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Do all plants grow roots when separated from parent?
Recently I bought my very first plant.
I thought it was doing well because it remained green, sometimes a yellow leave but all of my acquaintances which do know about plants told me not to worry, and remove the yellow leaves.
Until yesterday,
suddenly
a branch of the plant fell off,
I looked at it and it had rot through the whole stem of that branch and broke off.
Quite displeased of course,
Now, the branch is still alright, I guess, the leaves are still green,
now what am I supposed to do?
For now I planted the branch in the pot of the main plant,
I'm intending to get a separate pot for the branch and plant it again,
But I wonder, do all branches of all plants grow roots when put in ground?
If not it's not worth the effort to buy another pot of course,
Could someone help me out?

Dear respected person,
I am not a professional botanist, but I adore gardening, and would like to help you as much as I can from my humble garden experience.
As far as I have experienced, not all plants have stems which root when put in the ground. For instance, I have a plant called Bouganville Tom Thumb (I apologise for any spelling error). I once decided to clone this Tom Thumb variety by cutting its stem off and then burying its base in potting soil. I even tried rooting hormone powder (from a gardening store) but it did not root, even after a whole month.
On the other hand, I had a plant called Petunia whose stem I cut off on purpose to maintain the plant's shape and threw the stem into the soil. The stem shriveled, and I thought it died and left it there. However, to my surprise, I found the stem all fresh after 2 weeks only to find that it had rooted into the soil from side of its stem. Another plant called Jade Plant can be cloned by putting its leaf in soil.
I think it really depends on the type of plant whether its stems will root or not and how long the stem will retain its rooting potential after being cut.
If possible, you can try the following. Put the cut stem in a small plastic pot (they are very cheap) with soil and see if it roots (leaves will begin growing). If it does, transfer it into a larger pot later once it has grown. Wait for it to grow big enough to spread its roots thoughout the pot, then shift it into a big pot.
I believe if a plant roots, then all stems of that plant will root. Plus, congratulations on your first plant.

Hey Taimur, thanks a bunch for your in depth answer and the kindness it radiates... I'll surely follow your advice, I do hope the separates branch will survive, thanks for your elaborate answer and I wish you much fun with your gardening endeavors!!! Best regards, S.

Plants vary wildly in their ability at vegetative propagation. Not all plants grow roots naturally when cloned. Many plants have very slow response time to make new roots, and the branch dies long before the roots arrive, even in good normal conditions, so that it can only clone with very artificial environment.
You will find guides how to propagate your plant by searching google for clone+plant name... Lots of practical information is available online, it normally involves: 1/propagating by cutting new buds and putting the fresh branch underground while still attached to the plant
2/cutting new branches and taking off some of their leaves so they dont dehydrate, they evaporate passively drawing from roots, and putting them in controlled humidity for a week/months. the roots can take anywhere from a few days to many weeks to become visible, depending on species, i.e. conifer vs most broadleaves.
here's an interesting text on the subject:
https://gardening.stackexchange.com/questions/30685/are-all-plants-able-to-be-cloned


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Can cysteine alone change pigmentation?
According to this graph (from here):

cysteine contributes to pheomelanogenesis, and having a high enough concentration of cysteine makes the shift towards pheomelanin instead of eumelanin. So my question is: theoretically, let's say I would feed my dog a cysteine supplement daily, would that change its coat color over time? If yes, how, and if no, then why not? What am I missing in this process?
Disclaimer: this is just an example, of course I do NOT intend to feed my dog anything at all, it's just a hypothesis. What I want to know is that raising cysteine/glutathione levels can really contribute to pheomelanin production? I know that theoretically, in lab tests a higher cysteine concentration means a higher pheomelanin production, but I am interested in actual living things. If this is possible, it can be a huge breakthrough. If you have the opinion that cysteine alone won't make the difference, than what will? According to the graph attached, that's the only thing making the difference.

Surprisingly, it is indeed possible! But, the fact is that the actual process is a bit more complex and might actually require more compounds along with cysteine to give such effects in living beings. First of all, see this image1:

As is clear from the diagram, GSH (glutathione) is also a factor for pheomelanin production, along with cysteine. Another factor on which one might not pay heed is Tyrosinase protein expression. High amount of L-cysteine is thought to decrease the expression of tyrosinase in cells2 (but since I found just one article, I'd suggest to not pay much attention on this point).
Apart from gene expression, cysteine affects tyrosinase itself too. High concentrations of cysteine and glutathione have been shown to inactivate tyrosinase in cells, and the cause has been suggested to be the thiol-group of GSH and cysteine, which somehow generates oxygen radicals and inactivates tyrosinase3. A concentration of 10mM cysteine is sufficient to inhibit tyrosinase activity in cells4. It is because of these kinds of effects that GSH and cysteine are now being used in cosmetics as skin whitening agents as they, in higher concentrations, inhibit tyrosinase activity and hence, melanin production in skin cells5.
Just to add, when it comes to gene regulation, then it seems that cysteine has some more effects too. As pointed out by @Chris, eumelanin production in skin is stimulated by a cascade which involves a receptor known as melanocortin-1 receptor (or MC1R). When activated by one of the variants of MSH, typically $\alpha$-MSH, MC1R initiates a complex signaling cascade that leads to the production of the brown or black pigment eumelanin6. Now, a research has concluded that 0.07 mg/ml concentration of L-cysteine greatly reduces expression of MC1R gene, thus literally leaving no way (not really) for eumelanin production7!
Thus, in short, it is not as simple as "Hey, you want a red skin tone? Here is some cysteine for you!" Cysteine, and other related compounds like GSH, have more complex effect on melanin production than just promoting production of pheomelanin over eumelanin. You can also have a look at this answer (by @Chris) for some more information.
EDIT: To tell where you're going wrong, I'll make two reaction flowcharts. First, this is (IMO) what you're expecting as an answer:

But this is what is actually happening:

The red line is what we're interested in. But as you can see, the diagram is already quite complicated (and expected to get more complicated as more factors are discovered). So, giving a simpler explanation than this would be, very much, impractical or impossible.
References:

Malathi M, Thappa DM. Systemic skin whitening/lightening agents: What is the evidence?. Indian J Dermatol Venereol Leprol 2013;79:842-6
The Inhibition Effect of L-cysteine on Melanogenesis in B16F10 Mouse Melanoma Cells; In-Sook An, Ji-Hye Kim, Hoe-sook Yoo, Rui Zhang, Sang-Mo Kang, Tae-Boo Choe, Tae-Jong Kwon, Sung-kwan An, Gi-Yeon Kim
The effect of catalase on the inactivation of tyrosinase by ascorbic acid and by cysteine or glutathione; Lindbladh C, Rorsman H, Rosengren E.
Inactivation of human tyrosinase by cysteine. Protection by dopa and tyrosine.
Jergil B, Lindbladh C, Rorsman H, Rosengren E.
Mechanisms Regulating Skin Pigmentation: The Rise and Fall of Complexion Coloration; Jody P. Ebanks, R. Randall Wickett, and Raymond E. Boissy
Melanocortin 1 receptor - Wikipedia
Substantial Effect of Melanin Influencing Factors on in vitro Melanogenesis in Muzzle Melanocytes of Differently Colored Hanwoo; Touseef Amna, Kyoung Mi Park, In-Kyung Cho, Tae Jeong Choi, Seung Soo Lee, Kang-Seok Seo, and Inho Hwang

Nice answer. There is also a genetic component which is important: The status of the MC1R gene. It is responsible for the shift between the eu- and pheomelanin production - how, is not really understood so far. If you have mutations in this gene, this will get less signal into the cell and people are prone for pheomelanin. And I doubt that this can be influenced by diet.

@Chris Wow I didn't know about this one! Thanks, I'll add it in as soon as I get some citations :)

Besides, this paper should be interesting for MC1R (and a ton of others, too ;-) ): https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2678743/

@another'Homosapien' thanks for your great answer! So it seems that my hypothesis isn't just a fairytale after all? To quote myself again: so if I would give cysteine to my dog/kangaroo/pigeon/myself/whatever(the accent is on actual living things, not plants or lab tests) then it could change pigmentation to some degree? This is actually a huge thing. Now I'm not sure how those numbers from those studies would translate to human consumption. In other words: in theory how much cysteine would a human need to reduce the expression of the MC1R and inhibit tyrosinase activity?

@Chris so you don't think that pheomelanin/eumelanin switch can be induced by diet/supplementation? Do you really think that we humans reached a point in research where we can say :that's it, we just don't know how to make the switch between eu and pheomelanin, we can't influence pigmentation? If you think that pigmentation, either darkening/tanning or lightening can be influenced in any other way and I am dead wrong than could you post some links? If cysteine is the building block for pheomelanin, than why cysteine supplementation won't make a difference? Legit question, I want to know really

@user30255 I don't think it's that easy. This is a heavily regulated process, that can be influenced by certain drugs. I am not sure (actually I doubt it at the moment) that this can be done by nutrition alone.

@Chris  What would those specific drugs be? Never heard of any, to be honest. On the flipside, I found Melanotan to increase eumelanin production(the stuff bodybuilders use to get 'tanned'), so I figured there must be something which does the exact opposite. This is scientific banter on my part, I do not recommend nor advocate the use of things like Melanotan or any other potentially dangerous drugs. I just want to investigate all the theoretical solutions to increase pheomelanin as well. So if my cysteine hypothesis might be wrong, care to mention those drugs/substances?

@user30255 your hypothesis is partly correct. It is partly wrong because this process is not as easy as you are supposing, there are many processes involved in it, and its difficult to get a simple answer for any situation

@another'Homosapien' could you tell me more about those processes? what am I exactly missing here? I don't mind if this gets complicated

@another'Homosapien' thanks! sure, take as much time as you need and make it perfect!

@user30255 does it make some sense now? :)

@another'Homosapien' yeah that's a good graph, but according to it cysteine is pretty much a super drug which influences everything in there, if it's in abundance. So my question stands: do you think that dietary/supplemental cysteine can influence pheomelanin/eumelanin balance? Not to a drastic measure, but still noticeably. Because right now, in 2017 cysteine seems to be the best bet which could do that, and it could be a breakthrough.

@user30255 of course it is! That graph was just to mention the complexity at molecular levels. Yeah, cysteine does influence pheomelanin/eumelanin balance quite noticeably. That graph involves only pigmentation factors, if I include other factors as well, its gonna be a long flowchart then ;)

@another'Homosapien' so you agree with me that dietary/supplemental cysteine excess can influence pheomelanin/eumelanin balance? I heard that l-cysteine, as a supplement is poorly absorbed, what do you think?

I can't be definitely sure about this point. The acetyl group makes cysteine more water-soluble, and functions to speed absorption and distribution on orally ingested cysteine yup thats why N-acetyl cysteine is ingested orally for better absorption.

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How can highly virulent but uncommon diseases (like ebola) maintain a stable equilibrium?
I'm wondering how can very uncommon diseases remain in a relatively stable equilibrium. For example, if it started to spread, the spread could accelerate and become an epidemic. However, if it doesn't spread, why doesn't it wither away?
As I understand, the ebola for example, is highly contagious, nearly always fatal, and kills quickly. So quickly, hat the target has not much time to pass it on to others. If it spread just a little better, it would become an epidemic, just a little slower and it would disappear. How is it possible, that its spread did not change significantly in the last couple of decades? It kills a few dozen, maybe a few hundred people per year, these numbers remain largely unchanged.

They do not maintain an equilibrium. They show up, kill a few people and are gone again. Something stable would be like the measles which are present in humans (and only there) and take the chance to cause local epidemies. And we are lucky that ebola kills so fast and is not better transmittable. This would end in a big catastrophe. A very interesting book on this topic is "Spillover" by David Quammen.

I did not mean that they intentionally maintain an equilibrium. I was just meaning, that it stays a it was decades ago. Not growing, not shrinking.

What do you mean by "it stays as it was"? That there are no mutations? That it is not moving to other hosts?

No, the number of people infected per year.

Speaking of Ebola it is not stable. It stays in its reservoir hosts and only occasionally moves out. Even the great apes are not good host and die from it. We only "stumble" upon it from time to time.

It still has approximately the same average kill per year as it had 40 years ago. Not growing, not shrinking. I assumed if it started to grow or started to shrink even just a little, the tendency would continue stronger and stronger. Why isn't it like that?

Why should it? This virus exists in its reservoir hosts (most likely bats). From there is breaks out every now and then, when people cross the way of this host or probably eat them. This virus kills its host quite efficiently, so it doesn't stay in the human population (additionally humans do all to prevent it staying there). I really recommend the book by David Quammen, although is popular science. It is interesting to read on this topic (not only Ebola).

@Chris : thanks, this made it a bit more clear. Don't you want to add it as an answer?

I can do that. But not before tomorrow.

Viruses and other disease causing organisms are usually in an ecological steady state in different organism, called a vector.  When they start to infect another organism similar enough that they can reproduce, they may turn out to be more virulent or fatal than is optimal for the organism.
The classic example is the case of influenza outbreaks, the flu virus is causing mild infections in other animals such as birds or pigs and then a human being catches it and it may be serious or even fatal.  This is classically because the viruses lytic cycle (where it reproduces and then kills host cells) is not tuned to the equilibrium ideal for viruses in the new human environment, which is not fatal which gives the virus the best chance of reproduction and retransmission.
In the case of Ebola and Marburg viruses the vector is not known but there is speculation and research going on. So in the extremely rare handful of events where these hemorrhagic fevers have been caught by people they fatal.
Its the non-equilibrium case where the virus is not adjusted to human hosts and adjusted for its vector population where it is usually most dangerous.
If these viruses were allowed to persist they would theoretically come to the point where it wasn't fatal.  The problem being that people would die and there is always the risk that the virus would burn through all possible human hosts before it adjusts...
I want to say that this is all driven by evolutionary forces.  If the environment encourages pathogenic characteristics then human pathogens can persist forever.  Flesh eating bacteria and MRSA and other antibiotic resistant bacteria have found a competitive environment where causing disease and death are the only way to go - hospitals with antibiotics. In the case of Ebola/Marburg, there may be a disease reservoir of monkeys acting as a pool for the high fatality strain.  Anything can happen with the right geography and dynamics.
If you've been thinking to yourself, 'what are the odds that a virus or bacterium would be extra virulent versus not infectious at all?', you are right. One should also note that fatal outbreaks are rare and exceptional.  There are clearly plenty of cases where viruses or pathogens from other organisms can't get any traction at all in humans.  We are practically swimming in viruses and bacteria all the time.

They mostly getting less dangerous over time, but not necessisarily harmless. The Myoxomavirus, which was imported to kill rabbits, still kills about 70% of all infected animals, and this is more than 30 years after it was set free. In the beginning the rate was around 99,6%, but 70% is still far away from being nice. The example is from the Quammen book, the data has been published [here](Biological Control, as Exemplified by Smallpox Eradication and Myxomatosis).

Adding a comment for @PlaysDice  - recommending this book that explores emerging threats from reservoirs of infectious biotica.  http://www.amazon.com/dp/0393066800/?tag=stackoverfl08-20

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Could the proteome of E. coli be fluorescently labelled?
What proportion of the total number of proteins in E. coli could be fluorescently labelled for PALM/STORM imaging?

If (G)FP labeling is cumbersome or it changes diffusion co-efficients then you can try quantum dots or click chemistry based probes too. But as pointed out in the answer, you have to do one at a time. If I am not mistaken there are libraries with each protein GFP tagged (at least for yeast afaik there is one)

One at a time, you could potentially label all of them.
If you're asking how many proteins you could label at once, your biggest limitation is probably your microscope. In order to distinguish between different types of proteins you need different color fluorescent labels (dyes, fluorescent proteins, etc). Even the fanciest fluorescent microscopes tend to be set up to excite/record labels in <10 distinct wavelengths.
In practice I've only seen experiments where there were tracking 3 distinct types of proteins at one time.


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What are the evolutionary benefits for herbs having beneficial health effects on humans?
There are many types of plants which produce chemicals which can be beneficial in treating human illnesses, or at least alleviate painful symptoms.
Why would they do that?
Is it just random chance, like some plants being poisonous, some having no effect, and some having beneficial effects? However, for poison there are evolutionary benefits, as it might reduce the chance of animals eating the plant.
Many plant species produce tasty fruits for the purpose of having animals eat them and disperse the seeds. However, for most plants used for medicinal purposes, the leaves, roots or flowers are used, the cultivation of which doesn't seem to be useful for the plant itself.

Fruits serve a purpose, they contain seeds which are dispersed by the consumer. There is generally no benefit to having leaves and roots eaten, any effects on consumers are likely to be coincidental... I think that's the general principle - that may be wrong and there will probably be exceptions so I'm not posting it as an answer

Also note that not everything evolves for a reason, there are four mechanisms of evolution - only selection leads to adaptation (ie gives things a reason to have evolved) see illustrations here http://biology.stackexchange.com/questions/5007/how-is-evolution-possible-in-contemporary-humans/5058#5058


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What kind of predators do the snail's shell protect against?
Growing a shell is a significant material and energy investment for a snail. They have lots of predators which can easily eat them, having beaks which can pick them out or teeth strong enough to break the shell. Those which are not big enough to have a strong enough jaw, are small enough to be able to reach inside the shell.
Why do snails still have shells? Is there a large group of animals which cannot eat snails because of their shells, and would be able to if the snails had no shells?
I'm thinking of commonly known land snails.

What research have you done before asking it here?

Just think about what animals eat animals the size of snails but do not eat snails. lots of small predators do not eat snails. Its like turtles, are there things that eat turtles yes, but there are far fewer turtle predators than predators of other reptiles of the same size.

@John : my argument would be that if a predator is small enough, it can reach or crawl inside the shell though the opening where the snail retracted itself. Could you please provide an example of a predator which is incapable of eating a snail, but would eat one if it had no shell?

You may want to familiarize yourself with snail anatomy, the opening is not left open.


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Correct structure of RNA
Of the 2 figures, which is the correct structure of RNA,
This is the link :  1: https://i.sstatic.net/IYgyv.jpg
Sorry, the figure is not to scale.
If there's any problem with the question please inform me.

Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy. It is also bad practice to have figures as part of the question as they are inaccessible to partially sighted people. In addition the figures are incomprehensible and neither represents RNA.

Both figures include A,G,T,C.
Those are abbreviations for the bases adenine, guanine, thymine and cytosine.
RNA does not contain thymine, but its unmethylated form uracil, abbreviated with an U.
Thus, none of the structures represents RNA.

Please do not answer homework questions where the poster has made no attempt to research the question himself.

As Marzipanherz said, RNA does not contain thymine. Furthermore, none of those resemble any kind of RNA structure you usually see, for example two dimensional secondary structures showing watson-crick basepairing such as this example:
http://www.rna-seqblog.com/wp-content/uploads/2014/02/secondary1.jpg
Familiarize yourself with RNA by e.g. reading the wikipedia article or something https://en.wikipedia.org/wiki/RNA
After you've done this, you can e.g. go to the vienna webserver http://rna.tbi.univie.ac.at/cgi-bin/RNAWebSuite/RNAfold.cgi and predict secondary structures of your own RNA sequences.

Please do not answer homework questions where the poster has made no attempt to research the question himself.


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What if our whole body is made up of cancer cells?
Today I learnt in my biology class that cancer cells are immortal.  That left me wondering what if our whole body is made up of cancer cells?  Will that make us immortal? Is it possible or why is it not possible?

Many cancers are deadly for a reason you know. Vote to close being pob

I'm voting to close this question as off-topic because it lacks research.

This question shouldn't be closed; it's a good question and has an objective answer which @JayCkat gives. There is a difference between immortality as seen in stem cells and immortality as seen in cancer cells. There is tons of research on this kind of thing as well; you can discuss stem cell transplantation vs teratoma formation assays.

@Artem Thank you XD I really wish they don't remove my question.

No.
One aspect of cancer cells is that they no longer follow their programming, ie they stop doing all the work that a normal cell in that particular part of your body would do.
The next aspect is that cancer cells keep growing even when they are told to stop, even when there is no more space to grow.
Cancer cells also tend to destroy surrounding extracellular matrix in the quest for more nutrient. SO stuff like bone get deformed or just broken down leaving holes.
So if your entire body were made of cancer cells... well it would fall apart as cell stop doing their assigned job in the body, start growing without care and break down existing structure for better access to more nutrients.
What you want are immortal cells that still do their job.. stem cells.


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what is the meaning of the genotype values in each snp
I understand that snp is a single base variation. For example, if person 1 has the sequence in DNA , AAGCCTA the second has AAGCTTA, then the allels are
C,T.
My question is what is the meaning of 0,1,2 genotypes under each snp id (rs#) , and how it is related to the snp ?

I won't post this as an answer, as I really can't find any comprehensive source. Basically you are looking at SNPs from a diploid individual. Therefore it can either be homozygous for an allele or heterozygous. Heterozygous SNPs are encoded by 1. For homozygous ones it is usually 0 if the individual is heterozygous for the major allele (in the population or the one found in the reference in pairwise comparison) and 2 if it is heterozygous for the minor allele. Although this might in fact be different in different formats. 0 and 2 are always homozygous and 1 heterozygous, though.

Note that there is now a beta bioinformatics stackexchange site where this question might receive answers: https://bioinformatics.stackexchange.com/


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Are left-handed people more likely to be colorblind?
My friend, uncle, and I are left handed and also suffer from Protan colorblindness. Is it more likely for left-handed people to be colorblind?
Disclaimer: I was originally Right handed and due to a physical handicap I developed left-handedness.
EDIT: We also suffer from either ADD or ADHD.

I myself am left handed and also suffer from Protanomaly colourblindness. What gets me the most is that I’m also diagnosed with ADHD. Rarely do I ever come across someone who shares the same as I do.

In research literature, colorblindness and handedness appear to be correlated through male-ness.
Genetic causes of colorblindness are on the X chromosome, which explains why males are much more likely to suffer from colorblindness than females, as high as 16x more likely for red-green colorblindness.
Handedness is a complex polygenic trait governed by dozens of genes. A recent paper, Brandler et al., PLOS Genetics 2013, studying handedness implicated genes in chromosome 10.
However, males appear to be 25% more likely to be left-handed than females.
I wasn't able to find any studies directly addressing whether or not handedness is correlated with colorblindness, but it appears that if the only thing you tell me is that you are left-handed, then I can guess that you are more likely to be male than female, which means you are more likely to be colorblind than a person picked at random. So yes, a correlation appears to exist through maleness.
However, it's possible that being left-handed is conditionally independent of being colorblind given that you are male. In which case, for males, there may not be a correlation between left-handedness and colorblindness - there haven't been any studies addressing this question that I have seen.
To put this another way: if you tell me that you're male and left-handed, then insufficient scientific studies exist for me to guess whether or not you're more likely to be colorblind or not.

To answer you,  I am Male.

Are there any other aspects of your question you feel like weren't adequately addressed? Otherwise, it would be useful if you accepted this answer.

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When do 3 germ layers form in embryo? And why is there only one mature egg formed?
During the process of pregnancy, when do the 3 germ layers form in embryo? Is it after formation of gastrula? Also, during oogenesis, why does only one mature egg form? Why don't use polar body egg instead? During oogenesis, is there a crossing over occurring? If yes, at which stage?

This seems more like a homework question, but still I answered it because the second part of the question (polar body egg) is rather interesting.

I'll bifurcate the question and answer each part one at a time.
Germ layer formation: Gastrulation is a phase early in the embryonic development of most animals, during which the single-layered blastula is reorganized into a trilaminar ("three-layered") structure known as the gastrula. These three germ layers are known as the ectoderm, mesoderm, and endoderm i.e. the layers are formed with gastrula, or simply gastrula is the structure which contains these 3 layers.1

Polar body egg: Polar bodies generally don't have the ability to get fertilized as they are just residual parts of oogenesis. They are formed just to maintain haploid number in oocyte, so they don't even get sufficient amount of cytoplasm to survive (most of the cytoplasm is given to oocyte to provide nourishment to embryo). So they apoptose and disappear, but in some cases (like this), they are considered important and can even lead to unusual phenomena like polar body twinning, in which twinning occurs when the egg cell and polar body are both fertilized by separate sperms.2.
Cross over: In oogenesis (or specifically, ootidogenesis), cross over occurs during the conversion of primary oocyte to secondary oocyte and first polar body. Meiosis I of ootidogenesis begins during embryonic development, but halts in the diplotene stage of prophase I until puberty. For those primary oocytes that continue to develop in each menstrual cycle, during puberty, synapsis occurs and tetrads form, enabling chromosomal crossover to occur. As a result of meiosis I, the primary oocyte develops into the secondary oocyte and the first polar body.3
(In mammals, the first polar body normally disintegrates before dividing, so only two polar bodies are produced.)
References:

https://en.wikipedia.org/wiki/Gastrulation
https://en.wikipedia.org/wiki/Polar_body
https://en.wikipedia.org/wiki/Oogenesis
Polar bodies—more a lack of understanding than a lack of respect
Rare Forms of Twinning


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How do CAM plants keep stomata closed by day and open at night?
I understand how plants open stomata, with the H+ ion removal and the resulting K+ ion influx in the guard cells to induce turgor (wikipedia article here), though not how this process relates to presence/absence of light.
However, I don't understand how CAM plants manage to keep their stomata closed during the day and how it relates to CAM photosynthesis (if at all). I know that malate ions are involved in the opening of the stomata in C3 plants, could the malic acid production in CAM photosynthesis contribute to this?
So my question is: How do CAM plants induce closing of the stomata and what signal triggers this?

This isn't homework, I'm just genuinely curious. CAM and C4 photosynthesis isn't part of the Scottish curriculum, so I haven't covered this  and nor can I find anything about this online.

Yeah I've been searching for this casually for about 3 months now and am yet to find anything, thank you for the link but it hasn't turned over anything new. I apologise if the wording makes it out to seem like I haven't done reading of my own. I asked my interviewers at a university interview this question and they said they knew someone who could answer my question, so I know this has been answered and I'm just hoping someone on here will know it.

I think the biggest problem is we don't know the signal transduction pathway in CAM plants in response to CO2 levels.

Is it known what conditions in the cell trigger the H+ ion pumping in normal plants? Again something I've been looking for

@Phototroph Blue light phototropins activate the membrane H+-ATPase through phosphorylation events (1). Therein voltage-gated potassium channels open in response to the membrane potential generated by the H+ pumping.

As others already say in comments, the complete answer to this question is still unknown. However, the basic mechanism has been understood and has been summarized in the following diagram (from Wikipedia):

As you see, the mechanism is regulated by temperature instead of presence of light, keeping in mind that high temperatures are generally observed during the day and low tempertures at night. Temperature regulates, at the expression level, the activity of an enzyme PEP-C kinase. This enzyme phosphorylates PEP carboxylase (or PEPCase in short), which increases its activity. So lets see what happens when temperture is high:
During day:

high temperature inhibits expression of the enzyme PEP-C kinase, which decreases the activity of PEPCase.
activity of PEPCase is further reduced by an enzyme PEP-C phosphatase (this enzyme is active all the time, but its effect is reversed by PEP-C kinase).
due to respiration and photosynthesis, the amount of cytoplasmic malate is reduced (malate is converted to pyruvate to yield NADPH for photosynthesis, and pyruvate is used up in TCA cycle, whose by-product, $\ce{CO_2}$, is used up in calvin cycle).
due to this, malate is released from vacuole into the cytoplasm. This malate is not only used up in photosynthesis and respiration, but also further inhibits activity of PEPCase and expression of PEP-C kinase.
because PEPCase is inhibited, it results in depletion of malate in cytoplasm as well as vacuole.

During night:

at night, stomata open leading to increase in amount of $\ce{CO_2}$. Also, low temperature is unable to inhibit expression of PEP-C kinase.
when activity of PEPCase increases, PEP is converted to malate, which is then transported into vacuole. Also, increased concentration of $\ce{CO_2}$ increases photosynthesis.

Where is light required? As already said, the exact mechanism is still unknown. The mostly accepted mechanism is potassium ion pump hypothesis, but problems arise when we think about the initiation of this process in CAM plants. There are many hypotheses regarding this, and I will follow the one presented by Lee, 2010. Lets begin with the diagram (don't pay attention to the spellings):

initial stomatal opening is mediated by phytochrome in guard cells. The $\ce{H^+}$ pump in guard cells is also activated by darkness.
the maleic acid synthesized in other cells is also transported to the vacuoles in guard cells. There, the intracellular $\ce{H^+}$ (from maleic acid) is exchanged for intercellular $\ce{K^+}$.
increased concentration of $\ce{CO_2}$ also regenerates glyceraldehyde-3-phosphate and ribulose-1,5-bisphosphate, which lead to formation of sucrose via calvin cycle.
this sucrose is again transported to vacuole of guard cells, adding up to osmotic pressure. However, the major effect comes from maleic acid.
increased $\ce{CO_2}$ concentration and increased activity of PEPCase (as already explained) form malate and lead to further increase in the osmotic concentration. All this causes stomata to open.
during the day, malate is decarboxylated to pyruvate (as already explained), leading to decrease in osmotic pressure and thus, closing of stomata.

I hope this makes the concept more clear, but bear in mind that the above mechanism could later prove to be wrong as further studies on CAM plants help to find out the actual mechanism.

@gerardofurtado +1 for explaining what I call healthy competition :)


text:
Lookup for transporter locations in humans
I am interested in several transporters and cotransporters (eg SLC12A1/2 and many others), more precicely, in (human) organism that are made of cells containing those transporters. So does anyone know a lookup table or database where I can find information about that? My google search unfortunately left me in the dark :/ So I am thankfull about any hint!

Welcome to Bio. It's unclear what information you are after; cell types? transporter proteins? What characteristics in the latter case you wish to know?

It seems to me like the OP just wants a database of all the types of transporters (especially proteins as he mentions 'cells') to get information about them.

Ah, sorry if my question wasnt clear... Basically I am looking for a database containing the transporter proteins linked with a list of human organisms where they occure. For example the transporter NKCC1(resp SLC12A1)  would be linked with the Inner ear, sensory neurons, the distal colon, salivary gland epithelial celss, etc...
So I would be happy about anything like, or just similar to this  :)

This site can help you locate RNA expression of a particular gene (if you know the gene for the protein in context) in various tissues. Its called biogps.
http://biogps.org/#goto=welcome
Hope it helps :)

Cool, this already is a good step forward :)

Update: So yes, the source helps a lot! Also I found another similar source which seems very nice: the EMBL-EBI expression atlas.
Just one confusing thing I don't understand about either of the sources: I cannot find any gene expressions for the inner ear, corti, or cochlea... Is there a reason for this?

Haha! I got no clue. I don't use these stuff. All I knew is, while i look up proteins and all on wiki, it shows up this colorful bargraph on the right. Which happens to be an RNA expression thing from the site. I just pasted the link :)

BioGPS and related sites stem from research projects where RNA from a number of tissues and cell types are obtained, and (relative) mRNA abundances were measured (using microarrays or RNA-sequencing). See literature references on these sites for the primary papers. But not all tissues are easy to get enough RNA to measure accurately; cochlea would be a very small amount of material. Also they may not have found anyone willing to part with their inner ear for the sake of research ...

Ah, that explains a lot! thanks for that explanation :)


text:
Do lysosomes play any role in cell division?
My biology textbook includes a point that lysosomes stimulates cell division without further elaborating. But studying it, I felt eerie about this function of lysosome. Then, I checked on the internet; found nothing relating cell division to lysosomes.
Maybe, autophagy of lysosomes can play a role in this regard. Killing cells and thus 'stimulating' cell division. But this reasoning doesn't seem plausible as autophagy doesn't occur without extreme conditions.
Nothing else is coming into my mind.
So, is this point included in my book wrong or right?

You're incorrect about autophagy - it occurs all the time.

Really? I thought it occurred when there is a shortage of food or other extreme conditions.

Nope. Read Wikipedia for an intro, then go to PubMed for recent review articles.

It is actually not completely correct to include it as a fact in textbooks. The main cause of it is that there is not much research on this topic. See this article for reference. According to Allison and Mallucci (1964), during cell division, lysosomes either released an unspecified activator or some hydrolase that inactivated a repressor. Apart from this, Allison and Paton (1965) showed that treatment of human embryonic lung cells in tissue culture with photosensitizing agents allowed high frequency of chromosome breaks on irradiating the cells with light from a high intensity tungsten source. They claimed that these effects were observed only at lysosomal sites, from which they concluded that a cytoplasmic event was giving rise to structural alteration in chromosomes. This event was suggested to be release of deoxyribonuclease from the lysosomes. However, Chevremont et al, 1959 showed different results through their experiments. They grew mammalian cells in tissue culture in the presence of acid deoxyribonuclease. This treatment inhibited cell division, but allowed DNA synthesis to proceed and did not appear to alter the nuclear DNA. Hence, the contribution of lysosomes in cell division is not yet completely established and still comes under debate.
So, it should not be considered a total false, but is also not reliable enough to be printed in textbooks. Overall, we don't yet know whether lysosomes do play a role or not.
References:

TUATARA: VOLUME 18, ISSUE 1, JULY 1970
THE LYSOSOME
ALLISON AC, MALLUCCI L. LYSOSOMES IN DIVIDING CELLS, WITH SPECIAL REFERENCE TO LYMPHOCYTES. Lancet. 1964 Dec 26;2(7374):1371–1373.
Nature 227, 707 - 708 (15 August 1970); doi:10.1038/227707a0;
Chromosome Breakage by Deoxyribonuclease;
GILLIAN R. PATON & A. C. ALLISON
CHEVREMONT M, CHEVREMONT-COMHAIRE S, BAECKELAND E. [Action of neutral and acid desoxyribonucleases on living somatic cells cultivated in vitro. III. Histoautoradiographic study after incorporation of tritium-labelled thymidine]. Arch Biol (Liege) 1959 Oct-Dec;70:833–849.

Well, how can acidic deoxyribonuclease inhibits cell division without inhibiting dna synthesis?

I ain't sure, but nuclease would simply cut the DNA due to which cell would prioritize DNA repair instead of cell division. Thus it could inhibit cell division by creating breaks in DNA continuously.

Well. I can show how they could be seen to be linked.
Taking cell division to mean the full process of mitosis – producing identical copies of a particular cell.
The mitotic apparatus would be present to aid in the separation of chromosomes during metaphase. One protein associated with the mitotic apparatus is "Nuclear mitotic apparatus protein 1"
In order to carefully control and regulate the amount of this protein present, the lysosome is able to degrade the protein.
So the lysosome is responsible for regulating a key protein associated with and vital for mitosis. `

Jeffrey Van Ness, David E. Pettijohn, A. Klug, Specific attachment of nuclear-mitotic apparatus protein to metaphase chromosomes and mitotic spindle poles: Possible function in nuclear reassembly, Journal of Molecular Biology, Volume 171, Issue 2, 5 December 1983, Pages 175-205, ISSN 0022-2836, http://doi.org/10.1016/S0022-2836(83)80352-0.

`

Please add some references to your answer. Has this process ever been reported in vivo or in vitro?

Would you elaborate "In order to carefully control and regulate the
amount of this protein present, the lysosome is
able to degrade the protein."?

From what I have read and what is indicated however a mechanism is not provided.

Would you please elaborate the passage I pointed out?

@Mockingbird The article which I read merely mentioned this in passing. It said that the protein was degraded by  lysosomes. This as deep as it went into explaining the mechanism.


text:
How Anopheles crop doesn't digest gametocytes of P. vivax?
Background
According to my A-level textbook: When Anopheles mosquitoes inject their proboscises and suck up blood from human host of malaria agent, they suck all stages of malaria parasite present in the blood like merozoites, cryptozoites, gametocytes etc.
But, Anopheles mosquito's crop digests all other stages of malaria schizogony except the gametocytes.
Question
Well, how does the digestive system of Anopheles distinguish the gametocytes from other stages of malaria parasite?
Or, is there any protective mechanism for gametocytes to stay untouched in face of digestion in Anopheles crop?

Short Answer: Nothing prevents it, most Plasmodium (gametocytes/gametes/zygotes/ookinetes) are killed.
Background: After lots of search, I finally found a definite answer about this. According to Smith et al, 2014, the survival rate of Plasmodium in the Anopheles gut is very low. At each developmental step during their life cycle, a large proportion of Plasmodium face the deleterious effects of the gut (albeit they are not certain that the effect possesses contribution from enzymes). As an example, even if an Anopheles mosquito ingests thousands of Plasmodium gametocytes, about 50-100 are able to develop into ookinetes while only about five survive to form oocyst. This is why even in high transmission areas, majority of Anopheles mosquitoes are not infected by Plasmodium parasites. See this image:

Pay attention to 'parasite #' and see how the number of parasites keeps on decreasing during different stages of development of Plasmodium.
Reference: Smith RC, Vega-Rodríguez J, Jacobs-Lorena M. The Plasmodium bottleneck: malaria parasite losses in the mosquito vector. Memórias do Instituto Oswaldo Cruz. 2014;109(5):644-661. doi:10.1590/0074-0276130597

Perhaps worth emphasising the points made in the paper (and shown in the Figure you have reproduced) that much of the reduction in parasite numbers may be attributable to factors present in the blood bolus such as complement, that come from the blood meal.

Why is there a sudden increase after a continuous decrease? O, I get it it's cleavage in epithelium.

@Another After this answer, do you still think the primary host of Plasmodium is Anopheles? I don't think without paleontological data, nothing can be said about which was the prior host of Plasmodium, mammal or Anopheles

"blood bolus such as complement, that come from the blood meal." Do you mean complements from human blood?" Do you mean complement proteins gathered from human host blood? @Alan Boyd

@Mockingbird yes, the paper that is linked to in the answer includes extensive discussion of the role of human complement in killing during the early stages - it is shown in the diagram along with blood-derived antibodies. The article also suggests a role for reactive nitrogen species generated  by incoming haemoglobin, amongst other things.

@alanboyd the paper said that the gametocytes (inside bolus) are resistant to complememnts while ookinetes (which come out when complements and bolus are digested) are sensitive to complements. Enlighten me if I got this wrong, but this is why I didn't bother to add it.

@mockingbird well I don't specialize in this field, so I can't say anything definitely

@another'Homosapien' I thought that you had broadened the scope of the discussion beyond gametocytes. If you didn't mean to do that then fine, but looking at the information in the Figure I don't think it is fair to say that 'most of them are killed' if 'them' means gametocytes only.

'nitrogen species' What kind of nitrogen species? @Alam

@Mockingbird why not read the paper?

Okay. I will do it

@alanboyd nope I didn't mean to broaden the topic, 'them' meant Plasmodium in general, not just gametocytes (does it convey that meaning?)

Disclaimer: I am trying to answer the question without finding any academic research on the topic. So, appreciate hypotheses and feel free to point out mistakes.
Short Answer : Co- Evolution

Broad Answer: 2 hypotheses

The gamete stage of Malaria parasite simply co-evolved with Anopheles sp. to develop a protective mechanism to survive digestion in crop. Whereas, the other stages of Malaria parasite didn't co-evolve,  so they get digested.
Parasites had already the protective mechanism for surviving digestive enzymes in Anopheles crop. They entered mammals later and evolved a life cycle with a new protective mechanism for new host's immune system.

Why is that?
The answer to this question is not so clear according to known biology, as I haven't found much research in this phenomenon.
But, we have to remember that biology sometimes (or always?) doesn't explain why rather explain how.
The following words are corresponding to what I think about the mechanism of this co-evolution
Hypothesis 1:
It could have simply happened that some point in ancient times, the gamete entered the Anopheles crop from a mammal, but not only that; it tried to continue its life cycle on this new host. But, the environment of crop was unsuitable for the gamete to survive due tto digestive enzymes. So, the first few million or billion tries went into vain. But, the parasite slowly started to evolve to adopt in the Anopheles crop.
After 'some' time, the parasite developed a working protective mechanism from digestive enzymes and continued it's life cycle in Anopheles.
As @Another Home sapien points out, there should be some benefits for this evolution. While it's hard to tell exactly what the benefits could have been; I think it's simply to adopt to new potential host's physiological environment.
But why didn't other stages evolve of Malaria parasite in a same way?
This is another hard question to answer. However, it's not so that only the Anopheles and the parasite co-evolve; the mammal host co-evolved too in this period. And the whole system evolved gradually to get to the present life-cycle of malaria.
Hypothesis 2:
It might have happened that the original host to malaria parasite was indeed Anopheles. So, it had developed a protective mechanism long before entering any mammal host. Then, after entering the mammal host it developed another protective mechanism to survive host's immune system and continued  it's life cycle.
I think hypothesis 2 is more probable as insects pre-existed mammals. Another hypothesis can be drawn the life cycle of parasite is shaped up simultaneously in mammal host and Anopheles host. But, it's hard to hypothesize what could have happened in this scenario.
Reference : 1. Wiki: Co-Evolution
2.Article on this co-evolution

I must say, you are assuming just too much in your answer. How do you know that Anopheles wasn't the original host of Plasmodium? And what benefit would sporozoites get even if they developed a protection against digestive enzymes? In evolution, selection pressure can be both in favor of or against a trait. Also, I won't recommend using phrases like "it chose to..." Also, usually its the parasite that co-evolves with the host, while the host just evolves to get rid of that parasite (which Anopheles too seems to be doing now)...

Thank you @Another You are free to edit my 'answer'. I too felt that my understanding is limited in this case. So, I will edit now.

@Another Do you think you would be able to add some quality reference on this phenomenon?

well, I've already been searching for the 'how' part for hours :P regarding the 'why' part, I'd love to improve the answer, but I feel I should first wait for somebody more specialized in evolutionary biology (since I ain't)...

@Gerarddo Furtado Thank you for your comment. I hope you can add some reference and details to my answer.

@Gerardo Are you sure about it?

Then, the 2nd hypothesis is more probable, I think.

@Mockingbird indeed a very imprtant & essential question to ask...@Gerardo Furtado said its totally correct.The Plasmodium's primary host is the Anopheles.There r reasons why but this logic is merely basic level only:The encysment of oocyst is due to partially secretion of cyst material by the stomach of the primary host and partially by the zygote itself.Without encystment sporogony doesnot initiate in them. This could be an important phenomenon which makes the mosquito not just a vector but a vector host.Otherwise they could hve cmpleted the entire cycle in humans alone.

@Catharanthus What's the difference between vector and vector host?

vectors only transmit the disease and vector hosts not only transmits the disease but also plays the role of a host during one phase of a digenetic life cycle like in malaria.I only read the term in a textbook on a digenetic cycle.

Would I have to award the bounty to myself?

What if Nobody answers without me? Would I have to award the bounty to me?

Umm sadly AFAIK you cannot award a bounty to yourself. Its probably gonna go to nowhere.

@Another Ha Broke my heart

Sorry for that, but now you have another option :P

@gerardofurtado lol :P yeah that would be injustice with the whole purpose of bounty

@Furtado I understand.


text:
Why does crippling pain exist?
Some kinds of trauma can cause pain so severe that it makes you unable to move or do anything at all.
It may put you out of action and unable to help yourself because of how excruciating it is.
Although I understand that pain is necessary to alert the brain that something is wrong and need to be fixed, I imagine it like an alarm going off alerting about trauma. But a crippling pain would be like a deafening siren hooked up to your ear making you unable to do anything to correct the problem, instead it might send you into a shock. It would be total disaster which could prevent you from taking any step about it. So, why does excruciating pain exist? Or in other words, why has this feature not gone extinct during the course of evolution in spite of its harmful effects?

Pain tells your body that something is wrong and needs to be fixed. Crippling pain is telling you that the "something" is an immediate danger to life or limb, and needs to be paid attention to NOW. Continuing on with your normal activities will be severely detrimental to your health.

@MattDMo but what good is it if you can't do anything more than moaning, rolling and eventually dying from shock while if it wasnt crippling you could have done something to save yourselves like moving to safety or applying pressure to bleeding wound etc that would have avoided death

To this point, I would like to tell you an incident which I saw once on TV (so I don't have reference for it). Once a mountain climber fell from height ~300m straight on a rock. Her hip joint, both knee joints, and some bones broke & she fainted. When she was unconscious, her brain decided that the pain is too excruciating to do anything and should be switched off (by endorphins). When she woke, she didn't feel any pain and somehow reached paramedic camp. When she reached, then she started feeling pain again.


text:
Miscarriage in early humans
Today, about 10 to 20 percent of known pregnancy end in miscarriage. Pregnancy is a biological process that has been very well studied by medicine. As a result, modern medicine helps a lot to prevent miscarriages and to prevent death of pregnant women.
What was the percentage of pregnancy ending in miscarriage before modern medicine? Typically, what was the percentage pregnancy ending in miscarriage in early Homo sapiens, during the paleolithic age?

Would it change your question if you knew that modern medicine can actually do very little to prevent miscarriages? Because there is actually very little modern medicine can do to prevent miscarriages. Death in childbirth? We've got that nearly covered. Healthier babies? Got that covered to a fair degree as well. But nope on the miscarriages.

Yes, that would indeed already be a nice insight. I assumed that modern medicine had an important impact but I actually had no idea. You can totally write an answer inspired by how modern medicine "fail" to prevent miscarriage.

@anongoodnurse - My guess is this would make an awesome answer, as the data on 2.5 million - 12k years ago is likely to be small or non-existent.

@anongoodnurse What about diet and overall health status? Doesn't this affect miscarriages rates? Even if this isn't only dependent on modern medicine and direct measures to specifically decrease miscarriage rates, I would still expect miscarriage rates to differ between modern humans and paleolithic people. But I'm only speculating and could definitely be mistaken.

@fileunderwater - nutrition affects age of menarche and number of ovulatory (vs. anovulatory) cycles, but it's not known to prevent miscarriages.

@anongoodnurse Ok good to know and you are probably right about this. See comment under your answer for further ideas on infection and miscarriage rates.

Pregnancy is a biological process that has been very well studied by medicine. As a result, modern medicine helps a lot to prevent miscarriages and to prevent death of pregnant women.

While the latter clause is correct (maternal - and infant - mortality is reduced with medical care), the former is not.
Miscarriages have been a problem as far back as recorded history. The written record includes medicinal recipes to prevent miscarriages. The problem then, as now, is that it just can't be done very well.
From a 2000 Obstetrics journal article:

Human reproduction is extraordinarily wasteful. The reasons for this have taxed all of the contributors to this book. As we move into the 21st century it is sobering to reflect on the fact that we have failed to harness the power of the evolving revolution in molecular medical biology to answer the fundamental question: why is the fate of a fertilized egg so hazardous and so unsuccessful? The following account summarizes our limited knowledge of the epidemiology of miscarriage and then moves on to consider some of the medical causes of miscarriage...

Miscarriage is difficult to study, and the causes difficult to establish, so the literature showing that any interventions help (antibiotics, bed rest, supplements, etc.) is not plentiful. Smoking seems to have a deleterious effect on pregnancy. How this relates to early populations is a matter of conjecture.
Some good studies do exist, however. One good study in the New England Journal of Medicine followed an ideal group: women who had no history of infertility, who were trying to become pregnant.
Of 221 couples followed for 6 months, a total of 199 pregnancies were detected, of which 126 ended in live birth (therefore a 37% miscarriage rate). Because of the methodology, failure of blastocysts to implant could not be measured. The findings of this study were supported by others (31%), etc.: early loss increased when implantation occurred later than 10 days after ovulation. While the authors were hopeful ("There may be opportunities to increase fertility by extending the time during which implantation can occur."), they were also realistic ("Such interventions should be approached cautiously, however, because they may have unintended consequences with respect to the quality of surviving embryos.") Basically, you can't fool around too much with Mother Nature in this realm.
Has modern medicine been able to change this rate? Not really. Even with IVF, where thousands of dollars are spent trying to preserve a single pregnancy (certainly not the norm), miscarriage is common. The best way to increase the viability of IVF pregnancy is to select better oocytes, embryos, etc. In other words, maternal factors remain refractory to manipulation.
Even things obstetricians long took for gospel (for example, bedrest with pre-eclampsia) have little evidence of benefit to the fetus.
The literature is vast in this area (reproduction is an important field to study). I can write a book on how little can be manipulated on average (I will consider spending thousands of dollars on one pregnancy not average), but it wouldn't sell. What does sell are false claims, this one being as good as any claimed today:

To prevent miscarrying or if one that is apt to miscarrie goe a journey let her take this powder morning and evening whilst shee journeys: Take of Dragons Blood the weight of a silver two-pence, a dram of red corrall powdered, the weight of 2 barly corns of Ambergrease, Besar ye weight of 3 barly corns, mix all these together and keep them close stoped in little vial glasse when you use take as much of it as lie upon a penny in a little clary water at nighte when you goe to bed, and in ye morning fasting and sleep after it to use it till you are out of danger.

From what I've heard, some infections during pregnancy, such as Rubella, can cause miscarriage. In the case of Rubella, this is now part of standard vaccination programmes, which should have decreased miscarriage rates. WebMD: causes of miscarriage also mentions Rubella, along with some other causes of miscarriage, some of which are prevented/treated by modern medicine (also see this WHO page). However, this is not my area and I'm only relying on secondary sources.

@fileunderwater - I did mention smoking. As for rubella, it's still not uncommon (though it's much better) but there are plenty of things that have come along to replace it as new causes of miscarriage. I'm not saying in no way are we better off; we are. But in the case of miscarriages, not by much. You can point to a number of things, such as cervical cerclage to prevent preterm delivery, but that doesn't help reduce miscarriages; it only helps the fetus to mature a bit more in occasional cases of preterm deliveries. A book can be written, but it probably won't be, and not by me.


text:
The Evolution of Fruits
I was cooking rice this morning and was fascinated by the color and it's sweetness and began to ask...

How did fruits evolve?
Did they come from a single cell?
Which cell?
How did that cell branch off from  the cell that became animals? Is there any evidence for this kind of thinking or just a lotta theories? How did we get rice, mangoes, beans, orange, coconuts, peanuts, apples, bananas, if there is no "Designer", where did ALL these come from and how did they evolve?

This question is too broad. Please narrow it down to (preferrably) single question to get better answers.

Too broad with shades of a creationism agenda.

@AlexDeLarge You are right, sorry. In the popular culture it is never considered a fruit but botanically speaking it is a fruit. I'm removing my comment.

@GbolahanFaluade. Welcome to Biology.SE. What have you found so far? Have you tried to google fruit evolution?

Turn the "Designer" question around: Why would a sensible designer have wasted time on all these randomly-different seed dispersal methods, instead of using just one good one?

I'm flagging to close this as it's opinion-based, although it's also far too broad.

Fruit did not evolve from a single cell( except in the sense that plants did)  it evolved from seeds and their casing in angiosperms. Fruit is a means to disperse seeds. This will get you started on the different methods of seed dispersion.
https://www.britannica.com/science/seed-plant-reproductive-part
By enclosing their seeds in material animals want to eat, plants get animals to transport their seeds long distances and deposit them in a warm pile of fertilizer. Sugar is the easiest macronutrient for plants to produce so that is the what they pack their fruit with. animals tend to eat new growth which often contains seeds so it is easy to see how animals with seeds tough enough to survive digestion (which many seeds do) would quickly spread. Any adaptation that made animals more likely to eat these parts and spread their seeds would likewise spread.
I suggest familiarizing yourself with basic plant phylogeny first, since if you had you would know only one group of plants produce fruit, and so would not have asked half your questions. So please go do a few minutes of research and come back with a more coherent question.
If you want a complete retelling of the entirety of plant evolution you can do that yourself, show a little initiative and start here.
http://bmcevolbiol.biomedcentral.com/articles/10.1186/1471-2148-14-23
https://www.accessscience.com/content/plant-phylogeny/524400
Also rice is not a fruit. It is the plant's seeds you are eating, it did not evolve to taste good, you evolved to think it tastes good becasue it is nutritious, in much the same way meat tastes good. You are essentially murdering their offspring.
I also suggest learning what a theory is.


text:
Do I have to chew for digestion to kick in?
Liquid nutrient-rich products (such as Soylent) are consumed without chewing. But if I have to chew to initiate digestion, are those nutrients really "processed"?

If you had to chew to digest, then beverages like sugary sodas would never be digested or provide calories or nutrients, as you (generally) don't chew when you drink them. No, chewing is not required for digestion or nutrient absorption. Chewing is important when eating solid foods, as the chewing action breaks down and begins to solublize the food, and stimulates the production of saliva, which contains enzymes that begin to break down the food prior to digestion in the stomach and intestines.

So digestive fluids are always there, waiting..?

Yes, there is always acid and digestive enzymes in your stomach, and more are produced when food enters it.

what, other than chewing, triggers more acid to be produced upon food intake?

@Sparkler the presence of the food itself. You can read all about the process of digestion here - it is directly linked from the other article I linked in my answer.

@Sparkler Also, saliva production and other digestive enzymes are increased in anticipation of food or from seeing/smelling it.


text:
What is the mechanism by which bactericides kill bacteria?
"Bactericides kill bacteria". What is the meaning of "killing" in this context, and how exactly is this "killing" happening chemically?

This is rather broad. Each bactericidal agent has a different mechanism of action. For example, alcohol denatures proteins necessary for function and the lipids in the plasma membrane dissolve into the alcohol. "Iodine can penetrate the cell wall of microorganisms quickly, and the lethal effects are believed to result from disruption of protein and nucleic acid structure and synthesis." [CDC]

Each bactericidal agent has a different mechanism of action. For example:

Alcohol denatures proteins necessary for function and the lipids in the plasma membrane dissolve into the alcohol.
"Iodine can penetrate the cell wall of micro-organisms quickly, and the lethal effects are believed to result from disruption of protein and nucleic acid structure and synthesis." [CDC]
other mechanisms include tampering cell metabolics, tampering DNA replication, and more.

See also:

The 2008 CDC guidelines for sterilization and the such for healthcare settings. Each method will contain a comprehensive description along with a statement of "mode of action," i.e. how the method actually kills the bacterium.
Another good link here from the CDC examines factors affecting the efficacy of sterilization.

Otherwise, it would be best therein to split the specific mechanisms you perhaps don't understand into separate questions. But an important take-home message in the efficacy link above just adds to just how broad this question is:

Microorganisms vary greatly in their resistance to chemical germicides and sterilization processes.

Could you please also give a few examples of what's going on from a pure chemical point of view?

@Sparkler this question is far too broad. From What types of questions should I avoid asking? "If you can imagine an entire book that answers your question, you’re asking too much."


text:
What mechanism is responsible for germinating in the right direction (root towards gravity)?
Regardless of the initial seed orientation, the root always grows/sprouts/germinates "towards gravity" (see picture), sometimes curving around in sharp 180°. What is the mechanism responsible for the gravity sensing and for the growth adjustment?

@WYSIWYG -the answer of the linked question indeed covers this question. The questions are however different. What to do?


text:
Does the location of the double bond in chlorins yield a distinct biological function?
Chlorins differ by the number of double bonds and their location. Chlorin has 20 pi electrons, whereas bacteriochlorin and isobacterichlorin have 18 pi electrons, but at different locations.

Do chlorin, bacteriochlorin and isobacteriochlorin have distinct biological function due to this double-bond difference?

I only found a hint that this might be the case in this publication by Singh et al., stating

Porphyrins, chlorins, bacteriochlorins, and isobacteriochlorins each have unique photophysical properties that are exploited by nature and can be used for diverse applications (1, 2).

I don't have access to "The Porphyrin Handbook" (The first citation in the quote above), but I suspect it would be your best guess in finding more information.


text:
Which ingested allergens can be transferred to a partner via bodily fluids?
Can some allergens, such as peanut traces, appear in bodily fluids (saliva, sweat, semen, vaginal secretion) after ingestion?
I would like to know in particular intake of which allergens should be avoided to prevent allergic reaction of a partner due to contact with bodily fluids.


text:
Is there a way to determine how many times a given cell divided?
Do cells divide into exact duplicates? If not, is there a way to determine how many times a given cell divided?

I suppose you implicitly talk about multicellular organisms and implicitely mean "since last fertilization" and not "since the origin of life" or anything else. Is that right?

Do you ask this question by curiosity or because you are trying to achieve something specific?

@Remi.b yes, multi cellular, since last fertilization. Curiosity, and maybe a way to determine "objective" age of an organism

There is no such thing as objective age except eventually the time separating fertilization to the current time. You are trying to find an estimate of this age, not a new definition of the age of an organism.

Telomere length is probably something that you want to consider.

Can you provide some clarification on what kind of cell you are interested in? While come cells do lose their telomeres, others do not. We are not even considering prokaryotes here, are we?

Yes, its called the HayFlick limit. A cell will divide until their telomeres reach a critical length,which is usually around 40 to 60 cell divisions. The cells then enter cellular senescence and cease to divide. However, cells may also stop dividing due to (ROS) or reactive oxygen species, cell to cell fusions, or activation of oncogenes, the latter of which is a gene that has the potential to cause cancer.


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Can the human brain be reduced to a binary system?
Does the brain really function like a computer as in, ultimately every response is related to a binary sequence based on whether particular neurons fire or not?

First of all, I would like to point out that making analogy between digital computers and the brain is often very misleading.
That being said, my answer is, some scientists believe so, some don't.
Several things to consider:

Some neural systems are not spiking. C. elegans for example has a nervous system that is entirely analogue. Human nervous system also contains neurons with graded responses (mostly in the sensory front-end though).
Spiking neurons may be binary at each time point, but time itself is continuous. Firing at 0.003 seconds later can represent something different. (in contrast to the usual synchronous digital architecture of computers)
The neuron doctrine is sometimes challenged. Glial cells that do not fire may have important functions for information processing. See:

Bullock, T. H., Bennett, M. V. L., Johnston, D., Josephson, R., Marder, E., and Fields, R. D. (2005). The neuron doctrine, redux. Science, 310(5749):791-793.

That's exactly what I was wondering; if in fact, some brain signals are propagated on a grade. Thanks!

Plus neurons have modulators that change the way they behave. Some modulators may cause hyperpolarization while others may decrease the threshold for depolarization.

While action potentials are usually binary, you should note that synaptic communication between neurons is generally not binary. Most synapses work by neurotransmittors, and this is a chemically mediated graded response that, for example, act on voltage-gated ion channels. So even though action potentials are often binary, communication between neurons are most often not, and action potential firing can involve the integration of synaptic information from many different neurons. Therefore, the brain as a whole cannot be reduced to a binary system.
See this as a complement to @Memmings answer.

Many neurotransmitters (also) have metabolic G-protein-coupled receptors as their target. E.g. Glu has NMDA-receptors (Na,Ca-channels) and AMPA receptors (Na ion channel), but also a gamut of metabolic GLuRs as target. I slightly adapted your answer by adding 'e.g.' Fine answer. +1, therefore removed the intro line - unnecessary :)

Very interesting. Thanks for the response. I am not familiar with voltage-gated ion channels and will definitely be reading up on them. Thank you!

John vonNeumann, the famous computer scientist, tackled this idea in his last book, 'The Computer and the Brain.'  He personally landed on the side of the brain being a binary system, due to the behavior of neurons which either fire or do not fire.
While that is an important observation, and will have significant consequences to people trying to create artificial brains within computer systems, I think a more important observation has to do with computational complexity.  It is very easy to build systems which, at least theoretically, have the potential to be universal computers.  From that fact, it is fairly trivial to see that whatever definitions you choose to work with in terms of brain input and output (sensory nerve cells feeding electrical impulses from organs of perception being a possible definition of 'input' and propagated impulses to muscles, or changes in the neural structure itself being possible definitions of 'output' for example), yes it is possible to construct a binary system which can perform the same calculations as a human brain.
However, there is a catch.  Because it is impossible to perfectly know the complete state of the brain, and because any degree of inaccuracy in the starting state of the binary system, no matter how small, will cause the behavior of the binary system to diverge completely from the behavior of the specific brain being modelled, it is reasonable to say that no particular individual brain can be reduced to a binary system.

It's theoretically possible, because all information can be well approximated/copied in binary, and it's
practically impossible because of size, energy, and program size/depth.
A fly brain is <1mm wide and an intel fly brain equivalent is >1000mm wide... much slower than the fruit fly. (Thats why flies see your hand coming in slow-mo).
This intel chip has as many neurons as a slug, far less than a fly:
https://www.cnet.com/google-amp/news/intel-packs-8-million-digital-neurons-onto-brain-like-pohoiki-beach-computer-loihi-chips/
he binary model has to include "chemical modelling" and "physical modelling" like a graphics card which models light and creatures as binary.
Except that there is an added issue: processing speed. The brain can grow direct connections which are very fast. Silicon signals have to travel 1000 times further for every calculation.
2d chips take as much space as a skyscraper and a small nuclear station for energy, and future mythical 3d transistors would take space and would be slower because they require direct chemical processing and flexible internal connection to be as fast.
AI is very performant and is one of the future paradigm changes like "internet/mobile phone / electric car / AI "

as far as I know the brain processes data in stages the neurons themselves are not purely binary as in a computer in that every action has a predetermined output. the neuron response tends to be goverened by sigmoid function output and hence the use of this function in artificial neural networks. further, the synapses have strengths that is depended on the amount of neurotransmitter in there which obviously varies from cell to cell and even in the same cell and hence one speaks of the probability of a neuron firing given a certain stimulus. additionally the neurons from sensory organs fire pulses at a frequency that increases with the strength of the stimulus. furthermore, the data from sensors is processed in layers of neurons lower layers have rapidly firing neurons whule higher layers fire at much lower rates.
you also have to consider the fact that the brain is actually a complicated network of "recurrent" neurons meaning that the output is fedback as an input and this is different from simple computer gates such as AND gates or XOR gates it is similar to counters may be but obviously on a very bigger scale. one more point is that recurrent neural networks have built in memory that enables the pattern recall and recognition and so the study of the brain as a binary system is very complicated and will fail to explain how the brain works.
on the macro scale the human brain operates as a bayesian inference engine more or less I mean when it comes to thinking and inference i.e. it relies on probabilities and knowledge gained from past experiences to deal with current problems and new data

human brain is strictly digital device using defined action potentials (0 volt as logical 0 and specified (fixed) voltage potential as logical 1). these two potentials work same way as complex logic gates systems. brain processes all types of analog-like variations (signal amplitude or response strength) as very short time based sums of logic gates operations. there is no other applicable description of brain functionality

Welcome to Biology.SE! This seems to conflict with the accepted answer and could easily be mistaken for an opinion rather than an answer based on facts.  Consequently, I think will find that supplying supporting references (primary literature is best) will help your answer receive a more favorable response. ——— You may also wish to take the [tour] and then consult the help pages on the standards for additional advice on [Answer] effectively. Thanks!


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Is it possible to process electrical signals from the brain and interpret the results as exact thoughts?
If the brain uses extremely low voltage signals to communicate (from what I understand around 100 mV), what sort of breakthroughs would be necessary to intercept these signals and interpret them as exact thoughts? I know we interface with the brain's electrical field through already at a much higher level, but what is stopping us from being able to interpret it more precisely?

No, it is not possible at all. There is no technology whatsoever at present that can "read" a thought. Only a brain can interpret electrical impulses as thought. I can imagine nothing that can even foreshadow this.

I think it is not possible for one brain to interpret the thought pattern of another brain.

Define "thought", please, and "exact". You can pick up EEG signals for creating brain-machine interface and move your PC cursor around, is that good enough?

The brain activity is electric and chemical. The male adult human brain contains about 86 billion neurons (Azevedo et al). There is about 100 trillion connections between them. Solving a puzzle like that is not easy..

what sort of breakthroughs would be necessary to intercept these signals and interpret them as exact thoughts?

What you are referring to would be called solving the neural code in neuroscience. With today's methods, it is probably not possible.
Consider electroencephalography (EEG). It records the electrical activity of the brain. Ag/AgCl sensors are placed along the scalp (typically 64-256 in research settings). When about 50,000 parallel neurons fire simultaneously, a change in a recorded signal can be seen. While the time resolution is about 1 ms for EEG, the spatial resolution is several centimeters (it is not easy to find which areas produced the recorded signals; it is an inverse problem). A newer technique, called magnetoencephalography (MEG), is becoming more and more used but is expensive. It records the magnetic fields related to the electrical activity and allows better localization.
Is there other complications? Well... lot's of them. Blink your eyes during the recording and there will be a major artefact masking the brain signals in most channels (10-100x greater in amplitude than the brain signals).
Anyway, you would probably be interested in the new research involving the use of machine learning techniques: it has been possible to decode the contents of dreams, reconstruct what a subject is seeing, etc. The best papers have been published by Science, Nature, and PNAS, so using their search engines with the keywords decoding and brain should allow you to explore the topic easily.
PS. I did not have time discuss fMRI; someone else can may be do that..

I disagree to some extent. If you read "thought" as "intention to perform a motor action", then BrainGate (http://braingate2.org/) has been reasonably successful.

Very thorough! That is precisely what I was referring to when I mentioned, "interpret as specific thoughts". In essence, understand the function the brain is performing as specifically as possible. This is part of what fascinates me about machine learning. I will take a look at those sources! I am curious as to how fMRI works and how accurate it is compared to other methods. I have read articles that employed this method.

Possibly but not for a very long time.
Professor Gallant is in the embryonic stages of researching this and is having some success. Right now the computer needs a pool of possible images to draw from to make the possibilities small enough to search and the image resolution is rough at best. But the fact that even something as simple as color of a remembered image can be read means it is possible. But that is space shuttle level technology while we are still at the stage of strapping cardboard wings to our arms.
In all likelihood even when this technology is mature the machine will have to learn your brain similar to how a speak to text program has to learn your speaking patterns, before it works. To me this is hugely interesting for the possibility of seeing what parts of our brain architecture is universal and thus likely genetic.
I am including two other sources for the research but I warn you they are behind pay wall. http://www.nature.com/scientificamericanmind/journal/v25/n6/full/scientificamericanmind1114-40.html
http://www.sciencedirect.com/science/article/pii/S1053811910009109


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What are the total number of action potentials in the human brain?
Is there an approximate figure of the total number of action potentials in the human brain? It's my understanding that there are ~ 60 billion neurons in the brain with ~ 100 trillion connections between them. Plus there are graded responses between those connections. Is there an estimated figure for what the total might be?

If firing rate is from 1 Hz to 200 Hz, 100 trillion to 20 quadrillion synaptic firings. Neuronal (say, measured from soma) firings  will add up to 86 billion to 17.2 trillion action potentials per second.
It important to remember, that synaptic firings "sum up" in soma or interfere between each other, so the are more of those.
Read more: http://neuroblog.stanford.edu/?p=4541

Awesome, thank you! I will check out the link.


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Is it possible for a human to get rabies from a rabies vaccine meant for dogs?
What would happen if a human was injected with a rabies vaccine meant for dogs? I know vaccines can contain weak or dead strains of the virus, but is it possible that the human could become infected with rabies from a vaccine meant for dogs? My thinking is that maybe a dogs' immune system is more suited to deal with a weak strain of rabies that would otherwise infect a human.

The question here is if the vaccines used in human and dogs are different. Or if there are really big differences between the immune systems of both, which I doubt. Generally living strains are weakened so that they trigger an immune response but not the full blown disease, which would be fatal in the case of rabies.

It would depend on which vaccine you're talking about, as there are several. Some use attenuated strains of the Rabies virus, others use killed, and some are recombinant glycoprotein vaccines. Here is a list from the CDC of all the rabies vaccines available in the US in 2011 (I wasn't able to find anything newer). Generally speaking, through, one would expect the FDA in the US and the relevant authorities in other companies to require vaccine manufacturers show that their product is safe in other species, in case of accidental exposure, such as you are talking about here. This is especially true of something being given to an animal that is quite often a family pet.
If you think you've been exposed to any type of medication which has not been prescribed for you, including dog rabies vaccine, you should seek medical attention immediately, if not sooner, but based on my experience in the pharmaceutical industry and dealing with regulatory agencies, you should be pretty safe, as the regulations surrounding vaccines are quite stringent.

Vaccines can generally be considered safe for this case. The charges are tested individually and are not released if there is any doubt on their quality or safety.

@Chris, I think the question then becomes: Is it possible for humans to get rabies from human attenuated rabies vaccine?

@CRags that's what I was trying to address, in part - pet vaccines have to be tested for possible transmission to humans. They wouldn't possibly use potentially contagious vectors in a vaccine meant to prevent disease in both species.


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What is the difference between gene and CDS annotations?
I have a bunch of sequence files fetched from the EBI ENA and I'm trying to find the end of the 5' UTR for specific genes.
The UTR itself doesn't seem to be annotated in most sequence files I have. My original idea was to simply use the CDS annotations, as the start of those should clearly identify the end of the 5' UTR. But I also noticed gene annotations in many of the sequences, most of them starting and ending at exactly the same locations as the corresponding CDS annotation. But there are also cases where there are small differences between the gene and the CDS annotation.
So I'm wondering how exactly the gene annotation is defined (if there is actually an agreed definition) and how the gene and CDS annotations are used in practice.
Which annotation would be the most reliable to identify the end of the 5' UTR?

Realistically speaking, there's no guarantee that UTRs are in a given gene definition unless you're looking at a well annotated species (e.g., mouse or human). There are many species for which there is simply very little information on UTR sequences.

CDS is based on ORF prediction and unless the protein product is known it is classified as an mRNA for a hypothetical protein (Refseq id: XM_*).
As Devon Ryan said sometimes UTR ends are not accurately annotated. If you are interested in finding the 3' end of 5'UTR then the problem is basically to find the translation start site. You can have a look at ribosome profiling experiments or try doing eIF2 CLIP-RNAseq (I don't think it has been done); peptide sequences may not be of help because N-terminal region in many cases, gets clipped.
If you are interested in finding the 5' end of 5'UTR then the problem is relatively simple. You just need to do a 5'-RACE followed by Sanger sequencing (this would work in most cases or you can do a deep-RNAseq).
There are official GTF files that provide the most reliable annotations. For human I would recommend GENCODE.
In the annotations the term Gene denotes the entire DNA region that is responsible for all of its RNA products (splice variants, alternate start/termination etc). Other features include Transcript, Exon, CDS, UTR and in some cases translation start site is separately annotated. CDS comprises of just the protein coding region.
You should read more about the GTF/GFF annotation format.


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Is there a database of known riboswitches?
I'm looking for sequences and annotations of known riboswitches, but so far I haven't found a resource that actually fulfills my requirements. The best database I found so far is Rfam, which has entries for many riboswitch classes. The biggest drawbacks of Rfam for my case are that it doesn't contain any information about the expression platform, only about the aptamer. I'd like to know if a riboswitch is translational or transcriptional, and where the terminator/Shine-Dalgarno sequences that are regulated by the switch are. Another limitation of Rfam is that I can't easily see which sequences are validated biologically in some way, and which are just predicted.
Is there a database of riboswitches that also contains information about the expression platform?


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Do Penicillin based antibiotics affect birth control?
I wasn't sure whether to ask this question on Biology or Chemistry Stack Exchange, since it is really biochemisty, but this is something that's been puzzling me.
Most pharmacists (all that I've encountered) tell you that antibiotics decrease the effectiveness of birth control. There are side-effect warnings on all Penicillin based antibiotics that say they decrease the effectiveness of birth control, and advise you to use a back-up method when taking antibiotics.
However, most health organization websites (Planned Parenthood, Mayo Clinic, NHS) explicitly state that ONLY two antibiotics have been shown to sometimes decrease the effectiveness of birth control-- Rifampicin and Rifabutin.

NHS Website: http://www.nhs.uk/conditions/contraception-guide/pages/antibiotics-contraception.aspx

Yet websites of Pharmacies like Walgreens or CVS say that to a lesser extent Penicillin based antibiotics can decrease birth control effectiveness, or in general remain vague about antibiotics affecting birth control :

http://www.walgreens.com/topic/faq/questionandanswer.jsp?questionTierId=600006&faqId=600022

So--do Penicillin based antibiotics affect birth control?

As I recall from pharmacy teaching, this is one of those things where it was theorised that it might happen due to damaging gut flora which reduces reuptake of oestrogen in the gut, therefore physicians took a cautious approach and gave advice to use barrier methods in addition when taking antibiotics and the OCP

Evidence on the association between antibiotic use and combination oral contraceptive (COC) failure remains controversial, with recent studies reporting no evidence to support decreased effectiveness of birth control with the use of antibiotics except rifampin and rifabutin.
The reasoning is antibiotics might interfere with the effectiveness of COCs by decreasing steroid hormone’s plasma concentrations by hepatic microsomal enzyme induction or inhibition, interference with enterohepatic circulation of
COC metabolites, interference with absorption from the GI tract, competition between two drugs for the same metabolizing enzyme, alterations in plasma protein binding, induction of an opposite physiologic effect, or increased urinary or fecal excretion of the contraceptive.
As you stated, the strongest evidence is for rifabutin and rifampin: a significant decrease in the hormonal levels was noted in women taking rifampin even after a single dose.  Dirithromycin slightly decreased plasma ethinyl estradiol levels, with questionable clinical importance. A recent study in the Netherlands did find a relationship between the use of antibiotics and breakthrough pregnancy in a population-based prescription database; also, individual patients do show large decreases in the plasma concentrations of ethinyl estradiol when they take certain antibiotics, notably tetracycline and penicillin derivatives.
Because of earlier studies, anecdotal reports, and the above (it's not possible to identify whose levels will drop with antibiotic use), a cautious approach is advised. Physicians and pharmacists (80-90% of both) still lean towards believing that broad-spectrum antibiotics decrease the effectiveness of COCs, and continue to advise the use of back-up contraception.
The tide is shifting, however, as new studies come out. Here are a few excerpts of recent studies:

Available scientific and pharmacokinetic data do not support the hypothesis that antibiotics (with the exception of rifampin) lower the contraceptive efficacy of oral contraceptives. (J Am Acad Dermatol 2002;46:917-23.)

Since dermatologists treat acne with antibiotics, and a significant percentage of these patients are young women of child-bearing age, they certainly have a vested interest in knowing if this is true.

Rifampicin and griseofulvin induce hepatic enzymes and do appear to have a genuine interaction with the COCP, leading to reduced efficacy. The situation with the broad-spectrum antibiotics is less clear. There are relatively few prospective studies of the pharmacokinetics of concurrent COCP and antibiotic use and few, if any, demonstrate a convincing basis for any reduced contraceptive efficacy.
We did not find an association between concomitant antibiotic use and the risk of breakthrough pregnancy among COC users. However, due to limited power and potential carryover effects, findings from this study cannot rule out an elevated risk of COC failure among antibiotic users. (2011)

So, the answer is (except with your noted exceptions) the penicillin-class antibiotics probably do not interfere with effectiveness of COCs. However, one unwanted pregnancy is one pregnancy too many, and the use of a back-up method is not a huge deal (just ~14 days).
Until more and larger studies demonstrate a lack of interaction between most antibiotics and COCs, this will likely be the advice people continue to receive. When you look at the risk to benefit ratio of back-up, it's probably the wisest course for people prescribed a short course of antibiotics. It is more significantly problematic for people prescribed continuous antibiotic use for acne, Crohn's and other conditions/illnesses.
Oral contraceptive efficacy and antibiotic interaction: A myth debunked
Interaction between broad-spectrum antibiotics and the combined oral contraceptive pill: A literature review
Antibiotics and oral contraceptive failure — a case-crossover study
Are antibiotics related to oral combination contraceptive failures in the Netherlands? A case-crossover study
Drug interactions between oral contraceptives and antibiotics.
Survey of pharmacists and physicians on drug interactions between combined oral contraceptives and broad-spectrum antibiotics.

Great answer. Thank you for taking the time to type up such a thorough response.


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How could cyanobacteria survive the anaerobic conditions of ancient earth?
I was reading about cyanobacteria and came to know that they are the first organisms that filled the atmosphere with oxygen around 2.3 billion years ago but then I realized that they themselves are aerobic and I couldn't understand how an aerobic organism would be able to survive the oxygen poor atmosphere in the first place to make enough oxygen that filled the whole atmosphere and caused almost all anaerobic organisms go extinct

Kindly shorten the title :/

Suggest something please

Where did you read that they were obligately aerobic?

I am pretty sure they are as nowhere it is mentioned that they are facultative aerobes

The first cyanobacteria were probably anaerobic, and this matter seems to be a hot topic of contemporary research. A recently published studya that performed a phylogenetic analysis of various Cyanobacteria genomes states:

The most parsimonious inference from these data is that the last
  common ancestor of the Cyanobacteria did not use oxygen and that the
  three classes [of Cyanobacteria] acquired aerobic respiration independently after their
  divergence. The absence of aerobic respiration in ancestral
  Cyanobacteria suggests that abiotic oxygen sources on early Earth were
  insufficient to allow for its evolution until after the appearance of
  oxygen produced by photosynthesis.

Reference
a Soo, Rochelle M., et al. "On the origins of oxygenic photosynthesis and aerobic respiration in Cyanobacteria." Science 355.6332 (2017): 1436-1440 (http://web.gps.caltech.edu/~wfischer/pubs/Sooetal2017.pdf)

So, were the common ancestors photosynthetic themselves?


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Biological data source of trees
I need some biological data for many types of trees, but I can not find good source of this on internet.
Where can I find following type of biological data of any tree:

Biological Profile
Taxonomy
Distribution
Cultivation
Edible Medicinal Parts
Phenology

Wikipedia: Vascular Plant

All trees are either gymosperms or angiosperms

Wikipedia: tree

Wikipedia: Medicinal plants

The Ecological Data Wiki search for Woody Plants is a good start for some nice datasets. There is also the USDA Plants Database which has information for every plant in the U.S. Woody species are well represented with lots of species specific info. These can be downloaded handily with an R package.
Looking for occurrences? Put the species name into GBIF to get historical records of where and when a species was found. This has an R package as well.
Want distribution maps for all trees in North America? Someone has done that for you here.
Phenology? The National Phenology Network.
Edibility? I've never come across a specific data source for this. But the best reference I've used is the Handbook of Edible and Poisonous Plants of Western North America. It's an amazing book with years of research put into it. It does not have any pictures nor a key to identify plants, but it does have information on pretty much every plant in the Western U.S. at least at the genus level.