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What type of jellyfish is this?
Friends of mine recently came back from a visit in kenya and on the kenyan beach they said they found several jellyfish with "sails" on their head. We tried finding out what they were and found one image online that was exactly the type of jellyfish they found:

What kind of jellyfish is it?
The guide told them that they're dangerous and those are just the corpses without stings or something, but nobody knew it's name.

If the jellyfish your friends saw actually look like this and if they were small (Wikipedia says they're usually less than 7 cm in length), they're likely Vellela vellela or sometimes called By-the-wind Sailors for the way the raised part catches the wind and is blown along the ocean's surface.
Wikipedia writes

...all possess nematocysts, in some species the nematocysts and toxins
  therein are more powerful than other species. V. velella's nematocysts
  are relatively benign to humans, although each person may respond
  differently to contact with the nematocyst toxin. It is wise to avoid
  touching one's face or eyes after handling V. velella, and itching may
  develop on parts of the skin that have been exposed to V. velella
  nematocysts.

Some photos.

Source

Source


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What are some online databases that I can search to find the pathways for sythesis of Lignin, Cellulose, GAX?
I am trying to obtain the pathway information for synthesis of Lignin,GAX and Cellulose in Sorghum. I am quite new to biology and genetics (EE background). I would appreciate it if y'all can provide me with some websites or books where such info maybe available. I have already looked in KEGG. Thank you very much.

KEGG would be the first choice for pathway data (also/especially for specific species). If KEGG does not give you the data you need, maybe describe what else you need, to give people a better idea in which direction to go.

The other big metabolic database site besides Kegg is MetaCyc which certainly responds to searches for lignin and cellulose.
The problem with lignin is that it is a very complex molecule, so in both Kegg and MetaCyc there are a many reactions involved in its synthesis. Cellulose is less complex and I have no idea what GAX is, despite an internet search. If you are so new to biochemical reactions and metabolic pathways that you cannot handle the results of a MetaCyc search on lignin you should easily be able to find articles devoted specifically to cellulose and lignin, perhaps using Wikipedia as a start.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


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What is this creature I found on my house?
What is this creature and what species is this?
I found this on my balcony.

It's a caterpillar but please add your approximate location, it helps a lot the id.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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Virus culture in artificial/synthetic medium
I am looking for a publication/paper in a well a circulated magazine/journal/government study on growing virus culture in synthetic or artificial medium. I have found this link on SARS Cov 2 being cultured in  artificial saliva, but are there any sources handy?
https://www.tandfonline.com/doi/full/10.1080/22221751.2020.1777906?scroll=top&needAccess=true
Thanks a lot!

What exactly are you looking for? What is your "goal"? The linked paper is not "culturing" viruses in artificial saliva, but rather looking at viral survival (aka decay rate) in that medium.

In the linked study they didn't grow it in artificial saliva or artificial culture medium (DMEM) - it was grown in cells (as viruses need to be) and then aerosolized for stability testing in the saliva or medium.  In some manner all media used for growing any cells and viruses are artificial - we make and purify compounds that are then mixed to make the final solution. The exact compositions of these solutions are not found in nature at all, but were derived experimentally by cell culture researchers.

Thanks for responding. Apologies, I should have gone through the whole article. The other day I was having a discussion with a colleague (also a buddy from college) on whether viruses can be cultured outside living cells i.e in a synthetic or artificial medium, under the right stimulation. Is it possible? (We were discussing on some vector vaccine)

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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COVID-19 exposure risk from passing joggers versus walkers
What is the COVID exposure risk from passing close by someone who is jogging relative to passing close by someone who is walking?
The reason I ask is with regard to going out for exercise, or to run errands: going out early in the morning means passing fewer people, but a larger percentage will be joggers. I'm trying to figure out whether there is an overall risk reduction, whether early morning is safer than the middle of the day.
I have only been able to find answers to adjacent questions:
'Either way, the risk is low outdoors versus indoors.'
Right. But what's the relative risk between these two low-risk outdoor events?
'Ideally, you should keep 4.5m separation from joggers.'
Ideally yes, but as it turns out, sidewalks are not 4.5m wide.
'We don't have enough data to be sure.'
Right. But decisions have to be made based on the best currently available guess. What's the best currently available guess for this? 1.1x? 2x? 5x? 20x?

This is a well-worded question, but I imagine there is no research that will give you the precise answer you seek. There are a multitude of variables, each of which is hard to control and provides minimal useful insight: relative viral shedding of a runner v. a walker due to different rates of respiration, the differences in turbulent airflow caused by running v. walking, etc. Moreover, the applicability of results obtained from such a study would be constrained to situations where environmental variables are similar: temperature, humidity, wind, inter-individual variability in viral load

I agree with @acvill, you might see papers looking at 1 of the variables each, but it would be very hard to do it all in one study.

Questions relating to medical advice are off-topic on biology. You might get an answer on SE Medical Sciences, but there are many reputable sources of information on this topic on the Internet (see the Meta article).

@acvill Sure, I'm aware there is no precise answer, like I said, I don't seek one, just a best guess to an order of magnitude.

@David This is not medical advice, and there are plenty of not purely theoretical questions on covid on biology. As I said, I have searched the Internet, and found nothing that addresses this question, only the adjacent questions I mentioned. Which Meta article are you talking about? The ones showing in 'featured on meta' in the top right, are on completely different topics.

The Meta article is here and was a response to the "plenty…questions" that on covid which were imho not on topic here, and for which this  forum is not a place to get the most informed information on a topic for which answers intrinsically constitute medical advice.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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How much does each rotation coarse adjustment move the stage in a microscope?
I've been working with microscopes lately and have been trying to think of a way to somehow find out a way to some how find out a way to relate the rotaions of fine adjustment to coarse adjustment.
The main idea is to figure out how many centimeters the fine adjustment moves the stage, then compare the same thing for coarse adjustment.

This is unanswerable unless you specify the particular model of microscope as there are tens of thousands of different models with their own specifications. You would also need to show your research in alignment with the [help]'s requirement. It would be great if you'd also tell us the purpose of the question and how it relates to biology, as it seems to be a question of engineering at present.

The instruction manual for the microscope would help greatly.  But there is a simple method that should tell you what you need to know with modest precision.  Use micrometers (the instrument, not the unit) to measure the thickness of a microscrope slide.  Mark the top and bottom sides of the slide with an expo marker.  Put the slide in the slide holder firmly, and focus on the bottom of the slide first ... then count how many times you need to turn the knob to focus on the top.


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Are the seeds in a single capsicum fruit genetically identical?
Hopefully not a too-basic question for the venue. I'm a chile pepper growing hobbyist and have spent some time searching around and reading up on pepper (angiosperm) reproduction, but I'm not getting a clear picture of the details.
It seems like flowers have multiple ovules and it seems like one pollen-grain landing on the stigma leads to fertilization of a single ovule. And it seems like that process produces a single seed.
But that fertilization also prompts fruit growth and flower death and capsicum fruits have many seeds, never just one (that I've ever seen).
So, does each seed have a potentially different father? Or are the multiple seeds generated through a reproductive/cloning process that I'm not seeing written about? Or something else?

No, the seeds are not genetically identical.  Each seed come from the fertilization of an ovum with a sperm from a separate pollen grain.  Since each pollen grain can come from a different plant, the seeds will generally differ from one another.
Additionally, even ova from a single plant will not usually be genetically identical to one another.  This is because the process that creates the ova (meiosis) shuffles the genes of the parent plant on then places only half into the ovum.  The same kind of shuffling goes on in the creation of pollen grains.
In the chili pepper genus (Capsicum), plants are predominantly self-pollinating. This means the majority of the pollen for the seeds in a fruit will come from the very same plant.  This generally reduces the amount of variation seen in the offspring compared to complete cross-plant pollination. Some cross-pollination can nevertheless occur if there are other varieties in the neighborhood.  The fruit will not show the effects of the new genetic combinations present in its seed, but only a plant grown from the seed will make the differences evident.

Thanks! So, it sounds like if I grew a plant in perfect isolation, removed all but one flower, and removed the anthers from that flower, and then brought in a single grain of pollen, I'd expect to see a fruit develop with a single seed?

No more than one seed since the single grain might not be successful.  (Also, the fruit might not develop due to not enough seeds being present.)


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What does this graph explain?

I find this graph incredibly confusing. Is it saying that when there is a decreased affinity (of hemoglobin to oxygen, I think?), the partial pressure of oxygen increases with the same percent saturation of hemoglobin? What does that even mean if that's the case?

is there text around graph? can you add source link

A graph is generally meant to be interpreted as y being a response to a change in x. This graph highlights that as the partial pressure of oxygen $P_{O2}$ increases, so does the percentage of hemoglobin that are saturated in oxygen. The relationship is not linear (unlike you seem to suggest) but is logistic.
The graph also highlights how three different level of affinity would affect the relationship between $P_{O2}$ and the fraction of hemoglobin that is saturated and highlights side consequences of such affinity variation.
Finally, with vertical dotted lines, the graph indicates what the $P_{O2}$ is in the lungs and in the other tissues.

why a decreased affinity is a shift to the right and an increased affinity is a shift to the left?

Consider a single point in the x axis such as $P_{O2} = 40$ for example. If affinity is increased you would expect that the percent saturation of Hb would increase, right? This causes a shift of the left.

That all makes sense, I guess I should've been more specific. The only thing I'm really confused about is why a decreased affinity is a shift to the right and an increased affinity is a shift to the left?

@AliceD X and Y are rarely arbitrary choices. In no way do I mean that correlation implies causation but a person makes a graph as to imply a causality of X on Y. Also, when statistical analysis is involved as in any linear model (incl. GLM, ANOVA, ...) one of the variable is considered as a response to the other variable variation.

@AliceD Of course, thinking everything as causation can be very misleading but this is still what is portrait through graphic representation. Google what goes in x axis what goes in y axis for more info. Note that following your comment, I corrected my first sentence from "always" to "generally", which is much more correct. Thanks!

@PatrickSalas Pease, see edit in my answer

I don't see how a shift to the left shows that the percent saturation of Hb has increased. It is only shifting in the x direction, so it seems like it's saying an increased affinity results in the same saturation for a smaller partial pressure of oxygen. Is that the case?

At $P_{O2} = 40$, the "baseline" affinity curve indicate a Y value of about 75. The increased affinity curve (the left shifted one) indicates a Y value of about 95. So, yes shifting a curve toward the left here lead to matching a greater perceneage of Hb saturated for a given $P_{O2}$ which is what you would expect from a case where affinity is increased. Btw, your issue has nothing to do with biology. It is about basic of mathematics and how to interpret a graph.

This answer is exactly correct. @AliceD correlation does imply causation, but does not prove causation. Here, either of those statements are nonsensical. This isn't a cohort study, it's a fact about physiology. With a healthy Hb molecule, when $P_{O_2}$ goes up, $O_2$ saturation goes up, with exactly this pattern, every single time.

You're right- there is a lot going on in this graph and it is hard to understand it at a glance.
Let's take the lines one at a time. The middle line is the curve that represents the relationship between PO2 dissolved in blood and percent hemoglobin saturation under physiological (essentially, healthy) conditions. We can see that percent Hb saturation is very low when the PO2 is between 0 and 20 mmHg, that Hb saturation sharply increases between approximately 20mmHg and 50mmHg, and that Hb saturation reaches near-maximal levels after the PO2 reaches approximately 50 or 60mmHg. From just looking at the middle line, we can learn that coming out of the lung, Hb will be about 100% saturated, while in tissue, at a much lower PO2, the Hb saturation is still around 75%.
Now, let's look at the dashed line, to the left of the middle line. This line represents the shift in hemoglobin saturation that occurs when PCO2 drops, when pH raises (blood becomes more basic, which could also occur as a result of inappropriately low PCO2), or when temperature decreases. This results in an increased affinity of Hb for O2, so Hb saturation stays much higher at a much lower PO2, when compared to the middle line. Therefore, at a PO2 that is very close to what tissue might see, Hb is still very close to maximally saturated. This becomes a problem for O2 delivery to tissue, since O2 is less likely to leave Hb to oxygenate the surrounding tissue.
Last, let's look at the rightmost line. This line represents the converse of the dashed line- here, PCO2 has increased, pH has decreased (blood is now more acidic), or temperature has increased. This causes a decrease in Hb affinity for O2, meaning that even at a high PO2, Hb will, on average, be carrying less oxygen. So, when blood leaves the lung, Hb might be almost maximally saturated, but by the time PO2 reaches tissue levels, Hb is actually closer to minimal saturation under these conditions. This causes issues with O2 delivery since there is just less O2 to be delivered once the PO2 reaches the level it might be in tissue.
Hope this helps- LMK if more questions.


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Why is the Baldwin Effect-transformation of learned behaviors into instinctive ones-a likely result of natural selection?
The Baldwin effect is an evolutionary mechanism that describes how learned behaviors can influence the direction of natural selection. It is postulated that when a learned behavior is advantageous, the members of a population that learn it best survive and pass on the ability to learn that behavior.  Eventually the behavior becomes instinctual.
Why would there be a jump from members of a species being able to learn a behavior very quickly to the members of a species having that behavior instinctually hardwired?  It would seem to me that the ability to learn it quickly and efficiently would reduce the relative benefit of gaining that behavioral ability instinctually since the behavior could be taught and learned without hardwiring it as an instinct.

I think you are wrongly thinking of "instinct" and "ability to learn a specific thing more quickly" as somehow separate, rather than as the same thing to varying degrees.

How well accepted is this hypothetical mechanism? You may be asking a question that doesn't have a definitive answer because it's not accepted as fact.

https://www.youtube.com/watch?v=Sdqg-jn_tBk

@anongoodnurse Strictly speaking, I am suggesting a debunk of a conjecture, namely that good learners of a behavior would be likely, by selection pressures, to integrate the learned behavior into an inborn instinct.  So I am suggesting that the Baldwin Effect conjecture is not logically supported by natural selection.

@BryanKrause The Baldwin Effect "conjecture" is the conjecture that a) fast learners of a helpful behavior survive in a population and are b) likely to eventually give rise to offspring that don't have to learn the behavior at all.  I don't think that the progression from a to b is consistent with natural selection.

No one is going to watch a YouTube video to get information you can write in a post. What @BryanKrause said is enough to counter the hypothesis. Instincts are strong things, and in my experience (mainly with dogs), if a dog picks up a behavior, it's because there's an instinct there already that predisposes the animal to "learn" the behavior in the first place, not the other way around (epigenetic modification excluded).

@JosephHirsch I understand what the Baldwin effect is. I think you are not understanding that biological changes underlying "fast learning" can be the same as those underlying "not needing to learn". That's just the fastest learning you can have: already learned. The Baldwin Effect is not about general learning speeds or anything like that, it's about specialization towards a particular behavior, and suggests that if the random variation in a population that allows some individuals to learn a specific behavior more quickly is heritable, selection moves the population towards instinct.

@BryanKrause So mechanistically perhaps there were genetic (likely polygenetic) behavioral tendencies in a population which might have become unlocked easily by observing the behavior of others who had already learned it, but that those behavioral tendencies might still lead to that behavior emerging eventually.  Those with a stronger tendency, or more genes working in that direction survived and eventually the behavior emerges in individuals readily enough that they may end up doing it fairly early in their lives even if they don't see it performed by another.

Yes, that would accurately describe the Baldwin Effect as I understand it.


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Are there any known bioluminescent species of fungi found in the Pacific Northwest?
This might not be the best place to ask this but since mycology is included I though I'd try: Some 21 years ago in late May of 2003 I was walking with a group of friends in the woods near Olympia, Washington sometime after 9PM when I noticed a blotch on the trunk of a tree(the tree was standing) glowing blue-green. It's glow was much dimmer than a firefly but it was clearly visible. We had no flashlights or lighters and it was pretty dark so I couldn't see what it actually looked like during daylight. It appeared to be either a slime mold or a crust fungus but I didn't touch it so I have no idea what its texture was. I talked to someone who also saw something very similar in the woods near Astoria, Oregon. So are there any known slime mold or crust fungus species that are bioluminescent? Nobody seems to have any idea what is could be and it makes me wonder if it is some species that has yet to be officially calatoged by science.

https://www.reddit.com/r/mycology/comments/5o1mry/do_any_bioluminescent_mushrooms_grow_in_washington/

@BenBolker it clearly wasn't any of those. I would say it was not a mushroom in any sense of the word but more like a mold of sorts if you will. If I ever see it again, I will take a sample of it to a mycology lab.


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What can't the human eye see far-UV, X-rays, and gamma rays?
This is as much of a physics question as it is a biochemistry question. But how does rhodopsin(and the retinal chromophore itself) respond to ionizing radiation? Photons whose wavelength is longer than 700nm do not have the energy to photoisomerize retinal. But for photos with wavelength shorter than 300nm for sure have more than enough energy to do so.


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can we say that pumps are carriers that need ATP?
I know that pumps always use ATP , but i don't know what is the relationship between carriers and pumps .
are pumps a subdivision of carriers ?

see WP membrane transport protein

Yes, you can consider pumps are carriers used for active transportation (needing ATP).
A carrier is a specific type of transport proteins. They differ from channels or pores in the fact that during a certain instant, carriers only have one side of the protein open1. While pores are continuously open, and channels are either open or closed2.
Carriers can be involved in active transport3 or facilitated diffusion (passive)4. But as you mentioned, pumps always are used for active transport. Pumps, as Bryan pointed out in the comments, are just a name given to some transport proteins that use active transport, but not all active transport proteins are labeled as pumps.
I hope this clarified things for you.

Not all pumps use ATP. Some things named pumps use ion gradients. It's not very precise terminology.

Would a more precise terminology be to remove "that use ATP to function" and replace it with active transport? As ion pumps using gradients would be using secondary active transportation.

Yeah. I think the optimal answer would also address that "pumps" aren't a special protein category, just a naming convention for some proteins involved in active transport. Other proteins with nearly identical function are known by other names, like "transporters", without an obvious defining characteristic (that I am aware of). That is, all pumps use active transport, but not all active transporters are given the name "pump". Those that use ATP directly, like Na/K pump, are also known as "Na/K ATPase" etc.

thank you for your answers ;
but i have another question ; 1- can we say that all pumps do a kind of active transport but don't need ATP , 2- can you give me an example of one transporter that do active transport but isn't a kind of pump ? – user35622 47 secs ago   edit

1- All pumps do active transport, but not all use ATP to power (secondary active transport). 2- An example of a whole family of active transporters the don't use "pump" are the ABC Transporters (Wiki - ABC Transporter)


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Does overfishing in one ocean hurt fishstock in another?
If there's overfishing in the Atlantic or North Sea - will this affect fish stocks in the Indian ocean? Are there papers on this?
The question I'm trying to answer is whether overfishing by developed countries has an impact on developing countries fishstocks?
I could see two different scenarios:
-fishstocks are connected globally and if you overfish in one ocean biomass from other oceans will 'flow in'
- the oceans ecosystems are more or less 'disconnected' and somewhat independent of each other
I would appreciate citations if there are any.


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Non-cavitating ultrasound for denaturation of short strands of DNA (~20 bp)?
I know that there is existing research on ultrasound-induced transient cavitation bubbles that mechanically denature DNA by generating violent shock waves locally in solution.
I would like to know if it is possible for non-cavitating ultrasound to denature short strands of DNA, ~20 base pairs in length (please cite sources, if possible). The mechanism should be mechanical, without involving thermal or cavitation effects of ultrasound. The ultrasound acts as a pressure wave, of the order of 10 MPa, and the DNA helices require a force of ~15 pN to initiate unzipping. I just need proof that this has been successfully demonstrated.
Thank you in advance.

Does DNA denature?


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Variations in asexual reproduction
It has always been said that sexual reproduction produces offsprings which are superior to their parents, due to the variations which they acquire causing them to survive better in their environment. That's because we can think of meiosis occurring at some level of their life cycle resulting in the variations in the final offspring.
 But what when we talk about bisexual organisms, might they be plants, animals or any other life form? Can't there be variations in their offsprings if they produce them asexually? It's like when they undergo gamete formation in different male and female structure present in that single parent, they'll surely undergo meiosis(if the parent is not haploid undoubtedly) forming the gametes which are dissimilar in their genetic makeup. When these fertilize, shouldn't they show variations?

The question is rooted in a misunderstanding of what sexual reproduction is and is not.
Any good intro book to evolution has a chapter on the diversity of reproductive systems. Consider for example Evolution: Making Sense of Life. If you speak french, the book évolution biologique has a very chapter on the diversity of reproductive systems. If you want something more complete and more advanced, you can have a look at The Evolution of Sex Determination.

It has always been said that sexual reproduction produces offsprings which are superior to their parents, due to the variations which they acquire causing them to survive better in their environment.

Who said that? The common simplistic idea and sex increases mean fitness because it increases genetic diversity is both wrong because sex does not necessarily increase genetic diversity and wrong because increase in genetic diversity does not necessarily result in increasing mean fitness.
You can have a look at the work of Nick Barton, Sally Otto and many others on the subject. The above misconception is well explained in the introduction of this talk from S. Otto's

[..] But what when we talk about bisexual organisms, might they be plants, animals or any other life form?

I'm not sure what you meant here. You probably did not want to use the term bisexual. Maybe you meant dioceous.
Please note that sexual reproduction does not mean dioecy. Sexual reproduction does not even mean anisogamy and doe snot necessarily involved more than one individual (see selfing).

Can't there be variations in their offsprings if they produce them asexually?

There is a whole range of reproduction mode and saying sexually vs asexually is making gross categories that make it sometimes hard to really answer the question. It is also hard to know what you mean by "variations" here. But shortly speaking:
Asexual reproduction does not necessarily mean total absence of recombination (see for example Narra and Ochman 2006) and definitely does not mean absence of mutations (see for example Sniegowski et al. 1997).

It's like when they undergo gamete formation in different male and female structure present in that single parent, they'll surely undergo meiosis(if the parent is not haploid undoubtedly) forming the gametes which are dissimilar in their genetic makeup. When these fertilize, shouldn't they show variations?

If there is fusion, then there is sexual reproduction, even if it is selfing and even is they don't have genders (anisogamy).

Thanks for the answer, it had literally cleared many of my misconceptions. I agree with your point that sexual reproduction doesn't always result in better offspring but can you please explain what you meant by 'sex does not necessarily increase genetic diversity'? I mean it does create variations. By variations I meant genetic recombination. I'm not sure what you meant here. You probably did not want to use the termbisexual. Maybe you meant dioceous. No I mean the use of term bisexual and an explanation to this was selfing as I well understood it.

Maybe you meant hermaphrodite by saying bisexual. Bisexual is a term mainly used for humans in sociology and does not mean being able to reproduce with oneself (selfing when there is fertilization) and does not mean having both sexes (hermaphroditism, usually called intersex in humans) either.

Recombination does not necessarily increase genetic variance in the population. It rather diminish it actually. It is a common misconception that sex necessarily increase genetic variation. Have a look at the link to Sally Otto's talk, that will probably clear things up.


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What is this red orange insect with black dots found in Japan?
I searched with picture to Google, and they suggest it might be

Fire-coloured beetle

I also went through the list of insects from this page, http://www7a.biglobe.ne.jp/~yabuyama/koucyuumoku.html, it is in Japanese. The bug that looked like the one in picture the most was a ベニカミキリ (latin name: Purpuricenus temminckii), but it did not have the black dots, and it seems too small.
The insect was found near a pond in a Japanese garden in Fukuoka, Kyushu in June. I do not recall the size of it, but I think it was somewhere between 1cm and 3cm long.

I was able to find it in an insect lexicon. It is all in Japanese, but the description fits the image. The insect is in fact a カミキリ、a ホシべ二カミキリto be exact. And the binomial name is Eupromus ruber

Here is also some more information https://www.insects.jp/kon-kamihosibeni.htm
And a Wiki page in english https://en.m.wikipedia.org/wiki/Eupromus_ruber


text:
How do cellular conditions change the Gibbs free energy of a reaction?
How do cellular conditions change the Gibbs free energy of a reaction?
Taking glycolysis as an example, how exactly would cellular conditions affect the free energy released from this reaction?

https://en.wikipedia.org/wiki/Glycolysis#Free_energy_changes

Standard free energy or actual free energy?

And this wouldn't be a homework question by any chance? In any case, what attempt have you made to answer it yourself?

To understand that, you must have a basic understanding of Gibbs-Helmholtz equation. it states-
$\Delta G'=\Delta G^{'o} +RT\,ln\,(Q) $
Here, $\Delta G'$ = biochemical free energy change & $\Delta G^{'o}$ = standard biochemical free energy change.
Suppose you have a reaction,
$x+FADH_2\rightleftharpoons xH_2+FAD $
So, $Q=\dfrac{[xH_2][FAD]}{[x][FADH_2]}$
Now let's assume that $\Delta G^{'o}>0$.
Hence the spontaneity of the aforesaid reaction (in forward direction) will be dependent on the $\Delta G^{'o}$, which is a function of reaction quotient (Q) as well as temperature (T).
Now, if the body is in lower energy state, i.e. fasting; $\dfrac{[FAD]}{[FADH_2]}$ ratio will be high. So, in order to make $\Delta G'<0$, the following condition must be satisfied $-$
$RT\,ln\,(Q)+\Delta G^{'o}<0$,
or, $RT\,ln\,(Q)< -\Delta G^{'o}$
or, $RT\,ln \dfrac{[xH_2][FAD]}{[x][FADH_2]}\,< -\Delta G^{'o}$
With this reasoning, be it any metabolic pathway; we can predict its spontaneity.

I don't see how this answers the poster's question. You are just explaining how the free energy change allows one to predict the direction of one particular reaction from the concentration of reactants. 2. Strictly speaking the prime indicates "at pH7". So one answer to the question might be that if the cellular pH changes this will alter the free energy change. However, the poster has not responded to either of my pertinent questions, so it is not clear what he is about.

I guess the poster has asked about free energy change in different cellular environment. So I briefly mentioned about different factors.


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Light intensity effect on plant transpiration
In the graph of light intensity versus rate of transpiration, the rate increases up to a certain point but then remains constant. What is the reason that it stays constant, is there a limiting factor such as water?

Can you add the graph you refer to to your post and add more backgrounds and a link to the source of your information?


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scientific reasons behind a a sudden yet temporary growth sprout of the plant when the soil has No depth?
Sorry, I'm kind of naive when it comes to plant biology.

Mark 4:5-6( New American Standard Bible 1995 )
5 Other seed fell on the rocky ground where it did not have much soil;
and immediately it sprang up because it had No depth of soil. 6 And
after the sun had risen, it was scorched; and because it had no root,
it withered away.

When someone plants in soil with No depth then will the plant immediately spring up( i.e. a sudden yet temporary growth sprout)?  If yes, could someone please explain the scientific reasons behind a a sudden yet temporary growth sprout of the plant when the soil has No depth?

Welcome to Biology.SE. I’m voting to close this question because it is both unclear/unfocused (among other things the type of plant and the environmental conditions will matter) and not well motivated (religious texts are not a good source for biological information). If you wish to ask questions here  please take the [tour] and consult the [help] starting with [ask] for details of what is expected.

Normally a seed would germinate (start to grow) when there is enough damp and warmth beneath the surface of the soil, and the shoot would push upwards at the same time as the root pushes downwards. The root then would be in the moist soil, able to suck-up water when the young plant needs it.
But because there is no depth to the soil, the roots grow and are unable to penetrate the soil and go down, instead they push the body of the seed upwards:

Cress seeds grown on tissue. Copyright unknown, groseeds.co.uk (commercial) 2022 fair usage.
The roots and shoots will then dry out.
You can try this at home with cress grown on moist tissue paper.


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Why does the insulin taken from pig when injected into humans causes allergy but not the insulin taken from bacteria?
At earlier times, insulin was injected to human patients that were taken from pigs and horses. But that caused allergy it seems.
But why is the insulin produced by the recombinant bacteria not causing such types of allergy?

Some more info here https://www.nature.com/nrd/journal/v15/n6/full/nrd.2015.36.html (fig 1 show the amino acid diffrences between human and porcine insuline)

Proteins and peptides vary across species, even if we give them the same name. Some are very homologous among even distantly related organisms, others differ even within a genus. Of course there are also variations across individuals of the same species.
Insulin from pigs and horses is pig or horse insulin. It differs slightly from human insulin because the genes that encode insulin in pigs and horses are slightly different than the genes that encode insulin in humans.
We inserted the genes responsible for producing insulin in humans into bacteria, so the insulin produced by recombinant bacteria is actually human insulin. That's why it doesn't produce an immune response.
There is also the issue of isolation and purification, and it is easier to produce very pure insulin free of other contaminants from recombinant sources than from animal sources.
That's the idea, anyways. Many humans tolerate porcine insulin just fine, and it isn't necessarily clear that human insulin is actually better (for example, this study).

To the OP: Note that the insulin from bacteria is not something the bacteria produces naturally. We have hijacked their protein synthesis macinery via genetic manipulation and specifically tricked it into making human insulin rather than whatever toxin / secretion they were making before.

@Arthur Indeed, this is what is meant by "recombinant bacteria" and that's why it's human insulin.


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Does brain size matters for the intelligence of an organism?
It was shown in a local TV show that larger the brain, larger the intelligence of that organism.
Does that mean if more number of neurons present in the brain canit helps in improving the intelligence of that organism?

does this answers your question?


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How do tall trees transport water at night?
I was studying transportation in plants and I came across two ways in which plants transport water.
The first one is root pressure. In this method, epiblema cells of root hairs actively absorb minerals from the soil. This creates a concentration gradient of water inside the roots and outside the roots and hence leading to a formation of a column of water. But this method can only be used to transport water for short heights.
In tall trees, the method of transpiration is seen. The evaporation of water molecules from the aerial parts of a plant leads to a phenomenon like a suction pull therefore transporting water.
But in the night, the stomata are closed which means that transpiration can't take place. And root pressure also cannot satisfy the needs of the tree because it is a tall tree.
Then how tall trees transport water in night?

Welcome Xavier, were expected to show our researches here on biology. Please take the [tour] and refer to the [help] for info as to how we work. Why would the stomata being open during the day enable water to reach heights above that possible by that created by the osmotic gradient at the roots? Ie. what do the stomata have to do with it? Perhaps researching capillary action might give you an idea about what it is you want to ask, then you can [edit] to clarify a bit.


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Hypothalamus and posterior pituitary gland in ADH production
Concerning the role of hypothalamus and the posterior pituitary gland in osmoregulation and especially when water potential of the blood is low,
When the osmoreceptors in the hypothalamus detect the low water potential of the blood, they lose water by osmosis and shrink, my question is:
NUMBER 1 》does this shrinkage stimulates the syntheisis of the ADH in the neurosecretory cells in hypothalamus first and then ADH is sent along the axons where they terminate in the posterior pituitary gland secondly and released into the blood stream thirdly (just non stop) , OR
NUMBER 2 》 before the shrinkage happens, already ADH was synthesized in the neurosecretory cells and was sent along the axons where they terminate in the posterior pituitary and ADH was stored there in the axon terminals and whenever the neuroscretory cells shrink, impulses are sent along the axons stimulating the release of ADH from the posterior pituitary gland into the blood stream?
Because I have read both explanations from different resources and I am confused which is the correct physiology mechanism that releases ADH from posterior pituitary gland.

Your second hypothesis is correct.
Hypothalamus secretes vasopressin (ADH), transports it along the axons and stores it in the posterior pituitary, thereby when hypothalamus senses the stimuli(osmotic potential or H+ levels or some other indicators) it generates nerve impulse and sends along the posterior pituitary to release that stored ADH.
Comparison of Both Cases
To get insight into the answer lets consider both hypothesis one by one and compare them on the basis of speed of action, in the first case as you mentioned if hypothalamus starts to transport ADH on stimuli this will lead to slow effect (and a comparatively long time / lag to show effect) also once if hypothalamus feels it needs to secrete more ADH since it wasn't enough to meet the requirements it will take even longer time which could be a disadvantage to the mechanism overall. Whereas in second hypothesis these limitations are take care of - hypothalamus transports it to Posterior pituitary from where it can deploy the effect quicker than earlier situation, also it can store some extra ADH in it's own once it has bulked the posterior pituitary's potential which is useful as a secondary backup.
Supporting Citation:https://pubmed.ncbi.nlm.nih.gov/2046874/

Please note that speculation is not welcome on this site, particularly on subjects for which research is available — consequently your answer is much more likely to receive a favorable response if you edit it to include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion and thus is inappropriate for this site. ——— Please take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site and then [edit] your answer accordingly.

That speculation was from the mind which is well learnt to speculate upon that. Also it is not possible to provide for the citations in every kind of question which can be well defined with some dogma. Thanks for the concern.


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What is the name of this fruit?
I have attached a photo. I know the Nepali name for this fruit but not its common name in English and its scientific names. In Nepal we call it as 'lahare Aanp' (meaning Climber Mango). This fruit is a climber type like cucumber.
Does anybody know its common name in English and its scientific name?

Note that you can easily find the answer by using Google's image search feature. It returns a partially completed version of this drawing, https://scontent-lga3-1.cdninstagram.com/t51.2885-15/s640x640/sh0.08/e35/20837253_1095238210612152_3434464044126306304_n.jpg , which is labeled "Coloured Pencil Passionfruit wip".


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mRNA bonding to itself
Does a mRNA molecule bond to itself? I heard that only tRNAs have hydrogen bonds that let them have second structures, but after searching the web i found multiple answers. If yes, does anybody have a credible reference for that?(books, articles etc.)

Welcome to SE Biology. Please quote the source of the extra-ordinary and incorrect statement you quote. This will better allow us to help you. Often students misunderstand the subtlties of a statement and misquote — carefully writing out the quote often makes this obvious or allows us to explain the misunderstanding.

It is very common!
Let's have a look at a few examples.

In bacteria, a lot of the genetic expression is regulated at the mRNA level. Certain mRNAs can form complex secondary structure that prevent or allow translation, and can switch from one structure to another based on the presence or absence of a signal molecule. These structures are called riboswitches; a very well-described example is the riboswitch regulating the expression of genes responsible for the biosynthesis of tryptophan.
For more details see this short article or this one.
Some mRNAs include internal ribosome entry sites (IRES), usually just upstream of coding sequences in mRNAs that code for several distinct proteins (polycistronic RNAs). IRES are highly structured RNA structures recognized by ribosomes that allow translation to start at a point in the middle of the mRNA. They are very widespread, especially in viral genomes. You can find a detailed explanation in the case of viral genes here:
In eukaryotes, mRNA molecules undergo a maturation process called RNA splicing that results in the excision of unnecessary internal sequences. During splicing, the mRNA forms a loop and a covalent bond is created at the future junction point; this bond is very transient but absolutely necessary for mRNA maturation and correct gene expression. See here for more explanations.
What about engineered RNA molecules? Self-hybridization of mRNAs is very useful in biological engineering. People reprogram riboswitches and IRES, but also use very useful tools based on mRNA self-binding. For example: based on a similar principle as the riboswitches, the transcription starting site can be masked by articificially introducing a (fairly simple) secondary structure called toehold switch that hides the ribosome binding site; however when a competing RNA sequence (which nature is specified by the sequence of the toehold) is present it opens and binds a part of the toehold, thereby making the ribosome binding site available for gene expression. This website shows an explanation and a real-life application of toehold switches for diagnostics.

These are only a few examples of mRNA self-binding processes; all of these have been extensively studied and are well described in many articles and books. There are many others types of self-hybridization in mRNA, and in pretty much all other types of RNAs too!


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Do green algae form obligate symbioses with fungi?
I understand that obligate symbioses means that the two organisms cannot live without each other and are in a symbiotic relationship, but do green algae from this with fungi?

Yes, Lichen are composite organisms of green algae (or cyanobacteria) living togther with fungi.
In most cases the fungi-part is completely dependent on that symbioses and is completely dependent on the symbiosis. For the algae it seems that some species can survive on their own, but not necessarily in the same enviroment as the lichen, while other species may again be completely depedent on the symbiosis (see also the comments).

The wiki page you quoted states "The photosynthetic partner [so the algae] can exist in nature independently of the fungal partner, but not vice versa." That contradicts your answer, don't you agree?

@RHA, this quote does indeed contradict my takeaway from the part/quote is was focusing on: "Although some photosynthetic partners in a lichen can survive outside the lichen, the lichen symbiotic association extends the ecological range of both partners, whereby most descriptions of lichen associations describe them as symbiotic". I guess for the algae/cyanobacteria it really depends on the exact species and environment whether they'd be able to survive on their own.

It seems that way, but it might also be unknown. Maybe add some doubt to your answer?

@RHA I (hopefully) clarified it a bit


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Gene cluster of interest not being amplified in PCR
In a lab, I currently have a sample of Rhizobium sp. NT-26. This bacteria is a chemolithoautotrophic arsenite-oxidizer, and I want to clone the arsenite oxidase genes into another bacteria strain in hopes of expression of those genes and learning more about arsenite oxidation and resistance. My first step of this experiment was to purify the plasmid DNA of a colony of NT-26 that I grew on a TSA plate. For this, I used the Omega Bio-teK E.Z.N.A plasmid mini kit I. After using the kit, I was left with 40 microliters of plasmid DNA solution. Afterwards, I wanted to amplify the genes of interest through PCR. The sequence of this gene cluster is listed on NCBI Nucleotide right here: https://www.ncbi.nlm.nih.gov/nuccore/AY345225. My main challenges for this project are designing the right primers for correct amplification, and the fact that this sequence is 9 kilobases, so I would need a high-fidelity taq polymerase blend. The main problem that I will focus on is the design of the primers.
For one, I knew that I would be cloning this gene cluster into a plasmid expression vector for electroporation into a strain of E. coli. Because of this, I decided that I wanted to design my primers with restriction sites already attached. Long story short, I attempted PCR a total of 17 times, and I have not found the correct length of sequence in electrophoresis. I have tried PCR with many variations in the program and various other changes, and I have come to conclude that there is something wrong with my primers. I would like to go over the details of the project, and maybe I can receive a hint as to what I have done wrong.
The gene sequence that I am wanting to amplify consists of 6 total genes. The first four genes are aroB, aroA, cytC, and moeA1 (Santini et al. 2010). These genes are in one gene cluster. The other two genes are upstream, and they are AroS and aroR. These two gene clusters compose a two-component signal transduction system that encode for the autotrophic oxidation of arsenite. In her original publication, Dr. Joanne Santini added the link to the sequence of all 6 genes on NCBI Nucleotide. I have listed the link in the above paragraph. I went on Addgene's Genome Compiler and found the exact sequence from NCBI, and I have pasted a screenshot of that below. For some reason, the actual genes I am interested in amplifying do not start at the beginning of the sequence on NCBI. Instead, the first gene, aroS, starts at 424th nucleotide. From nucleotides 1-423, the Genome Compiler listed that as "unknown". For that reason, I decided to get rid of those nucleotides, and just amplify the rest of this. The same thing happened at the end of the sequence, where the last gene, moeA1, stopped at nucleotide 8,263. From then on, the Genome Compiler listed the rest as "unknown". I decided not to deal with the unknown regions, and just amplify the genes i am interested in.

The first gene of this sequence, aroS, starts with ATGAGCCTTCTCGAGC. I know that for designing primers, the forward primer should match the sequence of the beginning of the gene of interest. For this reason, the forward primer contained ATGAGCCTTCTCGAGC. Since I was cloning it into a vector, pBAD30 (the map is listed here https://www.addgene.org/vector-database/1847/), I wanted to add a restrction site to the forward primer. I found that kpnI would work for my sequence. The sequence of kpnI is "GGTACC", so I added it to my forward primer. The primer so far is typed like this: GGTACCATGAGCCTTCTCGAGC. I also learned that a sitting sequence should be added to the beginning of the primer, so I arbitrarily added four letters to the beggining "GTAT". After all three of these additions, my finalized forward primer is GTATGGTACCATGAGCCTTCTCGAGC.
Designing the reverse primer is where I am not completely sure on the correctness of my design. The last 18 bases for the last gene, moeA1, are GAACCGTTCGCAATGTGA. I knew that the reverse primer should be a reverse compliment, so I found the reverse compliment to be TCACATTGCGAACGGTTC. As for my restriction site, I decided to use xmaI. The sequence for xmaI is "CCCGGG", so I added that sequence onto my reverse primer. The sequence so far is CCCGGGTCACATTGCGAACGGTTC. Just like the last one, I added the bases "GATA" as a sitting sequence. The final reverse primer sequence is "GATACCCGGGTCACATTGCGAACGGTTC".
After I designed both primers, I pasted those sequences into Integrated DNA Technologies and ordered primers in solution (100 mM with IDTE). For a PCR kit, I used the Expand Long Range dNTPack from Millipore-Sigma. This PCR kit included enzymes, nucleotides, and all buffers needed for PCR.
After the primers were delivered, I set up a few mastermixes for PCR. I followed the manufacturer instruction for setting up the mastermixes and the program (https://www.sigmaaldrich.com/content/dam/sigma-aldrich/docs/Roche/Bulletin/1/elongnrobul.pdf). The melting point of my forward primer was 60.5°C, and the melting point of my reverse primer was 64.4°C. Because of this, I chose an annealing temperature of 57.5°C. I am slightly worried about the difference in melting temperature and the effect it could have on annealing, and I realize now that I could have adjusted the GC-content of both of the primers to generate closer melting temperatures. However, I do not think that is causing the lack of amplification. One concern that I have about my mastermixes is that I do not know the concentration of DNA in the purified plasmid solution. Each matermix should have up to 500 ng of DNA, but I have used 1-8 uL of DNA solution in each mastermix. Could there be a possibility of too much DNA? Too little? I have tried many different variations, and none have worked. For the most part, each mastermix has used 3 uL of the given DMSO.
On my 17th run of PCR, I did receive some sort of result. As I mentioned before, I did not mess with the unknown regions of DNA, so our final sequence of the 6 genes should be about 7.8 kilobases long. After PCR, I ran it under a gel, and this is what I saw:

In the third lane, the bands of DNA were the brightest. Suprisingly enough, for the third lane, I added a colony of our bacteria to the mastermix for the DNA source, and a band was produced. Most of the lanes show a band of DNA, but the bands are not quite at the 7.8 kb region, so I'm thinking that it is not our desired product. Could this possibly be our product, but impurities slowed the travel of DNA? If so, I would like to know if I should continue with restriction digestion of the insert and pBAD30, and then ligation.

A few things to consider:
Template:

Are you sure the template you want is on a plasmid, and not in the Rhizobium genomic DNA? (In which case it would not be present in DNA purified with a plasmid miniprep kit - you would need to do some kind of genomic DNA prep instead.)
Have you measured the concentration of your template DNA? I typically put ~2-10 ng of template DNA in a 50 ul PCR reaction. If you are adding undiluted DNA there's a chance it could be way too much template, which can adversely affect amplification.
What is your template dissolved/eluted in? Tris or water should be fine - if there is any EDTA in it (such as in TE buffer), it will interfere with PCR.

Primers:

Your primers look good, except that I would recommend using a longer "sitting sequence" - 5-6 nt.
I would not worry about the melting temps. I always use 55°C for annealing, except in rare cases where there appears to be erroneous/nonspecific annealing.
Do you dilute your primers to 10 mM working stocks? Is "IDTE" a buffer containing EDTA? That would likely interfere with the PCR, even if you dilute it 10-fold in water. I recommend ordering oligos dry, dissolving them to 100 mM in sterile water, then diluting 10-fold to 10 mM, also in water, for your working stocks.
One thing you might consider is amplifying first without any restriction sites on the primers, then cloning the PCR product into a blunt vector or TOPO vector, then PCR'ing from that with your primers with restriction sites. This can sometimes help with tricky PCRs, or when amplifying from complicated templates like genomic DNA or a cDNA library.

Polymerase / PCR cycle

It is advisable to try a couple different polymerases. I have had good results with long products using KOD polymerase.
I also recommend trying several different magnesium concentrations, as well as trying with and without DMSO.

As for the "wrong"-size product - if you have enough of it, you could go ahead with the cloning, in which case you'll find out soon enough if it's the wrong thing. You can also check it's identity by doing some diagnostic restriction digests, or directly sequencing the PCR product with a couple internal primers.

One of the reasons why region may not be amplified via PCR is that the region is much larger than is thought. This may happen if there is a repeat of variable length in the region that may be difficult to sequence precisely, or have a different length in your sample than is shown inside NCBI database.
In the case we hit it was Homo sapiens. I am not sure about Rhizobium but who knows? Repeats seem not uncommon, see here.


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Measuring transgenic gene expression with a microplate reader
I have been working on genetically engineering an E. coli strain to autotrophically oxidize arsenite into arsenate for bioremediation of arsenic contamination in groundwater. For my research, I have been finding ways to quantitatively measure how much arsenite the bacteria oxidizes over time.
After researching ways to quantitatively measure arsenite being oxidized, I have concluded to use the method of Johnson and Pilson (https://www.sciencedirect.com/science/article/pii/S0003267072800059?via%3Dihub).
The arsenate that is formed from arsenite oxidation forms a molybdenum-blue complex with phosphate in the water. As the concentration of arsenate increases, the absorbance value of the water should increase proportionally.
Here was my plan: First, after growing my transgenic bacteria on an amp-plate, I would pipette out various concentrations of cells and arsenite in wells of a 96-well spot plate. I currently plan to use the Fisher Scientific Multiskan FC microplate photometer. I planned on incubating the cells while shaking at 37 C. The main problem I have come across is that my experiment would not be controlled. Over time, the growth of cells will change the absorbance value, not just the molybdenum-blue complex. I need to isolate the variable of just arsenite oxidation.
I have thought of a few possible solutions, but I feel as if I may be missing something crucial. When learning about microplate readers, I know that researchers can use them to measure gene expression. How do these researchers eliminate the variable of cell growth effects on absorbance values?
For one, I have thought of finding a way to filter the cells to one side of the well where they will not affect the absorbance values. Would it be possible for me to cut out a dialysis bag to where it is dipping into the well? In that case, the cells could be suspended in the well, oxidizing arsenite (if my hypothesis is correct).
Anyway, I really want to find a simple method for quantitatively measuring arsenite concentrations over time using a microplate reader without having cell growth affecting absorbance values.

Spectophotometry
Does the photometer allow using different wavelengths of light? Perhaps using a spectrophotometer might give you a control and your desired value, i.e. blue light may be absorbed by your sample, but red might not? The absorbance spectrum of the molybdenum-blue complex is very specific and you could use this to your advantage using spectral photometry.
Photometry + correcting for absorbance due to cell growth
Another approach is to quantify over time how your bacteria affect absorbance as a function of time and then subtract this from your experimental values.  For example, in a wellplate, place the following adjacently: use a (i) well without cells, and only arsenite in solution, (ii) cells without arsenite, and (iii) cells with arsenite. This should allow you to quantify quite accurately how much the arsenite, the cells, and how much both affect absorbance.
Of course as you say there may be an interaction between the cells and the arsenite slowing or speeding up cell growth, so that would be a pickle to disentangle. You could try, perhaps in the wellplates (this would be best!), to find out what effect arsenite has on growth and correct your final data this way.
Periodically sampling the solution; removing bacteria from the measurement
Another idea would be to culture your cells in arsenite, and take samples to obtain time-points. For each sample, you filter using small syringe filters (these are cheap and are typically used for sterilizing solutions, i.e. getting rid of bacteria but keeping the solution, given their pore size of ~.1 microns) and then perform photometry for the molybdenum-blue complex. This is typical practice in microbiology.
PCR? An idea.
Last but not least, it's good to remember this is an indirect readout of transgenic gene expression. Similarly, you could use quantitative PCR to quantify the expression of any transgenes - here, you use housekeeping genes as controls for cell number, and the mRNA expression of your transgene as the readout. You would be reading out the expression of mRNA, but I personally don't think it would be more 'indirect' than measuring arsenate concentrations in solution, especially when there are confounding factors and awkwardness in getting a clean measurement. The PCR approach would be quite accurate and likely more reliable.
These are just some initial thoughts - perhaps you could add a comment or we could chat about this if you think it could spark up some concrete ideas!

Thanks for the advice! I will be collecting data hopefully over a 3 hour course. For the amount of time I have to complete experimentation, I might go with the periodic sampling method that you mentioned. I could try to grow multiple culture tubes on a shaker, and at 10 minute intervals filter out the solutions into the wells (containing LB, amp, sodium arsenite, and potassium phosphate dibasic). Also, I would create several stock solutions with known concentrations of arsenate and arsenite while accounting for absorbance values of LB and amp. I could just calculate all needed concentrations.

Also, I dont have any arsenate on hand to make a stock solution; I just have arsenite. I know if I have stock solutions, I can calculate the amount of arsenate based on absorbance, but would it be scientifically "acceptable" to have my measurements in absorbance instead of concentration?

Depends on what you are trying to demonstrate. If it is not feasible to measure arsenate concentration, you can use absorbance as a relative unit! Twice as absorbant doesn't mean you have twice the concentration, but you can compare different bacterial strains; you'll know which one oxidizes arsenite more. Very often in biology (and science generally) we don't have absolute measurements; we can only compare to a control, for instance. PS. It's good to check whether arsenite oxidizes by itself over time (it might not, I have no idea) - you'll have to correct for this if you want solid data.


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Using expression vector to express arsenite oxidase genes in E. coli
So I am trying to express a gene cluster that can oxidize arsenite into arsenite autotrophically. The arsenite oxidase gene cluster sequence is linked here: https://www.ncbi.nlm.nih.gov/nuccore/AY345225.3
I originally was going to clone this gene into the pBAD-DEST49 expression vector, and transform it into E. coli C600, but the vector is out of stock, and I need it quickly. I was looking through Sigma Aldrich, and I found this vector: PSF-OXB20. I plan to clone the genes into this vector.
I do, however, need some advice. I am not 100% sure on if this vector would work, or if the genes would be overexpressed. My question is would this vector work out, or is there any better ones out there. Any advice would be appreciated, and if I need to include more details, just let me know.


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Humans are Apes are Primates. But will they remain so?
Not a biologist here as you will propably be able to tell.
I understand that throughout the tree of life each species at the leaves at the same time also belongs to all the parent categories up the tree. So humans are apes and also are primates. The most frequent use of that fact in everyday discussion is in reply to the question "if humans evolved from apes, why are there still apes?". I also get why that question is silly.
I wonder, however, how biology would treat future evolution.
Assume that 10 million years from now our descendants are still around and have developed some trait that conflicts with the current distinction defining the branching of the taxonomic tree. Let them for instance grow some sort of tail again. Possibly to keep their hands free while still clutching some mobile device (I believe taillessness is one of the characteristics differentiating apes from other primates, if I am wrong about that please just substitute any trait that is).
Also assume that todays' other primates and apes are still around in that future.
Would we still say "homo futurensis are apes", even though they have tails?
Or would future taxonomists rearrange the tree and restate the distinctions? If so would that imply that looking back from that future to today us currently tailless humans would also not be apes after all but on a different branch together with h.futurensis? Is there a time-dimension to the layout of the tree of life? I don't mean corrections as we learn more. But changes due to evolution taking its course. The appearance of a new species forcing a remap.
Or would we just keep the tree and drop the tail-thing from the list of characteristics because there are enough other things that define the commonality? If so we could imagine even further evolution changing those traits too. What then?
Or does the new tail not pose a conflict in the first place because it would be something new. "Tail" being a naive name and the new appendage propably being called something else?
Or is the question plain silly, if so please explain why.
Thank you.

Very simple question that is at the root of systematics/phylogenetics. I think I offer a complete answer: when considering whether a species is considered part of something, it is very crucial to understand (and dependent on) whether the term that uses to group things ("Primates" "apes" "animals", "eukaryotes", etc.) is mono-, para- or polyphyletic. See here.

I'll give you a rudimentary example to explain. Let's say we make a term called 'multi-hearters' and we use it to group animals with more than one heart. This term would be polyphyletic. You'd group squids and roundworms with this approach, though they are not closely related in phylogeny. Whichever way you choose to use the terms ape, primate, simian or human, you have to be clear about what you mean. If "ape" is to be used monophyletically, then any descendants of humans will be apes, by definition. Any descendant of any ape will always be an ape since they are part of "ape" monophyly.

@S Pr: Though that definition runs into the obvious problem that it makes all land vertebrates into fish.  Any descendant of any fish will always be a fish since they are part of "fish" monophyly, no?

@jamesqf Yes, as is currently thought. Under our current system Cyclostomata would be the common ancestor I think. These would be the bony jawless fishes, similar to lamprey now.

Traits that are lost and then redeveloped are called atavisms and can be gained and lost several times in a evolutionary history. I suspect you need to learn about parsimony and why it's not necessarily the true course of evolution.

@bob1: Are you familiar with the logical principle of reductio ad absurdum?  https://en.wikipedia.org/wiki/Reductio_ad_absurdum

@jamesqf - yes I am. But your example isn't RAA in my opinion because land animals are part of the group descended from fishes, though the conclusion may seem absurd becuase most people (myself included) think of fish as scaly, water etc.

@jamesqf Oops I'm sorry, well spotted. Here's a small amendment to my second comment for OP to understand more clearly: I meant that if "apes" is to be used as a monophyletic designation, then all future descendants from any ape will be apes. One day we may of course designate "ape" as a paraphyletic group. Fish are a great example of a paraphyletic group. What I want to confer/re-state is that it doesn't matter what word you use, you have to understand that the word has to be defined with an explicit category in mind. One must know the categories. That is the crux of the answer IMO :)

Yes, humans will remain members of apes and primates.
The terms "ape" and "primate" are common names representing certain phylogenetic clades. A clade is a group where all members are eachothers' closest relatives compared to members outside the group. Another way to put it is that a clade exists if there is a common ancestor whose descendants include all and only members of that group.
All of today's apes share a common ancestor to the exclusion of all non-apes. The descendants of today's apes will also share that ancestor*, and so will still be within the ape clade. The terms "ape" and "primate" are best thought of as expressions of relationships rather than clusters of traits.
Could humans evolve something very non-ape-like? For argument let's say humans evolved a tail. I suppose colloquially it could become common for people to use the term "ape" to refer only to the tailless apes, but anyone speaking of evolutionary relationships could still use it to refer to all the descendants of today's apes. Then it would just be a matter of clarifying which meaning is intended. Since "ape" is a common name, it might get used more flexibly, but the scientific term for apes, Hominoidea, certainly wouldn't change.
If humans evolved a tail they wouldn't cease to be apes, because "ape" isn't defined as "primates without tails," it really means "all the descendants of [this one ancestor]," which we generally recognize by their lack of tails.
The term "fish" is a similar example. If one calls a shark, a salmon, and a coelacanth all fish, then really humans should be included as well. Otherwise, "fish" stops being a biological term and just means something like "aquatic vertebrates that have gills**."
I'll finally add that it's fairly common for a lost trait to re-evolve, or for a new trait evolved in an ancestor to be missing from some descendants. Often, some additional observation will show that the re-evolved trait is actually different from the lost trait (think, for example of salmon fins vs. whale fins), but not necessarily. This can make it more difficult to accurately reconstruct relationships, but doesn't exclude those organisms from their clade.

*This is ignoring the possibility of hybridization, which is extrememly unlikely for ape/non-ape, but can be common in other groups.
**Mostly


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Question on Viruses

A recent study has provided evidence that two types of equine (horse) herpes viruses have an unusually broad host range. This fact supports which of the following statements?
a. The lytic cylce occurs in horses while the lysogenic cycle occurs only in other species.
b. The virus is transmitted from one host to another by mosquitoes.
c. In a population of horses, many of the individuals will become infected
d. Horses, rhinoceroses, and polar bear can become infected
e. In an individual horse, many different type of cells will be infected

According to the answer key, the answer is D. My question is why isn't E also a correct answer? I thought host range means "the range of cells that can act as a host to a virus".

A host is an organism, not a cell of an organism.

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I think this is a good question because it highlights a critical pitfall in any field of science: making broad assumptions with too little or poor data. It also in part highlights poor test questions/mentoring that lead people into these pitfalls. See in my comments on Yordan's answer.

"host" refers to the organism as a whole. So two types of equine herpes viruses have an unusually broad host range means here that these two viruses have the particular ability to infect various animals, and not only horses.

And yet that statement still doesn't support any of the possible answers. Is that a fussy assumption?

@CMosychuk My guess is that the question is badely put. It should have been more like 'Based on this fact, which of the following statements can be considered as true?'. Then d. is the correct answer because the fact that these viruses have a broad host range is enough to explain why polar bear and rhinos can also be infected. However, it is kind of a circular reasoning.

The correct answer is D and there is nothing wrong with the question. @user34748, the very definition of host range is the range of species a virus can infect, not cell types. See the Wikipedia definition of host as used in biology: In biology, a host is an organism that harbors a parasitic, a mutual, or a commensal symbiont, typically providing nourishment and shelter.  This is why the answer is D, not E. If the question specified host cell types, then E would have been the correct answer.
The problem is that you are supposed to know the definition before you go to exam and host has very clear definition in parasitology in general as the organism the infectious  organism infects, not its cell types! In fact if the answer was to be E the very structure of the question had to be changed to include a special close specifying it is host cell types, not the hosts themselves the question is about. And this is clearly not the case here. This is why the answer is D, not E. Even from a testological point of view there is nothing wrong with the question. The methodology used to compose it is within the limits of what you are expected to know and the reasoning you are expected to be able to use. It's legitimate virology question.

As I understand it, the correct answer is that multiple species (polar bear, rhino, horse) can get infected because these viruses have a broad host range. But I guess that the very definition of having a broad host range is being able to infect various hosts. So, in the end the reason why d. is correct is that d. is correct...

No, the reason why D is correct is because you definition you should have known before entering this exam is " In biology, a host is an organism that harbors a parasitic, a mutual, or a commensal symbiont, typically providing nourishment and shelter." If you knew this definition, you should not have had any problems choosing D as answer. See definitions are important in biology, if you don't pay enough attention to them you can easily make mistakes later on in both interpreting and even noticing important tendencies in your data. You should have paid attention to the definition of host!

Basically the entire question revolves around knowing or not what the definition of host is in virology. If you have considered that host is always an organism and not just a single cell you would never had failed the question and ask it here. I advise you the next time you go take a test-learn your definitions better. Hope you make good lesson out of this experience.

Well, I did not fail the question, because I did not take the exam. I'm not the OP, I'm just confused by the way the question is asked. And for that matter, I am well aware that definitions are important in biology, as in every other field of science.

On Northwestern University's website in states that the definition of a host range is, "The range of cells that can act as a host to a virus or bacteriophage." So according to what you are saying, this definition is wrong? http://groups.molbiosci.northwestern.edu/holmgren/Glossary/Definitions/Def-H/host_range.html

I'm very sorry @Flo for taking you for the OP instead of the editor, I just didn't see it. Sorry again. Now I looked at the link you provided and this is what is says: 1. The spectrum of strains of bacterial species that a given strain of phage can infect.
2. The range of cells that can act as a host to a virus or bacteriophage.

It isn't "wrong" per se, but just more specific. It is designed specially for bacteriophages, not for host range in general. In the case of bacteriophages the cell is the organism, so one doesn't need to add anything more specific to understand any difference between a cell and an organism. In this case there is no need to specify any cell types. However, the OP's question has a possible answer specifying cell types, therefore, the lecturer should haven't ever used such definition for his/hers course or otherwise this questions would indeed have been wrong to ask.

Then my arguments is: Did the lecturer in the OP's course used the definition you provided or did s/he used the broad definition of a host in parasitology? If s/he indeed used the definition you provided the question was indeed wrong to ask. However, if s/he didn't used this definition, but one similar to the broad parasitological definition, then it's the OP's fault to have failed the question. Do you know what definition the lecturer of the class used or even what was the class about?

Without explicitly demonstrating the virus in a polar bear or rhinoceros, how would the statement "a virus has more than one host species" lead you to assume a polar bear or a rhinoceros can be infected? Why not bobcats or barn owls? That requires more data than this question provides, and here's the actual paper being referenced (1, 2). You can see how they can make that assumption, QED.

@CMosychuk , still the OP should have known the definition of a virus in parasitology and should have thought out the question carefully. If s/he drew on the information provided in the question and what s/he was supposed to know is a host range, s/he wouldn't have made the mistake. There is enough information provided in the question to come to the right answer.


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Trying to find the right plasmid expression vector for e. coli c600
I am very new to the concept of gene cloning and transformation. I am trying transfer the arenite oxidase gene cluster (9kb in length) to E. coli strain C600. I want the E. coli strain to express this gene in order to oxidize arenite for bioremediation of groundwater. I am just realizing how complicated it really is to select the right expression vector. I have not studies this topic at all at school (still in high school); I am just studying this topic on my own. I am worried that my 9kb sequence could be too big for the plasmid vector or the bacterium. I have been trying to find the right plasmid expression vector for days, and it seems like everyone I find isn't quite right.
I have been kind of vague, so here is the whole story: I am in possession of a gram-negative bacteria that can oxidize arsenite into arsenite very efficiently. The gene cluster that is responsible for this is Aro, which is 9 kilobases in length, and I am looking to use a heat shock method to transfer that gene cluster into a specific bacterium (I found that E. coli C600 might be a worthwhile candidate). I have everything I need for the extraction of the DNA and PCR, but I am just trying to find a plasmid expression vector that I can insert into E. coli C600. Originally, I looked at pUC19, but then I found out it is only a cloning vector and not an expression vector. Then I looked at the pET system, but there are so many selections; I cannot seem to find the right one.
Are there any suggestions for what vector I should use or any guidance on how to find one?

You can use an arabinose inducible promoter for expressing the gene(s) of your interest. There are several vectors that have this system. Search for "pBAD" expression system. PET system is generally used for protein purification. You perhaps don't want that level of overexpression. It's difficult to comment which vector would be the best without going into the details of your project. Note that expressing an entire pathway may not be that straightforward. Are the genes in this 9Kb cluster parts of the same operon? If not they will have their individual promoters.


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Highest bite force of a wolf?
Some sites say wolves can bite around 400 psi. But this site claims that when facing a peril they can deliver upto 1200 ?https://plexidors.com/myths-around-dog-bite-force/(skip to the 'How does that measure compared to cousins in the wild?' portion to save time)
  -That's a huge range, and could in theory put them on par with big cats.Is what the site says true?
-I looked online extensively in the internet but I only came across a reddit post where they discuss this and it wasn't conclusive.Why is there a maximum bite force of other animals like crocodiles,gorillas,hyenas etc but not for wolves?

@Specter writes about other units: PSI (pounds per square inch), but I don't know how it counts to N (newton).

The range from mean to maximum of wolve's bite force is huge.

Is it really? According to this Wikipedia page, (Scully, C. (2003). Oxford Handbook of Applied Dental Sciences. p. 151) claims that human masticatory forces range from 70 N to 700 N. Also, (Kim et al., 2018) claims that domestic dogs have a bite force of (147-3417) N, so I don't think it's too implausible for wolves to have the value of (774-2255) N of wolves that @Olga_Swider claims. We see also, on Table 4 on p. 550 of (Eng et al., 2013), the estimated maximum bite force (MBF) spread over the $M^2$ area of the jaw. Eng claims that Gorillas and Chimpanzees have MBFs of 3200 N and 1800 N respectively. I think there's quite a large degree of control of masticatory muscles, which wouldn't make it too surprising that you can have a large range of forces.

This range of wolves' bite forces could put them on par with big cats.

According to p. 621 of (Wroe et al., 2005), lions have a bite force of around 1768 N, while tigers have a bite force of 1525 N. So, it seems that wolves have a significantly smaller mean bite force than big cats. But bear in mind that while dogs and wolves might have a fairly similar jaw size, lions jaws are much larger so their bite force is spread over a much greater area. So exercise caution when comparing them. Similarly, note that PSI is a unit of pressure (force over area), while newtons are a unit of force.

Why isn't there a maximum bite force for wolves?

Says who? Of course there's a maximum. Wolves can't make arbitrarily large forces with their mouths, that's physically impossible.

I did not carry out these tests. I gave the data after literature. In addition, the values given refer to the mean. In another chart, in the second item I cited, it can be read that the "maximum estimated bite force" does not exceed 3000 N.

By the way: I do not think that we can measure the maximum bite strength. You will not get the animal to do it. Only estimation remains.

@Olga I never said you recorded it, I said you claimed it. Also, it's redundant whether the second paper is claiming that "the value is 2255 N" or "the value is estimated as 2255 N"; it's the same effect. There's tonnes of stuff in science that you can't measure directly but have to estimate.

Re "dogs and wolves might have a fairly similar jaw size", that depends on the breed of dog.  A malamute or husky might have a similar jaw size to a wolf, but a Pekinese or an Irish Wolfhound?  Which probably accounts for the wide variation in dog bite force cited.

@Jam - You wrote that you doubt the presented results. I just made it clea,r that it was difficult for me to discuss it, because I did not estimate or measure it. Have a nice day...

In this article (Bite forces and evolutionary adaptation to feeding ecology in Carnivores) they say, that bite forces of wolf (Canis lupus) is 774 N. Literature (Maximum estimated bite force, skull morphology, and primary prey size in North American Carnivores) gives that: "the wolf had a mean maximum
estimated bite force of 2255 N".


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Jellyfish gulf of Thailand
I found may such jellyfishes on the Hua Hin beach in 27.11.2018. They measure around 25 cm.
Since I'm more botanist, I have big problem to identify it. Google doesn't help me a lot (spent 3 hours googling and nothing).
Anyone know latin name?

So in a 3 minute search for blue-rimmed Thai jellyfish...Doesn't look like Rhizostoma pulmo, Aequorea, or Cyanea lamarckii,

However,  others have seen similar specimens to yours: see here, here, and here. I'll sleuth a bit more for you in a little bit....


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Where is ethanol detoxified? peroxisomes or smooth ER? Or both?
I am reading the textbook Biology (Campbell et al, 2005), and I am confused.
In Chapter 6.4, on page 104, it says that "In the smooth ER,  other enzymes help detoxify drugs <...>", and alcohol is mentioned later.
In Chapter 6.5, on page 111, it says "Peroxisomes in the liver detoxify alcohol <...>"
Googling the question also brought me mixed results.
As I understand it, alcohol detoxification happens in two stages, first oxidising ethanol to the also toxic ethanal, and then oxidising ethanal to acetic acid.
Do these processes happen in different organelles? Is that the reason that both of them are mentioned? Or do they both detoxify alcohol completely, but do it in different circumstances?

It seems that there are multiple (oxidative) pathways.
If you look here, there are multiple references showing how ethanol (alcohol) is detoxified.
Alcohol dehydrogenase (ADH) is found in the stomach and starts breaking down ethanol (see first-pass effect, see also the article Gastric alcohol dehydrogenase activity in man: influence of gender, age, alcohol consumption and smoking in a caucasian population). But it is further detoxified elsewhere like the liver cells where the smooth endoplasmic reticulum contains cytochrome P450 2E1 (CYP2E1) and ADH inside the cytosol. The peroxisome also contains catalase which can use peroxide ($H_2O_2$) to oxidize ethanol to acetaldehyde.
This article (Determinants of Alcohol Use and Abuse: Impact of Quantity and Frequency Patterns on Liver Disease) contains a nice figure (2), which shows the pathways which was reproduced here.
Check out this reference also for more details about the pathways.


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What is the 'job' of the byproduct water in the Electron Transport Chain?
I understand what happens in the Electron Transport Cycle, but I fail to understand that after Oxygen has accepted an electron, it forms water, but why? what happens to the water? I can take an educated guess but again its a guess.
Does it then react with ADP?
Thanks in advance! I'm doing an animal welfare course and as part of it I need to study basic biology.

The formation of water in the matrix at the end of the electron transport chain helps to maintain the hydrogen gradient between the intermembrane space and the matrix.

Thanks for your question.
One reason is, if this chemical reaction does not happen so there will be a lot of electrons in mitochondria in a short time consequently the environment inside the mitochondria will be charged in negative and as we know the environment inside the all parts of cells should not change during the time
and on the other hand, these extra electrons may carry out some chemical reactions which result in producing some materials which are not good for cell, for ex H2O2, as we know it is a poisonous material for cell.
But maybe you ask why H2O and not another product? because H2O exists in cell, in a large amount, it is solvent for many materials, it is not poisonous for cell, and many other reasons.

As we know, many other reasons all these things make you look ignorant to the answer. Maybe you ask why $\ce{H_2O}$ and not other product No, as much as I can see, the OP is not asking this in any way.


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This 5X binding buffers where experiment participates in?
I saw 5X bingind buffer maded by;

100mM HEPES, pH 7.6
5mM EDTA
50mM ammonium sulfate
5mM DTT
1% Tween-20
150mM potassium chloride

which reaction helps this buffer? I don't consider to this buffer participates in which experiment by name. Although this buffer have another name but they writes just '5X bonding buffer'..

From what kind of reaction/protocol did you take this description?

I saw that recipie at pre-made buffer selling site. there's no mentioned about buffer usage.

Can you give us the link?

http://www.biosesang.com/bbs/shop/item.php?it_id=B2003 <<here. Application used by 'Applications: Suitable for molecular biology applications.'.

The description says "binding buffer" without specifying. This is pretty standard stuff, containing a buffer (Hepes), some salt and detergents. Nothing too special, but I wouldn't use a "one fits all" buffer.


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Can I ask tip for tissue measuring(especially for RNA preparation)?
I extracted RNA at mouse liver and human blood, but degradation occurs. I think, at mouse liver, too hard to measuring 50mg liver(I am newbie for animal tissue preparation) so spend several minutes. liver is soft but very small, and too hard to keep the weight. (human blood spend time for defreeze, but It degraded, too.)
for example, I want to weight 20mg mouse liver,
1. cut liver by scissors about 10mg after set zero point of scales with ep-tube.
2. cut liver almost 10mg, but it's exceed weight 2~3mg, so I have to cut it 2~3mg.
3. this scale is too small... so I spend for keep the weight for 20mg, like this: 10->23->19->19.3->19.8->21->19.8->20.
I want to ask for advice about how it faster animal tissue measuring and preparation. When preparation genomic DNA, is it OK so DNA is stable than RNA. but, when extract RNA, keep the weight fast and incubate sample at ice for prevent RNA degradation.

I do not have specific experience with liver tissue, but here I would do a couple of things. First, to get around your issues with weighing tissue, set an acceptable range around 20 (say, plus or minus 5mg, so ranging from 15 to 25mg) and then normalize your RNA yield to that starting weight. Second, look into ways to preserve the RNA in your tissue as you're processing it. You could try RNAlater solutions or other chemical means of stopping RNA degradation, or just snap freeze your tissue in liquid nitrogen. Good luck!


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Why does vasodilation increase blood flow in the capillaries, but decrease it in the chest during inspiration?
From Guyton and Hall Textbook of Medical Physiology:

Every time a person inspires, the pressure in the thoracic cavity becomes more negative than usual, causing the blood vessels in the chest to expand. This reduces the quantity of blood returning to the left side of the heart and thereby momentarily decreases the cardiac output and arterial pressure.

Why does vasodilation increase blood flow in the capillaries, but decrease it here?
As I understand it, vasodilation results in decreased resistance. According to Ohm's law, decreased resistance should increase blood flow.

The passage isn't talking about a magical diameter increase in a physics problem. If negative outside pressure causes blood vessels to increase in diameter, something has to fill the vacated space inside: blood.
That means that some of the blood that would be flowing through the vessels into the heart is instead filling the extra space in the vessels themselves.
You could most directly model this in terms of analogy to electricity by thinking about the vessel walls as a capacitor, and it takes some time to charge that capacitor when the outside pressure is released. If you measure flow at the input, you'll see a higher flow because a good portion is charging the capacitor/filling the vessels, but if you measure flow at the output you'll find a reduction.
I'm not strongly familiar with the effect described in Guyton and Hall but I'm guessing that the "momentarily" word in there is doing a lot of work, as this effect is going to be brief relative to the respiratory cycle.

...if you measure flow at the output you'll find a reduction. This doesn't seem to happen in the capillaries (any capillaries, not necessarily in the chest) during vasodilation. Why?

@athlonusm It would momentarily if arterioles suddenly expanded. Once they are expanded and "full", though, there's nowhere to go but through. I don't know that it's possible for arterioles to expand via vasodilation as rapidly as you get in the chest from inspiration, though.


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Recommendations for good books on bacterial genetics & molecular biology?
I'm starting a new phase of my PhD soon, and am feeling very under-prepared with respect to my general bacteriology knowledge. I was recommended to read up on basic bacterial genetics and molecular biology.
All the textbooks which I am familiar with from my past (Molecular Biology of the Cell etc,) rarely go in depth on the bacteria side of things. I really want a text which focusses solely on bacteria, and nothing else - this seems relatively hard to find recommendations for. I have Googled and found a few, but it would be nice to hear some first hand accounts on what books people recommend.

Why not start with a microbiology text? They tend to be very strong on those subjects, by my fuzzy recollection.

@MaximilianPress thank you. Do you have any favourites?

Afraid I'm quite out of date on these texts. You can find some material online via searches (e.g. https://bio.libretexts.org/Bookshelves/Microbiology/Book%3A_Microbiology_(Boundless)/7%3A_Microbial_Genetics), possibly some combo of "microbiology", "microbial genetics", "bacterial genetics" etc. will get you there.


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PBS or TBS, where cannot use each buffers?
As you know, Tris buffered saline and Phosphate buffered saline is multipurpose. For finding each buffer's use, there's so many use experiment for PBS and TBS. TBS uses for western blotting, and PBS uses for cell culture.
but some experiment never use PBS and some experiment never use TBS, I want to ask this situation which when you use TBE but never use PBS, and the opposite situation(use TBS but never use PBS), For example, When you western-blotting with alkaline phosphatase never use PBS and PBS-T. this case, phosphate inhibits AP, and amine-coupling with NHS-EDC, never use Tris buffer because it have primary amine.

I think you answered your own question.
The buffer used in a given experiment depends on the requirements and limitations of the experiment itself. You just have to look at the properties of the buffer, and if it is relevant to your experiment.
You just gave two great examples... are you just looking for more examples of experiments when one would not use phosphate buffer vs Tris buffer?
PBS is supposed to closely mimic/represent the osmolarity of a cell, and buffer from pH = 7.0 to 9.0. Tris also buffers around neutral pH. It is pretty cheap, but as you've stated, has primary amine groups that are nucleophilic and thus interfere with certain experiments like disuccinimidyl suberate crosslinking, etc.


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Speed of evolution
I know that evolution can happen quite rapidly in single celled organisms. How about animals? Has there been any record of new speciations over the past 1000 years? In this video it is claimed that Darwin's finches arrived at Galápagos Islands just a few hundred years ago.

Wrong about the finches.

How do you know?

Depending on just how you define "species", it can happen in about 40 years for finches on the Galapagos: http://www.bbc.com/news/science-environment-42103058

Evolution ≠ speciation. So, it is unclear which one you are interested in!  I am voting to close.

The video is a simplification of the speciation concept in order to convey principles of evolution using Darwin's finches as an example.  Very rapid speciation (obvious speciation in 1000 years or less) for animals with much longer lifespans, is probably not documented.  However, much of a potential answer to your question depends on how you define "speciations". Species is a very fluid term. When speciation is defined as major genetic changes resulting in obvious differences that distinguish two different populations, it is easier to say "yes" it can occur in shorter periods of time. For those differences to accumulate and increase to the point where animal phenotypes and genetic differences make reproduction (genetic exchange) completely impossible probably takes much longer. Here are two links that I found helpful.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC21824/
https://en.wikipedia.org/wiki/Species

The speed of evolution is controlled by three things how fast the organisms reproduces (aka how short the generation time is)(faster/shorter = faster), how large the population is (smaller = faster), and how strong the selective pressure is (stronger = faster).
If you want a list of observed speciation events you can start here and a more indepth look and a longer list of speciation here. However a list of all know examples would be very large, outside the size available for posting here.
As for the finches they arrived on the island about 2.3 million years ago based on genetic evidence, some species on the islands may only be a few hundred years old but that is very different then when the first finches arrived on the islands.