they will provide a site-quality self-assessment, a certificate of quality/analysis, and specifications. They also have a notification system that customers can opt-in to for updates on quality control features. There's information on what each quality level meansand a breakdown of what they will notify you about on the Sigma website.


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Why is the start of my coding sequence ATG and not TAC?
I am engineering a set of genetic sequences and have come across a surprisingly basic point of confusion that seems to have fallen through the cracks regarding coding sequences.
The standard start codon is AUG, and since this is an RNA sequence, I would thus expect that the start of the coding sequence would then be TAC, since DNA is complementary to the mRNA transcript taken from it. Wikipedia and various introductory texts confirm this expectation, e.g., in wikipedia's article on the central dogma:

The ribosome reads the mRNA triplet codons, usually beginning with an AUG

Here's another example: in the Khan academy introduction to the genetic code, the codon illustration clearly shows an AUG in the mRNA sequence.
The coding sequences that I am composing into my design, however, are all listed as starting with ATG, rather than TAC, which would be the complement of AUG. I am certain the coding sequences are not wrong, since some are very well established parts like BBa_E0040.
Something seems to have gotten confused or elided in many standard explanations, then. Why do coding sequences start with ATG and not TAC?

This image from the Kahn Academy article 'Overview of transcription' might help:

Essentially, the sense/coding strand of the DNA encodes the sequence that is transcribed. The RNA polymerase binds to the antisense/template strand, for which the code is indeed TAC, but when it then transcribes this strand it is again complemented, giving us the AUG that is recognised by initiator tRNAMet (also known as tRNAfmet), as shown in this diagram from the Kahn academy article on 'tRNA and Ribosomes'.

(Note that this diagram is actually showing Met in the middle of a sequence, rather than the start. fMET binding looks slightly different.

Thank you, that is very clear. I'm surprised that this is not more clearly presented in more places, since everything I'd found either said nothing about which strand or else used terms like "template" and "non-template" that weren't clear about how they related to promoter location strands.

Yes! I think this is something that is intuitive to people who've been through the standard Biology training so it's often not explicitly explained to folks approaching SynBio from different angles. It's good to have a clear question here so that people can find it in the future.

When your start codon is 5'-AUG-3', it's clear that the template DNA strand should be 5'-CAT-3'
If you look at Noah's illustration, it's also clear that the RNA sequence is basically the same as the sequence of the non-template strand, and runs in the same direction.
People generally refer to the mRNA not in terms of its RNA nucleotides, but in terms of the cDNA which it could be converted to.  But they'll reported it in the direction that makes sense for talking about RNA.

I'm afraid that your answer contains the sort of mirror-language ambiguities that caused my confusion in the first place.  Which cDNA to convert it to, the template or the non-template? From @NoahSprent's answer, I now know that the template is the opposite from the strand with the promoter, but if I didn't have that answer to read, I would still be confused.

cDNA is double stranded molecule, so it contains the template and non-template strands.

Yes, of course: that's why there's the ambiguity that I was finding confusing.


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How hot water burn works?
At age of 6 I accidentally dipped my hand into a boiling indian curry(Sambar) which was in a large pot.
I got a Boiling Water Burn(Just like in the picture but with a little more radius) in my hand right away and my grandma applied some toothpaste on the area. It has been 11 years now and I still have that mark in my hand.

The question is why is the mark in the center(In circle form)  of my hand and not spread down the whole hand which was  completely submerged a little above the mark. The curry's temperature was pretty uniform around the whole mixture.

The heat takes some seconds to travel through the skin into the deeper layers of the skin, and the deeper it gets, the bigger the scar zone is, it also depends on the skin thickness. Perhaps when you shook and treated your hand, you managed to cool down all the zones further away than the scarred zone fast enough so that it was superficial, or the scar zone had thinner skin, or it was both. AFAIK you should dip a burn into cool water to prevent it getting deep ASAP?


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Yeast transformation plate confluent with growth
I have problem with yeast transformation. I tried to transform pyes3-tryp(my insert inside) into INVsc1 yeast cell by following the protocol in the manual for few times but failed(confluent with growth). In the manual, it states :INVSc1 will not grow in SC
minimal medium that is deficient in histidine, leucine, tryptophan, or uracil.I tried 2 media: selective media+ amino acids except tryp and selective media + amino acids except the 4 amino acids. There are confluent growths, no single colony on both of the plates including on the negative control plate( only yeast cell no plasmid).However, the confluent growth is less severe in the plate without the 4 amino acid. Everything i used is sterile except the old DMSO in my lab which had been opened outside of the laminar before. So, is it due to contamination by bacteria or...??.

Resuspend some of the cells from the plate in water and look at them under a microscope - it's easy to tell the difference between yeast and bacteria. What happens if you try streaking out your untransformed yeast strain on your selective media? Do you get any single colonies? (You shouldn't.)


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Linkage terminology in drosophila
Consider two linked loci that are 50+ map units apart. I perform a test cross between a female that is heterozygous at both loci to a male that is homozygous recessive. In this case, the phenotypic ratio of the offspring will be 1:1:1:1 suggesting that the loci are independently assorting. Then, I cross a heterozygous male to a homozygous recessive female. In this case I will have just two phenotypes due to the lack of recombination in male drosophila. Do I describe the loci as linked or unlinked in this scenario? Do we consider the loci to be linked for males and unlinked for females?

Is this a homework question? If so please tag it as such and read the site guidelines on homework questions.

No it is a hypothetical. I've never actually come across such a scenario nor have I found any information on it. I just want to know about the terminology.


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Do ringneck parrots reject eggs of other parrots in their nest / eggs touched by humans?
I've put up artificial parrot homes in my terrace. Parrots have been nesting there and have laid eggs in them.
Of late i have been observing a large gathering of crows and a few hawks perching in the nearby trees, like never before,  presumably due to the large number of artificial nests and feeders that i've put up for sparrows and parrots.
I observed that in one of the parrot nests, the mother/father haven't returned for almost a week now, and i'm worried for the eggs.
1) If i transport them secretly to another nest, will the host couple accept them ?
2) Can parrots sense if humans touch their eggs ? Will they reject them?


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Would a hole in a heart make it unsuitable for transplantation?
Would a hole in a heart instantly make it unsuitable for transplantation? Or could it be possible for a heart with a congenital defect to still be suitable for use is someone else's body?

I am assuming you are referring to a patent foramen ovale.
A Google Scholar search for donor heart "patent foramen ovale" returns many results about transplanted hearts with PFO, which suggests to me that this is not a contraindication for donation, though that may be up to the transplant team or hospital. In most cases, PFO is not symptomatic; it could also be potentially repaired at the time of transplant if it was deemed significant.


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What is an extinction test?
In Stolerman & Olufsen (2001) I read the sentence:

After drug-appropriate responding with the training mixtures reached
85%, generalisation to ethanol was examined in extinction tests.

Here is the entire section from the article on the subject of extinction testing:

Extinction test procedure
Effects of test drugs were determined in brief extinction tests of 3 > min duration that took place twice weekly, with normal training sessions continuing on the interven- ing days. Initially, rats were tested once with vehicle and once with the training mixture; they all reached a cri- terion of at least 80% correct responding and they were all used in subsequent experiments. The effects of saline, the single drugs used for training and the training drug mixture were determined in 3-min extinction tests. The different drug treatments were given in random order. Prior to each test, two injections were always given (via the appropriate routes) to equate handling.

What is an extinction test?

wow. I did quite a thorough search and couldn't find the answer. Problem is that the linked article is superbly vague and incomplete in their description of methodology. Extinction is a term used where folks neglect one stimulus out of a pair of stimuli and is used to diagnose hemineglect, e.g. in subjects that have experienced a unilateral stroke. Good luck with this excellent question. +1

By the way - if my lead to temporal neglect is right, you may consider re-posting on CogSci. If you do, let us know so the mods here can take appropriate measures. Up to you.

In the case of this particualr paper, I don't think it has anything to do with hemineglect. It has something to do with pharmacology. I've added the entire section from the article on it. The secontion is called "Extinction Test Procedure."

It's a behavioral thing.
The abstract of the paper says: "...mixtures of two drugs from vehicle in two-lever procedures with food reinforcers..."
In operant behavior, rats (in this case) are trained to associate a stimulus (a tone, an odor, a light, etc.) with an action that leads to a reward, the association is trained by delivering a reward only when the 'correct' action is performed, e.g.:
stim A -> press left lever -> get a reward
stim A -> press right lever -> get nothing (or a punishment, but that is a whole different question)
One can quantify the performance of the animal by looking at the probability of responding left (in this case) when stim A is presented.
Now, we think of the association between stim A and left pressing as being reinforced whenever a reward is present, we call it extinction whenever the reward is not present, basically because the reinforced behavior will eventually extinguish, and we say its extinguished when the probability of response to the left and right is 50%.
"...generali[z]ation to ethanol was examined in extinction tests..."
basically means that they substituted stim A for ethanol (I imagine its all olfactory, just read the abstract sorry) and characterize the response to ethanol without ever reinforcing it, hence the extinction.

Do you have any references you can add to this?

Any 1st year psychology text book will talk about classical and operant conditioning, extinction should be right there, it goes all the way back to B.F. Skinner (https://en.wikipedia.org/wiki/B._F.Skinner), speaking of wikipedia: https://en.wikipedia.org/wiki/Extinction(psychology) The reference section should be a good place to start.


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Is natural selection still at work in humans in the 21st century?
There has been some disussion on this site about some aspects (e.g. evolution of eye sight, or height, or the effect of medicine, or evolution the past $\sim10000$ years). My question is really more general regarding evolution and more specific regarding the current age. I'm looking for answer with references to original research if possible.

@Remi.b Thanks for finding this. The question is indeed similar, but the answers are not what I'm looking for, as they consider recent evolution (in the past 10000 yrs). I'm wondering about the today. Our cultur today is very different from that 10000 years ago and this might strongly effect natural selection.

You really cannot view evolution today.. But it is definitely happening..because humans are no more segregated populations but as a famous TV personality said a global community. But two hundred years from now when we have put colonies on Mars and then a thousand years from then you can expect Martian populations to carry traits that are a bit different from Earth humans.... I think you get my point.... That one of things required for viewing evolution is a niche population which has no exterior generic pressure...and lots of time....these are just my thoughts based on what i know till now...

Selection is still occurring because there are many genetic effects on reproductive output - some die before being able to reproduce, there are effects on fertility, behavioural traits (including those making one more or less prone to wanting children)... it is a duplicate as that is covered in the linked question which also focuses on very modern humans

@DavidBlomstrom Selection is most certainly occurring in all populations of humans. The modern cultural and social advances have altered the adaptive landscape, not flattened it. In some genes, net selection may even be stronger now. We also have continued evolution of the meta population, along with selection, by drift and mutation, as well as migration among populations leading to further evolution within sub populations.


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True examples of common variation due to Mendelian Inheritance
Classic examples of mendelian inheritance are genetic diseases such as sickle-cell anemia, Tay-Sachs, cystic fibrosis, and xeroderma pigmentosa. For some of these diseases, it is believed that they evolved because the genes gave a beneficial effect that outweighed the rare occurrence of the disease (e.g sickle cell and protection against malaria).
However, all of these are examples of uncommon phenotypes, usually less than 1% of the relevant population (where it is most common) has those diseases. I'm interested in examples of mendelian inheritance where variation is common (all of the relevant phenotypes have, say, >5% frequency or something like that).
Consider eye color. In European populations both blue and brown eyes are common phenotypes. Many people have probably experienced a typical high-school class of biology, where this was introduced as an example of mendelian inheritance with brown eyes being dominant and blue eyes being recessive. However, modern studies (for example, genome-wide association studies) show that things like eye, hair and skin color are all polygenic traits. See for example (Sulem, ..., Stefansson, 2007).
Throughout the years I've heard of other traits that some said were examples of mendelian inheritance. Being able to roll the tongue, for example. This question was inspired by this recent question where absence of teeth (Hypodontia) was taught to the OP as an example of a dominant trait. The current answer says that hypodontia is probably an example of a polygenic trait that interacts with certain environmental effects. This got me wondering whether there even are examples of common mendelian variation.
I don't quite know the best way to phrase it, but my question is the following:

Are there any examples of human phenotypes that are due to mendelian inheritance where all of the phenotypes are common?

Take eye color as an example again. By common, I mean that both blue eyes and brown eyes are common (over, say, 5% in for example Sweden). On the other hand, for example Tay-Sachs disease occurs only about 1 in 3,500 among Ashkenazi Jews where it is most common, according to Wikipedia. Way less than even 1%.
Preferably I want it to be verified by modern genomic studies (such as GWAS) that it is an example of mendelian inheritance. If such an example does not exist, then I will accept any answer that provides modern, relevant scientific literature that explores this topic. For example, it might explain why we would not expect to see common variation due to mendelian inheritance.

Generally, you don't need a GWAS to detect Mendelian traits (though it can and will quite reliably, precisely because those genes are Mendelian). That's why common Mendelian traits were identified before GWAS.

@kmm Fair enough. But there were also traits that were claimed to be Mendelian, and after GWAS were discovered to not be. (Though, to be fair, that could simply be bad practice by the people who claimed that, and perhaps it was not consensus.) But you're right. It doesn't have to be GWAS evidence. Just simply some good evidence that is consistent with modern findings.

GWAS aside, what you are asking for isn't clear to me. If I understand correctly, you are looking for phenotypes that are Mendelian (i.e., not complex traits), but which also have common alleles (I imagine 50:50 would be ideal).

@kmm Well, for example take any population, say The Netherlands. Imagine if a person from this population could either have blond hair or dark hair. Both phenotypes are fairly common. Then imagine if it were discovered that blond/dark hair was Mendelian, then that would be a nice example (It happens not to be the case; hair color is actually polygenic). Now I want to know if there are any examples like that. Sure, I guess 50:50 would be great, but I would be satisfied with, say, 95:5 or 90:10. (If you wish, you can edit my question to make it more clear)

Depending on how broadly you want to bin a phenotype, and what you mean by "all the phenotypes", hemoglobin disorders are among the most common mendelian traits. In Cyprus, for example, I believe around 17% of the population is heterozygous for a hemoglobinopathy.

@DeNovo I think that could be made into a satisfactory answer. This question has been open for long, and your example seems fine to me.

Earwax consistency is an example of a monogenic trait with dimorphic phenotypes in humans -- "wet" and "dry" -- where both phenotypes are globally common, though allele ratios are highly variable between human populations.  The population genetics and molecular basis of this trait are discussed at length by Dr. John H. McDonald as part of a series on the myths of human genetics (archived version here).  I reformat his discussion in my answer.

In The dimorphism in human normal cerumen, Matsunaga summarizes 30 years of research into the earwax of Japanese families, with two major observations:

Dry earwax parents never have wet earwax children, suggesting the genetics underlying the wet phenotype are dominant to those underlying the dry phenotype.
Because the allele for wet earwax is relatively rare in the sampled families, it is likely that most wet earwax parents are heterozygotes.  Following from this, if the trait is monogenic with two allele variants, we expect a 3:1 ratio of wet to dry children in wet × wet parent crosses, and a 1:1 ratio of wet to dry children wet × dry parent crosses.  Indeed, this is observed.

$$\begin{array}{c|c|c|}
\text{parents} & \text{wet children} & \text{dry children} \\ \hline
\text{w×w} & 35 & 12 \\ \hline
\text{w×d} & 205 & 195 \\ \hline
\text{d×d} & 0 & 634 \\ \hline
\end{array}$$
These results were later corroborated in Native Americans --
Cerumen in American Indians: Genetic Implications of Sticky and Dry Types
$$\begin{array}{c|c|c|}
\text{parents} & \text{wet children} & \text{dry children} \\ \hline
\text{w×w} & 32 & 6 \\ \hline
\text{w×d} & 20 & 9 \\ \hline
\text{d×d} & 0 & 42 \\ \hline
\end{array}$$
And in a different Japanese cohort --
Distribution and inheritance of earwax types: a study on inhabitants in Awa District, Chiba Prefecture
$$\begin{array}{c|c|c|}
\text{parents} & \text{wet children} & \text{dry children} \\ \hline
\text{w×w} & 27 & 3 \\ \hline
\text{w×d} & 137 & 109 \\ \hline
\text{d×d} & 0 & 345 \\ \hline
\end{array}$$
In the early 2000s, the molecular basis of human earwax consistency was elucidated in three major publications.

Toshida et al. mapped a single locus on chromosome 16
Yoshiura et al. identified a SNP at position 538 in the coding region of ABCC11.  At this site, G corresponds to a wet earwax phenotype, whereas A leads to a dry earwax phenotype.  A less common allele representing a deletion of 27 nucleotides in exon 29 also yields a dry phenotype.
Toyoda et al. found that the 538G>A transition encodes arginine in place of glycine, resulting in a loss of glycosylation in the mutant protein, leading to deficient cellular localization, rapid degradation, and loss of function.

To directly address your question,

Are there any examples of human phenotypes that are due to mendelian inheritance where all of the phenotypes are common?

I point you to the tables above, as well as Table 1 from Cerumen Phenotypes in Certain
Populations of Eurasia and Africa, which shows that the frequency of the dry allele ranges from 59% to 89% across diverse human populations --

To conclude, human earwax consistency is a dimorphic trait controlled by a single gene, where both phenotypes are common across human populations.

Thank you for the answer (upvoted and accepted), and nice site that "Myths of human genetics" by Dr. McDonald.


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Do chromosomes line up as pairs in mitosis or meiosis?
Here is a question from the book SAT II Success Biology E/M (where the SAT is the exam taken by the American high school students):

Homologous chromosomes line up in pairs in
  (A) metaphase of mitosis.
  (B) metaphase I.
  (C) metaphase II.
  (D) interphase.
  (E) prophase of
  mitosis.

In my opinion, we can definitely eliminate D and E since in both mitosis and meiosis, chromosomes line up during the metaphase.
Then, I would choose the answer choice B because as far as I know, after prophase I -- when the chromosomes are in pairs during crossing-over -- the chromosomes are still in pairs and become separated into the different ends of the cell during anaphase. In mitosis and metaphase II, however, they align along the "equator" of the cell, forming a line of single chromosomes.
However, I am confused here because of my book. Here is its explanation for this question:

The correct answer is (B). In meiosis, the homologous pairs line up as
  individuals in meiosis I in preparation for final segregation in
  meiosis II. Meiosis simply needs to ensure the pairs end up in
  opposite daughter cells in meiosis I. It is in mitosis that the
  homologous pairs line up as pairs, and interphase, of course, is not a
  phase where the chromosomes even appear.

You can see that even though the first line indicates that the answer actually is B, the phrase that's in the cursive contradicts that statement.
I suspect there is a mistake either in the bold or the cursive statement. Could you help me here?

You are correct.  The books explanation is mistaken, and badly written ("the pairs line up as individuals"???)
https://en.wikipedia.org/wiki/Homologous_chromosome

In metaphase I of meiosis I, the pairs of homologous chromosomes, also
  known as bivalents or tetrads, line up in a random order along the
  metaphase plate.

https://www.khanacademy.org/science/biology/cellular-molecular-biology/meiosis/a/phases-of-meiosis

So, during metaphase I, homologue pairs—not individual
  chromosomes—line up at the metaphase plate for separation.


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Why is the pressure pulse bigger after exercise?
Right after exercise, is the amplitude of the pulse smaller or bigger than resting period? And why is that ?

I would guess that pulse pressure increases after exercise. As I understand it,

Systolic pressure is simply resistance against the pressure wave of the ejected blood. Since the stroke volume is increased in exercise to deliver more blood, systolic pressure will be definitely be increased.
During diastole, the major resistance to flow is due to peripheral resistance (major arteries now assist flow by releasing stored energy), and this is reduced in exercise due to vasodilation. Although there is more flow, since the resistance is markedly reduced, diastolic pressure may drop.

Hence, pulse pressure should increase.

It'd be important to note that during exercise, there is systemic vasoconstriction but vasodilation in the vessels to the muscles. This sums up to a net vasodilation (due to the enormous bulk of musculature), resulting in a fall in net peripheral resistance and hence, the diastolic pressure.


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Why are there no WINGED flying arachnids?
There seem to have been no arachnids flying WITH WINGS of any sort at any location or any time in the present or in the fossil record.  Why is this?
Rationale for question :
If the process of evolution can be expected to explore all (or large numbers of) possibilities open for adaptation of any form, why has this never happened for arachnids which have been present on land in large numbers of species and individuals for about as long a time as insects?
Arachnids were among the first air-breathing terrestrial creatures so have had this option available for all this time, with apparently no sign of wings at all.
Winged flight offers major advantages to creatures that have evolved it, and has been evolved independently by many branches of the animal kingdom and apparently over relatively short timescales among those that have done this (e.g. bats have presumably evolved flight since the kT extinction of about 65 MY bp).
Flight is easier for smaller animals such as arachnids, as insects have shown, and insects have also shown that flight for small creatures is possible in oxygen levels at present, and levels have been much higher at times in the past.
N.B. !! We all know about spiders ballooning on silk ! This question is about WINGED flight. Please do not waste any of your time or ours on comments about ballooning ! That does not allow directed purposeful flight as wings do and is not a substitute adequate to account for this absence.

This isn't true on small scales: "evolution can be expected to explore all (or large numbers of) possibilities open for adaptation of any form".  If you take the entirety of natural history into account then you see incredible diversity and different ways of solving problems, but that doesn't mean every lineage gets to try out every solution. Because evolution is incremental and most mutations are bad, major changes to lineages happen rarely, for example flight's only evolved 4 times. Bats may have evolved it quickly, but they would have done so under specific circumstances.


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Do vitamin enriched foods preserve their value when exposed to higher temperatures?
At what temperatures do different kinds of vitamins are destroyed or lose their nutritional value?
Imagine you went to the store and bought vitamin enriched cacao powder. Then you made yourself a hot drink by pouring boiling water. How much in general(approximately) vitamins were destroyed by that heat.
"How to prepare/cook" usually doesn't have this kind of information. Thus any benefits of vitamins are lost(?).

There is already a lot of information on this topic (also for non-biochemists). Did you try googling "heat sensitivity of vitamins"?

@WYSIWYG yes, I have googled it. Bottom line every article or page that I have found just says - "yes vitamins lose their value when heated" (I am not very good at googling or finding this kind of data when it comes to biology). Not very informative, I understand that they lose their value. I wanted to know how serious those effects can be.

This question is not about biology in terms of SE Biology but domestic science, unless it is a personal medical question, which would be off-topic. It might fit Chemistry SE if it were not so broad/imprecise.

@David I see. I thought that since it's about vitamins and they have biochemical functions that occur in our bodies - it would be fit for biology. But since the question is more outside of terms of biology and closer to chemistry and reactions, I agree with you that it may better fit Chemistry. Although, it would be incorrect moving it after Jan's answer. Biology, chemistry and physics are tightly coupled together, so I guess it's not that big of an issue, is it?

I understand that the question is not of a nearly perfect quality. But due to my incompetence in this topic that is naturally what I could do.

Here's one estimation about how much vitamins or minerals can get lost due to various "food processing" (cooking, drying, freezing) methods:
According to NutritionData, cooking can result in a loss of vitamins:

Vitamin A: 25%
Vitamin C: 50 %
Vitamin B complex vitamins: 25-70%
Minerals: 25-70%; most important: potassium loss in cooking water. In this study with potatoes:

Leaching alone did not significantly reduce levels of potassium or
  other minerals in tubers. Boiling tuber cubes and shredded tubers
  decreased potassium levels by 50% and 75%, respectively.

According to USDA retention factors, the following vitamins are most affected by food processing:

Vitamin C
Vitamin B1, B6, B12 and folate

Vitamin and mineral loss is related to both the temperature and time of cooking.
Mineral loss can be prevented by cooking in vapour (steaming) instead of cooking in water.
According to this source, the following can be loses after heat treatment at 70 °C and (90 °C):

Vitamin A: 10% (30-40%)
Vitamin D: 15% (35%)
Vitamin B1: 15% (50%)
Folic acid: 5-20% (45%)
Vitamin C: 40% (85%)

But the minerals won't be truly lost if the cooking water is not thrown away.

@WYSIWYG,  most people throw away cooking water after boiling potatoes. Since potatoes are rich in potassium, a lot of it can be lost that way. If the water is consumed, of course no minerals are lost. I added one study about potatoes.


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Taq Polymerase's stability at high temperature
I was asked a question as to what is so special with Taq Polymerase that makes it quite stable at high temperatures though its functioning is the same as other DNA polymerases like that of mesophiles.
I just think it's the adaptation of that particular bacteria in that high-temperature environment. But I want to know if there is any strong reason for this stability.

Well, the evolutionary reason is the one you mentioned: the thermostability of Taq allowed its bacterium to colonize high-temperature environments. That, however, does not say anything about the molecular reasons for this difference.
I found this very good answer on Quora. The end of the post has several references for its claims.
Long story short, the stability of a proteins folded state depends on the difference of free energy $\Delta G$ between the folded and unfolded states. However, $\Delta G = \Delta H - T \Delta S$, which means the difference in free energy can either come from a bigger difference in enthalpy (for example, salt bridges, hydrogen bonds, hydrophobic interactions and such in the folded state) or a smaller difference in entropy (for example, a low number of "not-rigid" amino acids like glycin , or a high release of water from folding).
While enthalpy is often the reason for stability of folding, it seems like for Taq polymerase the difference actually lies in an unusually small difference in entropy between the two states.
Edit: here is one of the best references of the post. Open the link above to find more. https://www.ncbi.nlm.nih.gov/pubmed/24174290

Can you please cite an original source i.e. a research article/review?

@WYSIWYG As I said, the end of the post I linked had all the references. Anyway, here you go: https://www.ncbi.nlm.nih.gov/pubmed/24174290

Please edit your answer to include this reference information — comments are intended for suggestions and discussions intended to improve answers (or questions) and should not be used to post material that belongs in the answer itself.  You also might want to consult the help pages for additional advice on [Answer] effectively on this site. Thanks!