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Why did many species of Homo and their ancestors evolve in East Africa?
One thing I find interesting about the theory of evolution is the idea that Homo Erectus and Habilis evolved in Africa, began to spread around the globe, then was superseded by Homo Sapiens Sapiens which also evolved in Africa. Why did the vast majority of Homo species evolve in East Africa first?  What was it about Africa which encouraged speciation more than other areas?

Neanderthals probably evolved in Europe, not Africa, raising from a common ancestor that was present in both regions.  See The origin of Neandertals

Hi mate, thanks for this. Didn't know Neanderthals likely evolve in Europe, this changes my perspective somewhat.

Denisovans and floresiensis also probably evolved outside Africa. But all had a common ancestor that was African, and the division into "Homo" vs other groups is a little arbitrary

because of the trees, lizards evolved on the ground, and the apes lived on the trees, it wasn't until the extinction of the dinosaurs, that some of this apes returned to the ground and spread in the world. Africa was the safest place on those times.

Interesting idea, can you back this up with any studies? Don't think apes and dinosaurs had any overlap, first mammals were roughly 60 million and dinosaurs died out at a similair time. Also trees wouldn't explain the speciation, trees are found everywhere.

I know our shared ancestor with the opossums is contemporary to dinosaurs, but opossums are terrestrials which contradicts with my theory, its more likely that after dinosaurs went extinct other mammals became his predators and that's why they climbed the trees, maybe those predators existed in Africa only.

The main basis of my question want to do with the original evolution of Homo, but more to do with why East Africa was the hub of many stages in evolution. So as my question details you had Erectus and Habilis evolve in a very small area when they could have evolved ANYWHERE, then you had Homo Sapiens Sapiens evolve AGAIN in East Africa, even though there were Neanderthals in Europe too that could have evolved instead.

its more likely that homo sapiens killed them all, living outside Africa was probably relatively easier, away from danger, while in Africa homo sapiens was struggling to survive after descending from trees. that might be the original reason why many cousins left in the first place.

The question is based on a false opinion but I'll get back to that at the end.
Humans are still evolving

Why did all species of Homo evolve in Africa first?

Humans are evolving all around the world. Evolution is not a thing that stops once we made the arbitrary decision of naming a lineage. When we first named humans, Homo sapiens sapiens, indeed the lineage was living in east Africa.
Humans is a lineage of Old World Great Ape

One thing I find interesting about the theory of evolution is the idea that Homo Neanderthalis evolved in Africa

It would help if you could explain why you find that particularly interesting. It is possible that some falsy teleological view of evolution you may have might push you to make some unexpected conclusion from the idea that first Homo lineages lived in Africa (but might be wrong in your understanding of evolutionary processes). In any case, you can find an very introductory course to evolutionary biology here if you're interested.
If humans were a species of feline, it could have evolved elsewhere (it would look very different to what we currently call humans of course) but humans is a lineage of old world great ape. Old world great ape lived mainly in Africa. There is not much more to say about it.

why Africa did Africa encourage evolution more than other areas of the world?

Africa is a continent. It is big! You can find pretty much any biome in the world in Africa (except toundra and taiga if I am not mistaken). Did the specific location where humans lived in Eastern Africa affect their evolution. Yes, the evolution of a population is always affected by its surrounding. For example, the presence of large game was probably a big selection pressure for cooperative hunting (but you can/could find large game everywhere).
It will be near impossible to answer in the general sense. A lot of things happened in human evolution. Even if you tackle down to a single trait, it will be hard to tell you what would have happened if the world would have been different because it was not. (WorldBuilding.SE welcomes questions like "if it was like that what would have happened?").
Origin of Homo lineages
There are a number of named Homo lineages, some of them have not lived in Africa. This include for example Homo floresiensis.

The reason I described it as interesting is that to my understanding many significant stages in human evolution (the majority: Australopithecus, Homo Erectus, Homo Habilis, Neanderthals, Homo Sapiens) occurred in Africa; however, I'm well aware evolution is occurring all the time. My question was why Africa did Africa encourage evolution more than other areas of the world?

PS, I'm well aware there are exceptions to the rule and certain species evolved elsewhere.

I edited the post to try to address your comment. But I am afraid no one will be able to say much to such question (not so much by lack of knowledge but more due to the semantic of your question). But we'll some others might find more things to see that may be of interest to you


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What is Hamilton's rule for multiple generations?
What is Hamilton's rule as it applies to multiple generations?  Is it that the lineage success given up by the actor must be exceeded by the lineage success acquired times the relatedness between actor and acquirers?  How is this represented?

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Is agriculture really a net contributor of greenhouse gases?
A lot of scientific studies and credible sources indicate that agriculture is one of the major contributors of greenhouse gases. The exact numbers seem to vary a lot, I've seen everything from 8% to 45% of global greenhouse gas emissions.
What makes me unsure how to really interpret these numbers is the fact that the process of growing feed to feed livestock, raising livestock, and then eating that livestock, is a cycle. The very same plants that the livestock is eating has during the course of its growth acted as a sink, i.e. absorbing carbon dioxide from the air. This is totally different from pumping oil out of the ground and burning it, which is (in the relevant short term) only production of greenhouse gases, without the sink.
I would assume that any serious study on greenhouse gases would factor in the entire cycle of absorption through animal feed and release back into the atmosphere, yet none of the studies I have seen say exactly how they arrived at the emissions.
Aside from the fact that oil is used in agriculture, when only considering the actual gases released from animal farming vs plant farming, it doesn't really make basic sense to me that there could be a net production of greenhouse gases - where did the surplus come from?

The issue is that it is not always a cycle, when you drain wetlands or burn forests to make more farmland that's not a cycle that is permanent change. A change that can continue having effects for centuries. Then of course you have petroleum fuel used to run tractors and the production of fertilizer which are often not cycles either but pure extraction.
One of the reason the number varies so much is because of disagreements about what falls under agriculture, does the fuel used to run a cargo ship moving bananas count? How about mining equipment used to extract minerals used to make fertilizer? Many simply forget to include things like peat bogs or changes in soil bacteria.
For instance draining a peat bog releases tremendous amounts of carbon, as a functioning net carbon sink is changed into a carbon producer. Sometimes this happens as water is diverted to farmland but often it is done just on purpose to get more farmable land. Exact impacts vary from place to place leading to wide ranges of estimations further complicating it.

Wow, changes in soil bacteria was something I didn't see before... just got even more complex! Maybe I should have been more specific about what I'm really interested in is the claim by some that meat, dairy and eggs are a major (or even THE major) contributor to global warming... but then you need to know how the emissions would change - and a banana cargo ship clearly is still a banana cargo ship even in a 100% vegan world. If we replace meat calories with vegetable calories, wouldn't we sort of replace the farm animals emissions by our own instead (more fuel for harvesting plants, etc)?

Should I perhaps create a new question more along the lines of "How big is the difference in greenhouse gas emissions between today's diet and a 100% vegan diet?"? Not sure if the Biology StackExchange is even the correct place for such a question - it almost seems to be a mix of chemistry, physics and biology?

I reckon this is worth a new question, but off the top of my head, I think there's a figure that it takes 4kg of grain to produce 1kg of meat, or equivalent calorie content. Then methane is a major greenhouse gas and apparently cows are gassy animals, so still very complicated...

@OliverHouston Methane is a major greenhouse gas, but isn't stable in an oxidative atmosphere. We can't ignore it, but it doesn't accumulate. Water vapour (produced when methane breaks) is similar - it's by far the biggest contributor to Earth's greenhouse effect, but the atmosphere cannot really hold more of it - it spontaneously condenses out of the atmosphere.

@BadCash The whole thing is absurdly complex; it can't really be covered in a couple of SE questions. Consider that as carbon dioxide content increases, plants grow faster (lack of carbon is limiting the growth of most plants, not lack of energy; higher temperatures also promote growth, though only up to a point); this may very well cause agriculture to be more efficient (more food per square meter, which means less work for the same amount of food) or less efficient (more weed growth, disease...). Is transportation of meat cheaper or more expensive than fruits, vegetables, grains?

Thanks @Luaan, hadn't heard that methane oxidised in the atmosphere. I think some of the specifics e.g. does meat/crops produce more CO2. But I agree, it is hugely complex when you take into account shipping/growing methods, i.e. is it better to get local veg grown in a heated greenhouse, or naturally grown veg shipped from warmer climes?

@OliverHouston Transportation is ridiculously cheap, especially for non-perishable goods - I don't remember the exact numbers (and can't find the reference), but I recall that the break-even point is somewhere in thousands of kilometers over land (ships are pretty much unlimited). There is always something that can be produced and distributed locally cheaper than imports, but that's rarely a consideration - the main decision is political (self-sufficiency, nationalism, ...). But do consider that we mostly feed the animals with crops, so those can't be more efficient than crops, at least.

@BadCash the type of farming is often more important that what is being farmed, for instance small scale pig farms can often be closed cycle while it is nearly impossible to do with large ones, organic farms can pollute more than industrial due to yield, Many farms are horribly wasteful just becasue of where they are, a farm in kansas can be way more efficient than one in california. Even something as simple as what feed is used matter, in the US we favor corn as feed but not everyone does this, many countries favor barley which is more environmentally friendly

@OliverHouston - how much food per 1kg of meat depends on animal: short living, fast-growing chicken requires like 2 kg of cheap food (insects and leftovers), pig requires more, cow requires 10 kg of grains (suitable also as food for humans) and grass.

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Why are cells affected by time?
We as individuals die when we get old. But why are cells affected by time? We are constantly providing energy to the cells through food, but the cells die after a certain time. Why does this happen?

Anabolic processes vs Catabolic Processes. When you search on Google. what happens to cells overtime, there are many articles you can read through answering your question.

@Kamal I rolled back your edit: please don't ask people to upvote you. Users will upvote if they think the question is useful.

Sir if I do not get any vote stack exchange will ban me.

Individual cells don't live forever because they are damaged by their environment, for example by chemicals, radiation and mechanical wear and tear, or by other organisms (see this review). In multicellular organisms, such "worn out" cells are typically dismantled by programmed cell death and new cells are generated to take their place.
The life span of animal cells varies widely depending on their location and function. For example, epithelial cells lining the skin and intestines are exposed to a harsh environment, and consequently live only a couple of days. At the other extreme, neurons, which are safely lodged in the protected brain tissue, can live as long as the individual (or even longer).
Note that the life span of a given cell is very different from replicative age, which refers to the number of divisions a cell lineage has undergone, measured from some progenitor cell. Most animal cells are allowed only a limited number of cell divisions (known as the Hayflick limit) and thus their lineage is "mortal", while that of microorganisms are not.

Short answer: Not all cells do age and die, many symmetrically dividing unicellular cells are essentially immortal. In asymmetric species the occurs in many lines from the retention of old worn out cellular machinery. Triggered limited cell life only evolves later as organisms need to regulate multiple cells. It is likely a side effect of having cells specialize. However this origin is not conclusive, this is actually a vigorously debated subject in biology right now.

Can you cite some example of species where cells are considered immortal? I think life span is difficult to even define for unicellular organisms with symmetric cell division --- in one sense, such cells "die" in each cell division. For species with asymmetric division like budding yeast, cells generally age and die over time I think. See for example https://www.nature.com/nature/journal/v183/n4677/abs/1831751a0.html

"unicellular cells are essentially immortal" there's a search bar at top right corner (if you're on desktop version). Type "do bacteria die of old age?", hit enter and see what you get...

@another'Homosapien' Good catch I'll add a qualifier. symmetric dividing unicellular cells are essentially immortal. many asymmetric are not.

@Roland http://www.cell.com/current-biology/fulltext/S0960-9822(13)00973-1?_returnURL=http%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0960982213009731%3Fshowall%3Dtrue and https://www.ncbi.nlm.nih.gov/pubmed/20537537

@John, both of those studies actually claim that the cells studied have asymmetric cell division (defined by the old/new growth pole) and still do not age. That is very different from your statement "many symmetrically dividing unicellular cells are essentially immortal". My point was that the concept of cell age is meaningless if cell division is fully symmetric, as no cell is can be "older" than one division. (If symmetrically dividing cells would age and die, the species would die out ... )

@Roland I was just giving links for immortal lines, There is not a clear division between symmetric and asymmetric division it is a spectrum just like everything else in biology. Some cell lines are capable of both E coli is one of those. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4010982/.

Regular cells are built to expire themselves when they detect too much damage (taking one for the team).
There are plenty of examples of cells that refuse to do so. Often, they're called cancer cells.

I love questions like this! my reasoning is that while cells certainly have processes and mechanisms that exploit entropy, the bitter reality is that eventually something like our own cells will be subjected to entropy and will ultimately die and be disassociated. Every second a cell produces ATP to survive it is put under more and more oxidative stress and this is why cells age and ultimately die. It is also why less metabolically taxing lifeforms like a plant, can live for hundreds of years, as opposed to a mouse, which lives for like 3 years (an animal with a high metabolism)
my english is terrible so in short: energy is oxidation, oxidation reactions are entropy favored, this causes things to age. higher metabolism = more oxidation = shorter lifespan. Plants dont get up and run so they can live longer than animals which do

Sorry, but it sounds like you don't understand entropy. All reactions are driven by increasing entropy (that's the second law of thermodynamics) and oxidation is not special in this regard. And this has nothing to do with (oxidative) damage to cells. Also, the life spans of animals and plants is irrelevant here --- the question concerns the cell level.

Think of it this way:  If you took the whole sum of reactions taking place in a cell over 24 hours would
That Total
Change in Gibbs free energy be positive or negative ? It is the natural progression for ordered systems to evolve to a disordered state. Perhaps I am wrong about the oxidative stress in a mouse vs that of a plant, but you are being pedantic and not looking at the bigger picture. Entropy is the sole reason why TIME MOVES IN ONE DIRECTION and it applies to everything cells, planets, laptops, etc.

No, I think your bigger picture is wrong. The entropy law does not explain why cells degrade and die, because cells are not closed systems. As long as a cell has an energy source, it can maintain its state forever as far as thermodynamics is concerned. Cells die for other reasons.

the question is why are cells effected by time? Don't reduce biology to "all or nothing" level of thought, oxidation is oxidation, regardless of its Intent (metabolic oxidation does release damaging radicals regardless of its intent ) it drives the dG to become even more negative as well as other external sources etc. you may bring in glucose for example but I am talking about the sum total dG. If not entropy to explain why time moves in one direction, then what do you think is the reason cells are effected by time?


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What is this arthropod?
It is approx 2cm long and was discovered in house after a bush walk & BBQ at Riverside Garden Reserve in Mandurah, Western Australia. It has 6 legs.
Thanks! :-)

Welcome to Biology.SE. I edited your question slightly for improved readability. Please feel free to further edit.

It's almost certainly a beetle larvae/grub of some sort, but I'm afraid I don't know what species!

Lyn, I took the liberty to reedit your post to improve presentation.

This is a Sawfly larvae, and is most likely of the species Perga dorsalis or Perga affinis. The larvae you depict appears to be quite young, but as it matures it'll gain a much darker color, and, depending on whether it's P. affinis vs. P. dorsalis, the abdomen will grow fairly long.
I imagine the developmental progress of your larvae is somewhere between the two following larvae.

A few more images:


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Why are proteins always made in N to C direction?
Why are proteins always synthesized from the N-terminus to the C-terminus? Can there be any “reverse” peptide-bond formation to synthesize proteins in the C-terminal to the N-terminal direction?

Are you talking about natural processes only, or also about chemical ones? Because chemistry really doesn't care (in either case actually) and can do both directions. Nature just stuck with the direction that was easier 'to implement'.

@nicolai I think the OP wants to know about natural processes (lest this question would be better for chemistry.SE). I tried to make the concept as clear as possible in my answer, yet it basically comes down to what you say ;)

Actually 3′→5′ synthesis is possible … synthetically: http://www.news-medical.net/news/20120830/DNA-synthesis-in-the-3e28099-and-5e28099-direction-possible-using-new-template-directed-method.aspx

I have edited your question to remove the irrelevant and incorrect preliminary statements.

Nice question! As you already know, DNA is always shown in 5'$\rightarrow$3' direction because it is always synthesized in this direction (amino acids are joined by CO-NH peptide bond). So, a polypeptide looks like this (source):

In fact, if you just look at the polypeptide in the reverse direction, you could view it in C terminus to N terminus direction. But we don't do so because that is not the conventional direction of the polypeptide's biosynthesis.
Tracing the Roots: To know why there is no "reverse" peptide bond (NH-CO), we first need to know how peptide bonds are formed in polypeptides. Polypeptides are formed in ribosome, and the process of formation of peptide bond occurs in the peptidyl transferase complex of ribosome. Since ribosome is a ribozyme, this reaction is also catalyzed by the catalytic sites of RNA (i.e. 2'-OH) instead of proteins. See the image below for the mechanism (from Marina V. Rodina):

As visible from the diagram, nitrogen (in -NH2) from acceptor tRNA (A site) attacks the ester linkage at the peptidyl tRNA (P site). Carboxylic carbon cannot attack the nitrogen (for "reverse" bond formation) because it is already in ester linkage. One might ask then "if the nitrogen was joined to tRNA at P-site, the carboxylic carbon could have attacked on amino acid at A-site. Why is amino acid not joined to tRNA by the amine nitrogen?" To know why it is so, lets go a step further and see how tRNAs are charged i.e. how aminoacyl tRNA synthetase works. Aminoacyl tRNA synthetase charges tRNA in a two-step reaction. For displaying mechanism, I will take the example of histidyl-tRNA synthetase (diagrams from Proteopedia):

amino acid + ATP → aminoacyl-AMP + PPi
→
aminoacyl-AMP + tRNA → aminoacyl-tRNA + AMP

As is clearly visible now, whether amine nitrogen or carboxylic carbon will attach to phosphate of ATP is decided in the first step. See the image again:

You might ask that since nitrogen (in -NH2) also has a lone pair of electrons, it could also make a nucleophilic attack on the phosphate group, similar to the oxygen (in -COOH). Why doesn't this happen then? This cannot be accounted for by saying that the amine nitrogen is far away from the reaction site (look at the diagram again, and pay attention to how close the carboxylic carbon and amine nitrogen are. If we could move the amino acid even a little bit, this reaction could easily occur). Well, here's the twist: the optimum pH of this reaction lies near pH 6 i.e. in the acidic pH range (Lui et al, 1978). Now, as we know, under acidic pH, -NH2 exists in the protonated form i.e. -NH3+. In this condition, nitrogen lacks lone pair and thus cannot attack phosphate on ATP. Thus, it is not possible to attach amino acid to AMP via -NH2 group and, thus, form a "reverse" peptide bond. I hope this depth of the answer would be enough to satisfy your curiosity :)

Two comments. 1. You are explaining the directionality in terms of the way the activation of the amino acid occurs today. As long as you make that clear, that is fine. However the question of why it evolved that way is not answered. 2. Your arguments about ionization of amino groups at low pH do not hold water. The pH optimum of the charging reaction is irrelevant. What is relevant is the pH under which the reaction occurs, which is the cellular pH of, say 7.4–7.6. And if the amino group lacks a lone pair there, how does it manage to make a peptide bond, as per the first diagram?

@david 1. It evolved this way because evolving in the other direction was not possible (again, due to pH, I don't know if you understood what I wanted to convey through the pH factor) 2. I don't think you read Lui et al, the reaction does occur at a rather acidic pH (to make it faster). I don't know about peptidyl transfer reaction, most probably it occurs at cellular pH (about pH 7.5 or because the reaction occurs in almost isolated condition. Also, these are all suggested mechanisms, nobody has seen how the reaction actually occurs.

All the stages of protein synthesis occur at the same pH in a cell. If a particular reaction requires an ionization state of a group in the substrate different from that in aqueous solution (e.g. an unionized amino group in the peptidyl synthetase reaction) that is provided by the enzyme environment. In evolutionary terms, when one assumes there was a non-enzyme catalysed reaction first, you still have a problem. And one unexplained assumption of your answer is that activation of amino acids for attachement to tRNA has to be via ATP (not acetyCoA or something else).

@david the truth is that we don't yet know the true reaction mechanism, I used histidyl-tRNA synthetase as an example. The main point is that the $\alpha$-amino nitrogen is in the protonated form; if the cell can't provide this proton, the enzyme must. I did not explain acetyl-coA or other residues since the major (and I think only) substrate for aminoacyl-tRNA synthetase is ATP (I don't know if you have studied about aminoacyl-tRNA synthetase, or maybe there are some other enzymes about which I don't know).

This is just in addition to the other answers; some somewhat relevant thoughts I had.
Interestingly, even non-ribosomal peptide synthesis seems to proceed N to C terminal. Given the modular nature of such enzymes, synthesis in the reverse direction doesn't seem to be outside the realm of possibility, though I haven't found any known examples.
This might be a stretch as a counterexample, but if you consider the biosynthesis of the tripeptide glutathione, a γ-peptide bond is first formed between cysteine and glutamate, after which glycine is attached to the carboxyl group (ie C-terminus) of cysteine with an α-peptide bond.


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What is allele-specific gene expression?
I read somewhere that the two different alleles which we (and other species) inherit from our parents are not expressed equally in our cells. Which genes show allele-specific expression? How and why?

There are a few well known examples of allelic exclusion (which is what you've described):
In females (human and probably other mammals too) one of the two X-chromosomes is silenced (shut down) during embryo development. This means that some cells have one allele (from maternal X) active, while other cells have the other one (from paternal X) active. The actual mechanism behind this is quite complex, but ultimately results in the complete epigenetically-controlled prevention of gene expression from one X-chromosome. This is necessary because otherwise females would produce twice the amount of all proteins on the X-chromosome compared to males.
Another well known example relates to the genes that lead to the building of the B-cell receptors and antibodies. During maturation of the B-cells different segments of these genes are rearranged in a process call VDJ recombination. In order to make sure that the cells produce only one kind of B-cell receptor/antibody one of the two alleles for these genes is silenced after a certain rearrangement step has taken place.


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Synthetic life creation - status of attempts
First I apologize for my incorrect English and for lack of modern knowledge regarding the subject (I studied biology a long time ago).
I'm interested to find out:

if there were successful attempts of life creation from conditions that we suppose were dominant on early Earth
if there were not, are such attempts still being conducted?

To clarify, by "life creation" I mean the accidental creation of entire organism in conditions of organic compounds, water, electricity, radiation etc. being present (Abiogenesis).
If this is already answered here, I'm sorry for asking, I have researched this, this, this and this question with no luck.

You might be interested in this answer: https://biology.stackexchange.com/a/56363/6307

There have been lot's of attempts, no success so far, a few groups are still working on. However, many steps forward have been done in the last decades.
Starting from the Miller experiment which demonstrated that the building blocks of life chemistry can be obtained starting from fairly simple chemical compounds. Following, Luisi and Szostak showed that 1) nucleic acids can polymerize without the help of enzymes and 2) autocatalytic micelles form spontaneously in many different conditions. It is also important to remember the work of Otto that showed how different molecules can self-replicates.
There are many more examples reported in the literature, still, the complete "creation" of life from matter has not been yet accomplished. However, the results from the experimental work done so far suggest that it is only matter of time and lots of combinatorial work. Unfortunately, there are little to no investments in this field. It's very hard to get the funds needed to start an international cooperation (like the one made to sequence the human genome or to build the CERN's Large Hadron Collider) with the goal of actually making life in the lab. I think that the work of a few (uncoordinated) groups will not get to the goal in the next few years.

I would add that even these more basic results have really shown that abiogenesis is feasible. It is definitely feasible to show in a lab that certain steps are possible given certain conditions (like polymerization of nucleic acids). What isn't feasible is doing the experiment on whole-earth scale and waiting for potentially millions of years. It's really frustrating that some people take the infeasibility of that last step and conclude "oh so life must have come from a Creator!" That isn't what it means at all.

I agree. But I also think that it is possible to do it in the lab without having to wait millions of years. Actually, I hope that the pressure set from creationists will move some billionner to put money into this research. Is one of the great question of biology, is still lacking the final prove and it worth a Nobel price once solved. We can definitely do it, it's really just matter of money/organization.

Maybe, but if that attempt fails it doesn't prove anything, so really the experiment is quite flawed - probably one of the reasons there isn't much support for it.

I see lot's of support already from all the experiments reported in the literature. Surely it's not easy to solve, but again founding the Higgs boson wasn't easy as well, and same you can say or the first Human Genome. Now it's routine. Soon or later it will be routine also to create life in a lab.

I think that's a cool thought, but I'm skeptical. I think it is more likely that we will find life on another planet than create it here truly from scratch. I think we will continue to fill in some of the puzzle pieces here, though. The problem is that for those other projects you can engineer solutions that still answer the original question, like producing particles that are otherwise near infinitely rare to occur naturally. For abiogenesis, if the whole point is to say 'early earth could create life from scratch' you are sort of cheating if you add anything to the system.

@BryanKrause you say: 'early earth could create life from scratch'. My view of abiogenesis is more general: any complex mixture of chemicals, with enough energy and time, will tend to form complexity. Chemical complexity leads eventually to Life (the is, chemistry at the nth power). In this sense, there is nothing to "add to the system". It's just matter of finding the way of repeating the process in a controllable and repeatable way. I would expect different biochemistry evolve every run even if the initial conditions are the same. Eventually, some of them will evolve Life.

But you are assuming that that can happen on an experimental scale in a lifetime. The actual hypothesis is that it occurred at least once on a global/geological spatial/temporal scale. If you want to just say "tend to form complexity" we have already seen that to some extent.

Yes, I think it can happen on an experimental scale in a lifetime. Under controlled conditions, reaching a self-reproducing protocell should be doable. Then having that protocell evolving into some bacteria-like life form may take ages. But yes, I am speculating on that.

I find your speculations correct. However, there is a problem coming out precisely from running the experiment with a different outcome each time. See, scientists expect falsifiability of their experiments, it's heavily expected that if you run an experiment over and over again you should get the same result every time you run it. But it's not what you expect, or more likely shouldn't be what you expect when you run experiments for the creation of life-here one must expect that different outcome every time it's run and that destroys falsifiability.

That field of highly complex chemistry may indeed be the only case in science where you would expect to have unexpected result and that hampers your data analysis. If you produce different biochemistry each time you run the thing what about your statistics or any other interpretation of your data? Can you imagine doing the math of a different outcome of a highly complex experiment already? Do you think anyone could get enough funds to support such an endeavor? I highly doubt it, not with what we currently have as hardware and funds, at least.


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Segmentation in Platyhelminthes
My text book says:

Platyhelminthes are unsegmented worms.

Moreover, tape worm (Taenia solium), which is segmented, is one of the examples of Platyhelminthes.
My question is: why a segmented worm is included as an example in Platyhelminthes (unsegmented worm)?

Welcome to Biology.SE. Could you please add the reference to your textbook? Thanks!

The confusion here is quite common (at least it was quite common among my students): the "segments" in a tapeworm like Teania, properly called proglottids, are not really segments, or metamers.
According to Hickman et al. (2001), in the chapter 17, Segmented Worms:

Body segmentation, or metamerism, in annelids is not merely an external feature but is also seen internally in the repetitive arrangement of organs and systems and in the delimiting of segments (also called metameres or
  somites) by septa. Metamerism is not limited to annelids; it is shared by
  arthropods (insects, crustaceans, and others), whose metamerism may be
  homologous to that in annelids, and also by vertebrates, in which it evolved independently.

Some pages before, in chapter 14 (Acoelomate Bilateral Animals), the authors say:

Some zoologists have maintained that the proglottid formation of cestodes
  represents “true” segmentation (metamerism), but we do not support this view. Segmentation of tapeworms is best considered a replication of sex organs to increase reproductive capacity and is not related to the metamerism found in Annelida, Arthropoda, and Chordata (see pp. 193 and 371).

I'm citing Hickman, but all zoology books I'm aware of (Ruppert-Fox-Barnes, Brusca & Brusca, etc...) will say the same: segmentation is synonym of metamerism, and Plathyhelminthes (including Teania) are not segmented animals.
Source:

Hickman, C., Roberts, L., Larson, A., Ober, W. and Garrison, C. (2001). Integrated principles of zoology. 1st ed. Boston: McGraw-Hill.

...sir,also tell me that at one page in my text book it  has been written that Nervous system is well developed in platyhelminthes but at other;there mentioned a line (under heading of adaptation of flat worms );that there is degeneration of nervous system and muscles....What is truth?both line are contradict to each other...please make it clear!


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Why doesn't glucagon promote glycogenolysis in muscle?
Insulin stimulates glycogenesis in both liver and in muscles. Epinephrine stimulates glycogenolysis in both liver and muscles. But glucagon stimulates glycogenolysis in liver only.  Why is this so?

Glucagon needs glucagon receptors to have an effect on the tissue or organ in question, and your answer can be found there.  Glucagon receptors are found in the liver, like you say, but they're also found in other tissues like intestinal smooth muscle, and brain tissue (http://www.glucagon.com/glucagonreceptor.html) - but, crucially, not in skeletal muscle.  So glucagon-stimulated glycogenolysis isn't actually restricted to the liver, it's also found elsewhere.  Liver-based glycogenolysis has a significant role in blood-sugar control though, so it's often only the liver that gets mentioned.

Here is a better paper describing the distribution of the receptors: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X1998000200008


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At what stage is the nervous system developed enough to interpret neuronal signals as 'pain'?
According to this article in Live Science, one of the reasons the fetus can't feel pain until 19 weeks is because the nervous system isn't fully developed.
But according to this article, the heart starts beating at day 16.
And according to this article, the nervous system controls the rate beating of the heart.
Then my question is, **how can it be assured that the nervous system isn't developed until 19 weeks, when the nervous system controls the heart beating rate since day 16?

First, there is some confusion on your part about heart cells and pain perception. Heart cells generate an action potential intrinsically; they do not need the central nervous system to beat (your second article explains this; read the part about the importance of calcium.) So yes, long before a fetus can feel pain, the heart is beating, because there must be circulation of nutrients throughout the embryo.
Secondly, the vagus nerve and sympathetic nerves can affect heart rate (the former by slowing it down when firing). These nerves start to reach their endpoints late in week 4 of development. So 19 days is not correct.

Cardiac sympathetic system
Although the primitive human heart starts to beat at 21 to 22 d, heart development continues to day 50, and it is near the end of this period, during the fifth week, that thoracic neural crest cells migrate from the neural tube through the somites and form aggregations (ganglia) near the dorsal aorta. [emphasis mine]

To experience pain, however, requires maturation of certain parts of the brain, most importantly, part of the thalamus and the cerebral cortex:

Current theories of pain consider an intact cortical system to be both necessary and sufficient for pain experience. In support are functional imaging studies showing that activation within a network of cortical regions correlate with reported pain experience. Furthermore, cortical activation can generate the experience of pain even in the absence of actual noxious stimulation. These observations suggest thalamic projections into the cortical plate are the minimal necessary anatomy for pain experience. These projections are complete at 23 weeks' gestation.  [emphasis mine]

Fetal surgeons and anesthesiologists often use 20 weeks as the time at which a fetus can start to feel pain, because that is when the fetus reacts to stimuli that would be recognized as pain if applied to adults (e.g. recoiling from noxious stimuli.)
One must recognize that recoiling from noxious stimuli does not prove what the fetus is perceiving. But it's a step in the direction of protecting the fetus from unnecessary pain.
Autonomic cardiac innervation: Development and adult plasticity
Can fetuses feel pain?

Thanks, this is basically exactly the answer I would have wanted to give but felt I didn't have the time at the moment to track down some sources and nail down the timing of different developmental events.

This answer is very good, but it has risen many other questions. I dont know if post them here as comments or post them as new questions. The third article does state the nervous system controls the heart rate, doesnt it? " Your heart rate, both at rest and during exercise, is controlled by the nervous system "

@Pablo - if they are new questions, post them as new questions. :)

@anongoodnurse ok, I just will in a while

@Pablo It's probably better to say the nervous system modulates the heart rate, once the nervous system has developed connections with the heart. If you provide it with the correct nutrients and ions, the heart can keep beating for awhile even completely outside the body. In a developing fetus, the heart can certainly beat on its own without nervous input. The nervous input becomes important when your metabolic needs are changing at a moment to moment basis, like when you exercise: that doesn't really apply to a developing fetus.

I found one of the answers here https://biology.stackexchange.com/questions/35180/will-the-heart-keep-beating-if-its-separated-from-the-body "The brain regulates the rate of the heart beat sure, but it does not send the signals that cause the heart to beat in itself."

This answer might need to be updated. Aside of several sources stating things like "However, a mature cerebral cortex is not necessary in order for the unborn child to feel pain, as evidenced by scientific studies and observations that both children and adults who are born with no or minimal cerebral cortex, do in fact still perceive pain." https://downloads.frc.org/EF/EF15A104.pdf there are others sources which state hearing or purpose movement start before 20 weeks. If hearing and consciouness is present before 20 weeks is hard to believe pain isnt since the experiences are connected.

@Pablo - I personally believe that fetuses feel pain before 20 weeks, but I will not change the answer to help you confirm your opinions/biases. It's a good answer. Feel free to answer yourself, altough I noted you above that you misinterpreted what the 'science' is.

Development isn't my area of expertise within neuroscience, but without evaluating each of your sources (note: it might be better to read actual scientific articles; live science and especially livestrong are basically blogs; I haven't heard of iflscience but assume it is similar), it is important to recognize that the "nervous system" isn't all one unit, it is a collection of many networks and circuits.
There is no universal "on" switch where one day it is off and the next it is suddenly all working. Different pieces develop at different paces, and many functions are still developing even long after birth, through adolescence. In general, you can assume that the most basic functions necessary to sustain the body will develop first, followed by sensory and motor systems, followed by circuits that interpret sensory information to produce motor outputs (this is where awareness of things like pain would first come up), and lastly, executive functions that control whole patterns of behavior and higher-order decision making.


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Restriction enzyme type II
Why can't a type II restriction enzyme cut a nucleic acid with the following base composition:

A: 28% C: 15% G: 35% T: 22%

I don't really get your question... First, a restriction enzyme cut at recognition site, I never heard about base content distribution (can you link a source?) Second, in any DNA sequence the percentage of A is equal to the percentage of T and the same is true for C and G. What king of DNA sequence can have 28%T and 22%T? So it must be RNA you are talking about. But then T is not correct, it should be U. Please add more details to your question.

Welcome to Biology.SE. To me, this seems like a homework question (those are off-topic here, see link) so I put a flag to it. Please show some effort to answering the question yourself, if you want to avoid the question being deleted/closed. What do you know about the enzyme? What dies the base composition tell you about the sequence in question? Basically, let us know that you are trying. Thanks!

I suppose this is a homework, not a genuine curiosity. That being the case, I'm gonna give you two different answers here: the standard one, which is the one I believe your teacher/lecturer expects to see, and a more complicated one in the addendum.
The first thing that draws out attention in the question is the base percentages. Clearly, it doesn't follow the famous Watson-Crick pairing rule (A pairs with T, G pairs with C) and, because of that, we don't see the Chargaff's Rule in this nucleic acid.
Thus, this is not a double-stranded DNA (dsDNA), but a single-stranded DNA (ssDNA).
That being said, the answer to that question can be something along these lines:

A Type II RE can't cut that nucleic acid because that is a ssDNA.

Addendum:
There is a complication here, which may render the previous answer questionable.
Type II Restriction Enzymes only cleave regular, that is, double-stranded DNAs. So, they cannot cleave ssDNAs, which corroborates the answer we just gave.
But the problem is that ssDNAs can form loop structures, in which there is pairing between bases in the same strand. In those structures, DNA is technically dsDNA and, as such, can be cleaved by Type II RE. For instance, have a look at this paper:
Type II restriction endonucleases cleave single-stranded DNAs in general.
That being said, Type II RE do, in fact, cleave ssDNA (in places where ssDNA form loops and structurally resembles a dsDNA), which makes the question itself meaningless.

It is in fact a homework, the base percentage could only be possible if it refers to a ssDNA. Therefore, could the answer be anything related with palindromes? Although we cant say anything about the recognition site

I think that it is worth explaining that, at least according to the paper that is referred to in the answer, the observed cutting of a single-stranded phage DNA is due to the formation of dsDNA in stem-loop structures. This may seem pedantic, but clearly, from the point of view of the restriction enzymes, the substrate is still dsDNA.


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Why does crossing over take place at all?
I already know that crossing over causes genetic variation. My question is that since DNA is a stable molecule, why would it undergo process like crossing over during which it becomes so unstable and develop a chance of mutation?

Cross over often result in mutation, this is true. But of course, not all mutations are caused by cross-over. Note that cross overs do not lead to higher genetic variance (or only as an indirect effect of causing mutations). I am unclear whether your question is "Is there selection for increased mutation rate?" or "Is there selection for increased recombination rate?"

Of course it leads to higher genetic variation: Without crossover, genes must mutate for the chromosomes used to vary at all. Splitting up previously-coupled genes creates potentially new chromosomes out of existing genes. That is increased variation in the population: it provides sexual reproduction a new pattern of genes to mix things up with. If the permutation isn't new, a specific case might not, but that process certainly increases diversity in the population.

It exists for the same reason sex exists at all -- for recombination of alleles of genes.

@TheNate It really is not the point of the question but recombination actually reduces genetic variance (unless some funny type of epistasis) both 1) by allowing selection to be more effective and 2) by reducing genetic differences between haplotype lineages. The idea that recombination increases genetic variance is a common misconception (hence the two upvotes you received). You can typically look at the work from Barton and and/or Otto. You might also want to have a look at this presentation by S. Otto starting at 5'30''

@AKV I am voting to close as unclear until you have addressed my comment from yesterday.

Crossing over is believed to be beneficial for evolution. It does not cause only mutations, it allows for the switching and mixing of genetic information. Thanks to crossing over entire protein families evolved, like the hemoglobins. Indeed it is one of the mechanisms that shaped the chromosomes.
Some in-silico simulation proved that, in general, adaptation take place faster if crossing over is applied.
Here some extra references for further readings.
https://www.ncbi.nlm.nih.gov/pubmed/28565671
https://www.ncbi.nlm.nih.gov/pubmed/28564047
https://www.ncbi.nlm.nih.gov/pubmed/28563027
https://www.ncbi.nlm.nih.gov/pubmed/28557225
https://www.ncbi.nlm.nih.gov/pubmed/28555659

The evolution of recombination rate is a complex subject (and is typically closely linked to the evolution of sex). You might want to go further in your answer.


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Why higher plants lack centrioles?
Why do plant cells not have centrioles?

Not related to the question, but just an explanation to whoever voted this as too broad: "too broad" doesn't mean that the possible answer is somehow opinion-based or hypothetical. Too broad means that OP is making several questions at once. From the text of the option: "Please edit the question to limit it to a specific problem. Avoid asking multiple distinct questions at once". This may be closed, but not because it's too broad. I'll delete this comment soon.


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Does carbon dioxide from carbonated drinks enter the bloodstream?
When drinking soda or any other carbonated beverage, does some of the CO₂ find itself in the bloodstream? And if so, how long does it take until the carbon dioxide levels in the blood return to normal?

Is there enough CO2 to matter?
A can of soda contains about 2.2 grams of carbon dioxide (see this question from Chemistry.SE).
A human outputs about 1 kg of CO2 daily from respiration, though the rate can be much higher during physical activity. So, even if all of the CO2 content of a can of soda was absorbed into your blood, that's only 0.2% of your ~resting daily CO2 output.
A normal range for [partial pressure of CO in blood] is about 38-42 mmHg.
Gas exchange
The surface area of the lungs is something like 50-75 m2.
The surface area of the stomach is much smaller, closer to 1 m2.
Therefore, gas exchange is going to be much more efficient in the lungs than at the stomach.
Result
Any CO2 is going to be fairly efficiently cleared from expiration if it gets into the blood from the stomach. It's unlikely that you could detect any appreciable change in CO2 levels beyond what happens naturally as blood travels through the circulation and picks up CO2 from the periphery, and it's even less likely this difference would be greater than the difference between rest and exercise. That isn't even accounting for the buffering capability of the blood and diffusion into other tissues (both would smooth out any rise of CO2 over time) as well as not all of the CO2 will even make it to the stomach, and the gases that make it there can also leave via the esophagus.
As a sidenote, the Mythbusters partly addressed this issue in their episode on Mentos+coke. One of the factors they discussed is that much of the CO2 doesn't even make it to the stomach because it is released in the process of drinking, though they didn't quantify it. Therefore, CO2 is likely to have even less of an effect than described above.

As shown on MythBusters, most of the CO2 does not make it to the stomach.

@BrockAdams I assumed as much but couldn't find a decent citation to demonstrate it or estimate the quantity (and, once it was clear to me that even the full amount in the stomach would matter very little, I didn't look too hard). I'd be happy to add one if you find it.

IIRC, it was this episode (or similar): https://www.discovery.com/tv-shows/mythbusters/videos/exploding-stomach-minimyth.  PS:  who just drinks a lousy can of soda?  Double Big Gulp™ FTW!


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Why does the brain produce cannabinoids?
I've been reading lately about the brain producing cannabinoids. I was introduced to this idea by the Wim Hof Method which has been shown to increase the amount of cannabinoids (that is, compounds simulator to those found in cannabis) produced by the body.
Could anyone enlighten me on why the body naturally produces cannabinoids in the endocannibinoid system other than the shallow explanation that they have any anti inflammatory effect?

It's just a matter of terminology. The neurotransmitters, of course, already existed on mammals, such as Anandamite, and they had their own receptors (no matter the name we give them). Since it was discovered that cannabinoids act on these receptors as well, the whole system, including receptors and neurotransmitters, was named after the plant (Cannabis). The very same thing happened with endorphins (from endogenous morphine), which were named after Morphine.

Therefore, I believe your question boils down to just this: "There is a neurotransmitter X and a receptor Y in our brain. Why X was named endocannabinoid and Y was named cannabinoid receptor?"

The intention of my question was "what purpose do cannabinoids server in the body?" Why does the body produce them?

So the answer is: they are neurotransmitters. Please read the link I shared.

I will do, much appreciated.

It's interesting to me that cannabinoids, opioids, etc are naturally occurring substances in the body; it's a change of perspective for me. I've always believed those substances to be foreign substances in the body as opposed to something that's always meant to be there.

Yes, they are foreign substances, but you have to think the other way around. Something like this: I took this substance from this plant and it had a psychotropic effect on me. In that case, the substance is messing with some receptor in my chemical synapses. Therefore, I must have a naturally occurring neurotransmitter, which fits that receptor, and that resembles that plant's substance.

It's important to note that the foreign agonists are often either much more potent or in much higher concentration than the endogenous forms, which is in part why it was easier to identify those agonists first. Another type of neurotransmitter that is very common in the brain is glutamate, but even various ionotropic glutamate receptors are known as "AMPA", "NMDA", and "kainate" receptors. They all respond to endogenous glutamate, but they also respond to those other molecules selectively.


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Identify fuzzy black quarter sized spider with orange on abdomen, in Minnesota
Found this spider on my car in Minnesota near St Paul (USA). Total size including the legs (end of rear leg to end of front leg in picture) is probably about the size of a quarter.

looks like a harmless jumping spider

I'm having difficulty finding another image that matches https://goo.gl/YrXGKm

This appears to be some species of jumping spider (family Salticidae).

[Note that] All jumping spiders have four pairs of eyes, with the anterior median pair being particularly large.

In particular, I believe your specimen is Phidippus audax (Bold Jumper). Specifically, I believe yours is a subadult bryantae variant of this species.

 Source: David Hill 2014
From Wikipedia:

The average size of adults ranges from roughly 13–20 millimetres (0.51–0.79 in) in length. They are typically black with a pattern of spots and stripes on their abdomen and legs. Often these spots are orange-tinted in juveniles, turning white as the spider matures.

Your specimen shares the orange abdomen with connected black "splotches" that leave an orange triangular dot in the middle. Also, notice your specimen has two grey lines on the posterior cephalothorax as well as black/white striped legs. Finally, 20mm is close to the size of an American quarter (~24 mm).

If you get a good look at the front of your specimen, you'll likely see that the chelicerae are an iridescent/metallic blue or green (a tell tale sign of this species and genus).

 Source: David Hill 2014

 More typical coloration (L) vs. bryantae variant (R). [Source: David Hill 2014]
P. audax tends to prefer relatively open areas to hunt and is commonly found in common in fields and grasslands, as well as on fences, exterior walls, and gardens. Finding one on your car, therefore, would not be so strange, especially given that they can jump 10-50x their own body length (Ruppert et al., 2004).
Phidippus contains some of the larger species of jumping spiders in the family, and it is almost exclusively a North American genus.

Specifically, P. audax is common in southeastern Canada, eastern and central United States and parts of northern Central America, and it has become increasingly common farther West.

Citation:
Ruppert, E.E., Fox, R.S., and Barnes, R.D. (2004). Invertebrate Zoology (7 ed.). Brooks / Cole. pp. 571–584

Did you find this e-book [Invertebrate Zoology]? I have been looking for it for ages.


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How does the spindle fiber find the kinetochore?
I am curious if anyone knows the exact mechanism of how exactly does the spindle fiber find the kinetochore? it certainly seems like a fairly non-spontaneous reaction for a spindle fiber to reach all the way to a chromosome, how are these type of reactions carried out without producing new proteins? How Can cells execute complex "choreography" such as mitosis without making new proteins on the spot?

It's an interesting question, but don't assume that the requisite proteins are not already available or cannot be made.

But here is my confusion, we learned about the signal transduction pathway and the central dogma of molecular biology as the basis for how life exists, if DNA is bundled up into chromosomes during cell division, then how do we carry out such a complicated process ? to me its like cell division implies that gene expression isnt needed for cells to carry out complex tasks...which is crazy...You figure that  especially in the context of evolution mitosis is when a cell needs to be most responsive to problems and stimuli, you dont want your plane on "auto-pilot" when it is about to land...


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Why does olfactory sensation need lateral inhibition?
Why does olfactory sensation need lateral inhibition? If it's not helping in spatial discrimination then why is it needed? Don't we just smell the odour which is more concentrated?
My attempt: It is said that lateral inhibition is an important part of olfaction as it aids in odour discrimination by decreasing firing in response to background odours and differentiating the responses of olfactory nerve inputs in the mitral cell layer. But we also know that sensory perception is based on the pattern of receptors activated by the stimulus. So following questions arise:
Why don't background odours laterally inhibit the target odour? Isn't there more chance of inhibition of target odour being inhibited since its concentration is less?

Can you provide references to your claims?

Its in my textbook and some other information is from wikipedia.

Can you tell us about which textbook / chapter it's from, and which wikipedia article / section you are referring to?

About lateral inhibition here https://en.wikipedia.org/wiki/Olfactory_bulb

In the note below action potential https://goo.gl/sFAjqD

Background odours are downregulated. https://en.wikipedia.org/wiki/Olfactory_fatigue

Here is the paper which directly answers your question.
Urban NN. Lateral inhibition in the olfactory bulb and in olfaction. Physiology & behavior. 2002 Dec 31;77(4):607-12.
A few salient points:

It is true that the spatial gradient of sensory attributes is not as clear in the olfactory bulb-neuronal topography as it is at other places with lateral inhibition, but lateral inhibition still seems to serve a similar purpose in all these cases, namely sharpening the perceived stimuli. It is not settled how is this "edge enhancement" brought about in a nontopographical system ( "...Specific inhibitory connections between groups of cells with similar receptive fields may allow for functional lateral inhibition in such nontopographic systems, but no evidence for such specificity has been provided in the olfactory system...").

Unlike say for example in the Retina, where lateral inhibition creates the on/off centres, the lateral inhibition in olfactory bulbs is more widespread. That is, the area inhibited is relatively more expansive. This fact, coupled with the highly localised excitation caused by odours, suggests that "....lateral inhibition will be most effective at suppressing signals with low spatial frequency, in other words, signals that involve activation of broad regions of the olfactory bulb...". This is what I assume was meant by your source while referring to background odours.

The overall neurological effects of lateral inhibition is not settled, and the evidence is scanty. To quote the aforementioned paper, "... A simple prediction for the effects of lateral
inhibition on olfactory behavior would be that impairment
of lateral inhibition should impair performance on olfactory
discrimination tasks, and perhaps that these effects should
be strongest for tasks involving discrimination of very
similar odorants. Such a result has been obtained in experiments
in the honeybee in which inhibition is blocked by
picrotoxin. However, in these experiments, the blockade
of inhibition did not affect the odor-evoked firing rate of
the cells recorded, suggesting that the impairment of discrimination
ability was independent of a broadening of
tuning curves..."

Have a look at the cited paper, and the papers quoted therein, for further information.

Thanks for the link , but what I am unable to understand is how come background odour not inhibit the other odour? Shouldn't the inhibition be equal? If thats true then new odour must be more suppressed but its not the reality. So how can I justify this unfair treatment?

THe suppression of background odors happens by a different mechanism, namely receptor desensitization which is a phenomenon occurring in almost all receptors. After a while, these receptors reduce their firing intensity despite the molecules still being present. If this happens, it won't affect the lateral inhibition profile in the olfactory bulb.

Second, the paper suggests a different meaning of background odors, as odors with wide receptor specificity. These also have a different lateral inhibition effect. And one caveat that always looms overhead while studying neuroscience is that we might not know the thing perfectly well. I couldn't find any other simple papers regarding this, but if you delve a bit deeper, there might be more complicated yet explanatory papers out there


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How is it possible for monosomies to occur?
I was taught in biology class that a cell dies if it doesn't have at least one copy of a chromosome "type". If this is the case, that means that:

Zygotes without a copy of a specific chromosome (for example chromosome 21) die.
But this would also mean:
Gametes without a copy of a specific chromosome would also die.

If this is the case, how is it possible for monosomies to occur? Wouldn't there have to be at least one haploid cell with (n-1) chromosomes when fertilization occurs?

Your assumption #2 is wrong.

@GerardoFurtado Ok; can you please elaborate on this and turn it into an answer?

Gametes cannot be compared to regular (id est, somatic) cells for two main reasons:

Their lifetime and...
Their gene expression.

In human beings, gametes have a very short lifetime. Supposing the nondisjunction happened at meiosis I (which is the worst case scenario), a "nulissomic female gamete"1 has to be alive for some days, from the end of the dictyotene to the fertilisation. The male gamete would have to stay alive for a little more time, some weeks, from the spermatogonium stage to the end of meiosis. Those are not big time spans.
But the most important reason is that gametes are basically a structure to "deliver" genes. They normally don't express the genes they have, at least not as a somatic cell would do. Sperm cells, for instance, have densely packed chromosomes and gene expression, if any, is little and poorly understood.
Thus, the problem in your reasoning lies in assumption #2:

Gametes without a copy of a specific chromosome would also die.

Gametes lacking a given chromosome can and do exist, and they form aneuploid zygotes.
Note 1: the name "gamete" here is a wrong choice, since a primary oocyte is not a gamete, as it is the name "nullisomic", which doesn't apply to haploid cells.

Had I more points I would bounty this answer. Signed  – a technical editor


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Will charged water ions sprayed onto plants keep insects off?
I had stumbled on an article about a Dutch firm that devised an irrigation system that used mist of ionized water droplets that they claim keeps insects away from the plants.  This break through would revolutionize eco-friendly organic agriculture by reducing the need for insecticides.  They also claim nitrates are also formed by the process and embedded in the mist to supply nitrate fertilizers as well.  Thus eliminating the need for extra chemical fertilizers.
I tried to find the site again and the company but not coming up on search.
Are there any merits to these claims?  How would such a process or device work?


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Is there a reproductive barrier between Khoisan and other humans?
I have heard in an ethnology lecture that more or less all human ethnicities interbreed without a barrier (rate of reproduction of fertile offspring) except the Khoisan + any other human ethnicities, where fertile offspring is less likely than when other humans interbreed (as a an anecdotic side note, there are rumors about Zulu men who prefer Khoisan women as second or third spouse in order not to produce too many kids). My question is if some can confirm or falsify this (any literature coverage)?

Check the book "Genetic Nature/Culture: Anthropology and Science Beyond the Two-Culture Divide" edited by Alan H. Goodman, Deborah Heath, M. Susan Lindee. Page 205 states that that is a myth started by geneticist F Lenz of Gottingen that has been disproven.

Oh dear, which (FL) on top is a very dubious source, thank you for clarifying this!


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What is this brown spider with black and white stripes? (Atlanta, Georgia)
Location: Atlanta, Georgia
Spider mostly brown, with black and white stripes. Would fit on a teaspoon.  Ran quickly but not very far when I tried to catch it.
Click to zoom in the pictures below:

It resembles Dolomedes tenebrosus, commonly called the Dark Fishing Spider, and it belongs to the family Pisauridae.

Image Source: Bug Guide
Males are generally thinner in profile than the females, which is well depicted below.

Image Source: Spiders.Us
Based on the pictures provided, you seem to have captured a male Dolomedes tenebrosus.

Based on the OP's description of size, I'd say they found a male (7-13mm)

@theforestecologist I would agree. I have updated the answer to include that information.


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How do prions cross the blood brain barrier?
How does the PrP scrapie protein maintain its confirmation while going through the GI tract? How does the PrP scrapie protein cross the blood brain barrier?
Wouldn't the host immune system recognize the prion as "not self" and attack it?

Googling your title question gets about 231,000 results. What specifically are you having difficulty with?

hmm idk how to be more specific but i guess I could say: "what structural part of the PrP scrappie protein provides it transport across the blood brain barrier ?"

@anongoodnurse The vast majority of the results (56k without quotes, only 3 if you put quotes) are just combinations of some of those keywords. The very few results that actually do say that prions cross the blood-brain barrier just do that, like this one, whithout explaining how. That's what OP is asking. By the way, just for you to understand how search engines can be complicated (or even skewed), in my country (Australia) this very SE question is result number 3 in Google right now.

The link you provided raises more questions than it answers.. I dont see why we cant vaccinate against prions (or maybe just parts of it) if they spend so much time in secondary lymphoid organs?

@Confusedbyeverything You're literally confused! That link I shared was not for you, but for Anongoodnurse, showing that most sources we find online only affirm that prions cross the barriers without explaining how they do that. I didn't shared that link trying to provide an answer.

I am not sure if a perfect answer is possible owing to the fact that Prion diseases are still incompletely understood, and are actively under research. On a preliminary search, I found some papers which address the issue (cited at the end).

Since $PrP^C$ is normally found in the body, its role and its transport is also relevant to the issue. It seems to undergo bidirectional transport across the BBB using a saturable mechanism, mostly a specific transporter (1). It is taken up peripherally, and by several regions of the brain with the possibility that it is involved in various brain functions including modulating the BBB itself. Amyloid Beta-protein, with several kinetic and dynamic similarities with $PrP^C$, is shown to have BBB altering effects. (2) How far do the pathological prions follow this is seemingly unknown.
Autonomic nerves seem to play a role in their transport.(3) When challenged with prions, sympathectomy delays or even prevents the disease, whereas sympathetic hyperinnervation accelerates prion pathogenesis. There have been studies to elucidate the transport via the nerves, such as (4) and (5).

There are several other studies on this issue, and following the cited references might help you find them.
Reference number 3 also has information on the immunological response to prions.
References:

Banks WA, Robinson SM, Diaz-Espinoza R, Urayama A, Soto C. Transport of prion protein across the blood–brain barrier. Experimental neurology. 2009 Jul 31;218(1):162-7.
Giri R, Shen Y, Stins M, Du Yan S, Schmidt AM, Stern D, Kim KS, Zlokovic B, Kalra VK: Am J Physiol Cell Physiol. 2000 Dec; 279(6):C1772-81.
Aguzzi A, Zhu C. Five questions on prion diseases. PLoS Pathog. 2012 May 3;8(5):e1002651.
McBride PA, Schulz-Schaeffer WJ, Donaldson M, Bruce M, Diringer H, Kretzschmar HA, Beekes M. Early spread of scrapie from the gastrointestinal tract to the central nervous system involves autonomic fibers of the splanchnic and vagus nerves. Journal of virology. 2001 Oct 1;75(19):9320-7.
Glatzel M, Heppner FL, Albers KM, Aguzzi A. Sympathetic innervation of lymphoreticular organs is rate limiting for prion neuroinvasion. Neuron. 2001 Jul 19;31(1):25-34.

Thanks for the answer satwik, it certainly provided me with a lot more of an understanding than before.

'bidirectional transport'?


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Is aneuploidy/aneusomy only a problem for cell division?
One of my textbooks states that:

"recent studies suggest that aneuploidy can be seen in upwards of 10% of human brain cells without any noticeable effects"

I do know that trisomy 21 causes problems, specifically mental retardation by not allowing the brain to turn certain genes ON and OFF at certain protein levels, but I do not understand why plants are okay with aneuploidy?
Is it because plant cells are more "plastic" than animal cells that, they are okay with aneuploidy?
Because neurons never divide, do they never have to deal with aneuploidy?
Or is aneuploidy a problem of stress that results from failing to control gene expression?
or is it a problem strictly of mitosis?

I just want to understand WHY brain cells .... are okay with aneuploidy

Great question. The standard hypothesis has been that aneuploidy confers some kind of advantage to  the function of the organ (brain). After initial reports estimated a very high (>30% of brain cells) aneuploidy, it would be plausible that any potential negative effect would somehow have to be compensated. One hypothesis was that it increases the functional diversity of the neurons.
However, this notion is outdated. For instance, a recent study, which also nicely summarizes preceding literature, and has been published by Knouse et al. PNAS 2014 ( http://www.pnas.org/content/111/37/13409.full ), and has applied a more sensitive and accurate measurement, and also surveyed other tissues, found that the fraction of aneuploid cells in the brain is around 1-2%, and not higher than in most other tissues. One possible conclusion, which has also been drawn by the authors, is that for the brain aneuploidy is as much of a problem as for other organs, and that - given the low fraction of aneuploid cells, which is similar to other tissues - aneuploid cells in the brain do not contribute to some special organ-specific property. (Concerning your related questions to brain: the aneuploidy in brain is believed to result from cell division artifacts - also see paper mentioned above.)

I just want to understand WHY ... plant cells are okay with aneuploidy

Although plants appear more tolerant against aneuploidy than humans, aneuploidy can be quite harmful to them, and can easily lead to phenotypic aberrations. While the basis of the increased resistance of plants over humans isn't known, or at least hasn't been known at the time of the publication listed below, it appears linked to some genetic factors as different strains can have a different robustness - see Henry et al. , Genetics, 2010 ( https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2998307/ )

Is aneuploidy/aneusomy only a problem for cell division?

No, aneuploidy can create further problems (e.g.: also see second paper). For instance, in plants, it can also change the activity of genes, or the spatial organization of chromosomes - as described in Huettel et al. Plos Genetics, 2008 ( http://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1000226 )


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How effective is water purification by boiling?
Does boiling water kill all harmful bacteria, fungus etc from water, or it is just a myth and removes only few of microorganism?

To be precise, boiling water would not remove all bacteria as there are certain extremophiles that thrive at higher temperatures.
However, boiling of water is known to get rid of harmful pathogens. Boiling of water is a method of pasteurization, which means killing those organisms that can cause harm to humans.
Quoting from New York State - Department of Health >>

Boiling water kills or inactivates viruses, bacteria, protozoa and
  other pathogens by using heat to damage structural components and
  disrupt essential life processes (e.g. denature proteins). Boiling is
  not sterilization and is more accurately characterized as
  pasteurization.
Cooking food is also a form of pasteurization. For pasteurization to
  be effective, water or food must be heated to at least the
  pasteurization temperature for the organisms of concern and held at
  that temperature for a prescribed interval.

What is the difference between sterilization and pasteurization?


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Curved membrane effect

Curved Membrane effect: Movements of the  tympanic membrane are more at the periphery than at the centre where malleus is attached which provides some leverage. This is called as curved membrane effect.

I am unable to comprehend how movement is more at periphery than at centre.
Practically movement is more at the centre as can be seen from  this  .gif or from following image:
So, why it is said that movement is more at periphery?

Why down vote??

"...as seen from the gif" Is the gif not accurate in showing the curved membrane effect?

Yes, see a better picture here http://doctorlib.info/physiology/medical/medical.files/image540.jpg


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Are brown eyes healthier than blue eyes?
I have read somewhere brown eyes have more melanin than blue eyes and as melanin protects our body from cancers, I thought that brown eyes are more healthier.

Where did you read this?

I am voting to close until more information has been given on the source of the claim. It is for the moment hard to tackle the truth value of a claim we don't know the origin of.

Might be that melanin in our irises protects our pupils' dilator muscles but not much more.

People conflate "Dominant" traits to mean "healthier" which is a huge misconception. The previous answer provided a good example of how what is adaptive in one environment can be Mal-adaptive in another. Many Disorders can be dominant for example Huntingtons disease or achondriplastic dwarfism.

You're right to draw this distinction. However, polygeny and pleiotropy allow evolution to render many deleterious alleles recessive, and still-dominant examples (including HD) usually affect the individual late in life, resulting in little effect on fitness.

true: gene expression is often more like volume nobs than On/Off switches

Not an answer (I hope an expert provides one), but too long for a comment.
Although I'm unfamiliar with this claim, it's conceivable the optimum melanin content in eyes is subject to a trade-off as it is in skin. In bright areas, skin is dark to prevent damage from ultraviolet light; in dim areas, skin is light to produce enough vitamin D to avoid rickets. Eyes are different in their details, but they too may have adaptive geographical variations (or the distribution of light irises may be due to something more mundane, such as genetic bottlenecks). In theory their optimum colour would trade visual acuity against retinal protection, though I'm dubious about that as light enters through the pupil, not the iris.

@JG I agree with your point regarding adaptive geographical variations. Is there any place wherewe can discuss this more?

@AScientist I have no ideas about it besides those I wrote.

Well,That's a bummer.Do you know anyone who knows this stuff?


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What goes wrong in the immune system that leads to autoimmune diseases
As far as I understood so far, B and T cells are produced in the bone marrow, and during their maturing process in the bone marrow or Thymus, the are "programmed" to react to certain proteins. It is like giving them a particular key.
As I also understood, these "keys" are entirely created by random. Which means, that also "keys" are generated that match cells of the "host body."  Hence, if released into the bloodstream/lymph system, those B and T cells would attack the cells of the "host body."
As I understood further, there is a kind of a "security system" which checks if B and T cells are produced that would attack cells of the "host body." This security system would intervene and destroy those B and T cells before they are released into the bloodstream/lymph system.
As read lately - and I am not sure if I did understand this correctly - it is also possible, that B and T cells could also react to other cells even if the key doesn't match perfectly.
Now my questions.
Firstly, being an SW engineer interested in this topic is my understanding above correct?
Secondly, is it correct to say that autoimmune diseases are mainly caused by the following two points:
1. the "security system" in the bone marrow / Thymus failed, and therefore "bad" B and T cells were released into the bloodstream/lymph system
2. B and T cells react to other cells, even if the "key" does not match perfectly.

Welcome to Biology.SE! You need to keep in mind that this is one of the (many) riddles in biology which aren't completely solved yet. So, although you might get answers to many of your questions, don't expect an answer to everything

This will be a fun read for you. Note the publishing date: this is still a hot area of debate. Also note that there's another security system, clonal anergy, meant to stop rogue cells from responding to autoantigens: T cells require 2-3 signals during Ag stimulation for conventional activation, as do B cells require Th or Tfh cell co-stimulation. Otherwise they're made to become quiescent and die in the periphery.

There's also this notion that B or T cells regularly need to get survival signals, often times from very weak self-pMHC signalling that doesnt activate them, but says stay alive (ref). Whats interesting about B and T cell maturation is they need enough binding for self-pMHC at selection checkpoints that they don't bind too tightly, but also that they bind at all.

Consider you're a software engineer, consider an autoimmune disorder the equivalent of a bad antivirus update causing your AV to recognize C:\Windows\system32 as a threat and "quarantine" it.

Your understanding of the process is basically correct. There are of course a lot more details to it, but that wouldn't be in the scope of the question. Do note that only T cells mature in the thymus (that's where the T comes from ^^), whereas B cells mature in lymph nodes and the spleen.
As for why autoimmunity occurs you also understood the basics, however the devil is in the details: wikipedia does have a much longer list of mechanistically different causes. While its often sufficient to explain immune recognition using 'keys' (T cell receptor / B cell receptor = antibody) and their respective 'locks' (peptides bound to MHC / antigens), the exact process of immune cell activation becomes important in autoimmunity, where cells are wrongly activated. This means that there are many possible points at which the 'security system' of the immune cell maturation can (or rather has to) fail to allow autoimmunity.
As for the cross-reactivity of cells: the difference between the binding of B cells (via antibody/B cell receptor to protein surfaces) and T cells (via T cell receptor to peptide sequences) means that in general T cells are much more likely to show cross reactivity - just because the possibility space of a 10-12aa peptide is much smaller than that of a protein surface (even though the probability is still very low).
Additionally - as stated in the comments to your question - both the immune activation pathway and the issue of cross reactivity, while principally understood, are not 'completely solved'. The immune system is insanely complex just by itself and the addition of interactions with both almost all human proteins AND proteins any kind of pathogen, mean that it will take quite a lot of time until researchers can figure out all the weird quirks caused by the 'wrong' combinations.


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What type of nutrients can be applied foliarly?
I am interested in what type of nutrients can you spray on plants? Which ones do get used by a plant and which ones make no difference.
By nutrients I mean general fertilisers N,P,K and also micro elements.

Stack exchange has a beta site on Gardening and 'general care and feeding of plants' is on-topic there. I think this is better suited there as the question is framed along the line of Gardening and not Biology.


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Is Race the Result of Microevolution
I've been studying evolution for some time and was wondering whether the emergence of different races is an example of micro evolution within our species?
Bonus Question: is it impossible for homo sapiens to undergo to split into separate species via macro evolution?  I think it's impossible since were so interconnected (due to globalization and transportation), therefore speciation could not occur.
Thanks

Welcome to Biology.SE. If you don't mind me asking the question, what source (websites, books, etc...) did you use to study evolution?

I took Gr. 11 biology.  As for internet sources I used 'Understanding Evolution' and 'Talk Origins'.  I also glanced at the occasional youtube video.

Racial differentiation is illusory. We form a continuum that is currently understood better by some sociologists than by most biologists, regrettably.

Yes, but no humans are not plausibly going to diverge into separate species based on pre existing races.

Micro- and macro- evolution are terms vaguely referencing to arbitrary time scales
The terms microevolution and macroevolution have rather arbitrary and unclear meaning. For this reason, they are rarely used in the scientific literature. When they are being used, it is often in the first part of the introduction where general statements for which inaccuracy matters little are being made.
Typically, the existence of lineages called races (but see below) within a greater lineage called a species are limit cases between what one would want to call macro evolution or micro evolution. But in essence, it really does not matter where such arbitrary boundary is put, it changes nothing to evolutionary processes at play.
The concept of ethnic group
Note also that the concept of race (generally called ethnic group) is a human made concept that sometimes fail to match the reality of population structure in humans. If we were to name lineages based on genetic differentiation rather than socio-cultural cues, we would, if I am not mistaken, end up with a reasonably different result.
Bonus question
For your bonus question, you'll probably want to have a look at the post Does it make sense to classify all humans in a single species? and the post How could humans have interbred with Neanderthals if we're a different species? who discusses the concept of species.
You are right that the increased migration rate brought about by globalization causes increase interbreeding between humans lineages and will therefore rather prevent any further population structure that would have otherwise eventually lead to an event of speciation. There is, for the moment, no sign that any human speciation would evolve any reproductive barrier with any other human lineages. We are for the moment far from any speciation event in humans.

For the bonus question, would Homo floresiensis qualify as a species evolved from H. sapiens, or did both evolve from some precursor species?

I guess it is mainly a matter of what you decide to call Homo sapiens. As H. floresiensis is not called H. sapiens floriensis, I must be considered as a a sister lineage of H. sapiens and not a subspecies.


text:
Is the bipolar neuron of the retina considered a sensory neuron?
Any neuron that participates in sending impulses from receptors to the CNS are referred as sensory neurons. But I often see bipolar neurons of the eye (which according to the above definition should be sensory neurons) being called interneurons. Same is the case with the amacrine cells and the horizontal cells.
So what are sensory neurons? Are all the following retinal neurons sensory?

Rods/Cones,
bipolar neurons,
amacrine cells,
horizontal cells &
neurons of the optic nerve (ganglionic neurons)

Are all the neurons of brain interneurons? Obviously, there are neurosecretory cells in the hypothalamus that  I wouldn't consider interneurons. But, still.
Wikipedia tells us that only 20% of neurons in the cortex are interneurons.

Unlike the peripheral nervous system (PNS), the central nervous system, including the brain, contains many interneurons. In the neocortex (making up about 80% of the human brain), approximately 20-30% of neurons are interneurons.

Shouldn't that be about 80%?

In short, yes. Any neuron that is involved in conveying sensory information from the periphery to the CNS is a sensory neuron. So I would consider all of those neurons in the retina sensory.
Arguably amacrine and horizontal neurons do not convey information "towards" the CNS, but they are involved in the processing of sensory information, therefore I would call them sensory. However I wouldn't split hairs about it if the consensus on amacrines/horizontals was interneurons, not sensory.
I guess the confusion is that many categories of neurons are not mutually exclusive, so neurons can be both sensory and interneuron.
Once reaching the optic lobe (I assume you mean areas in the thalamus, midbrain etc.), then the CNS neurons can loosely be classed as projecting/interneurons. Interneurons will remain within a region of the brain, often inhibiting activity in other cells within the region (or exciting). Projecting neurons will carry information to a different brain region, or back out to the periphery. These are very loose, in a nutshell classifications though.
Once you start looking at a specific region, e.g. the Lateral Geniculate Nucleus, then the neurons will be further classified, either by shape, function, neurotransmitters, inputs or outputs, or a combination of the above depending on the requirements of the system.
Edit: To elaborate, the types of neurons in the brain will usually be described in an area specific fashion, e.g. the lateral Lateral Geniculate Nucleus has 3 major classes of neurons, magnocellular, parvocellular and koniocellular, as well as some interneurons and supporting cells. Whereas about a dozen types of neurons have been described in the cochlear nuclei, including pyramidal, stellate, giant, golgi etc. But at this level, you would be looking at very specific differences that are not necessarily relevant to the pathways involved.
I would argue that interneurons are small and restricted to individual brain regions, e.g. the visual/auditory cortex, many of the neurons, e.g. pyramidal neurons in layers IV and V  are generally projecting neurons that carry information around the brain. I don't have specific numbers for percentages, but about 20% interneurons sounds reasonable to me.

I like the overall message of this answer and gave it a +1, but I'd note that some people take a very narrow view of what "sensory neuron" means and intend to refer to the primary sensory neurons, which in this case would be the photoreceptors themselves. In my opinion it isn't an important distinction at all, as long as someone understands the actual functions, but sometimes textbooks or instructors can be overly precise on terminology even in cases where there is not a clear standard in the field.

I think the most generalizable definition of interneuron is what you wrote here: "Interneurons will remain within a region of the brain, often inhibiting activity in other cells within the region (or exciting). Projecting neurons will carry information to a different brain region" (though for "brain" you could substitute any component of the nervous system). By that definition bipolar, amacrine, and horizontal cells are all interneurons. Rods/cones and retinal ganglion cells are not: one is a sensory receptor cell, the other is a projection neuron.

Are projecting neurons textbook interneurons?

Thanks Bryan, that sums up the difficulties in the field. When studying inner hair cells, we would never consider them to be neurons, which would make the spiral ganglion neurons the sensory neurons, or there are no "sensory neurons" for hearing.

@DeechitPoudel, It depends on the textbook and the level of understanding you are expected to know. But in reality, no projecting neurons are neurons that carry information from one region of the brain to the other, e.g. from the brainstem to the midbrain. (In the UK, at approx. age 16, students are taught that all neurons in the brain are interneurons, which is a massive oversimplification).

@OliverHouston I agree, most people don't consider inner hair cells to be neurons: in that case I would say that spiral ganglion neurons are the sensory neurons; photoreceptors are usually considered neurons, however. It's really a developmental distinction more than anything else. I also agree 100% with what you say about projection and interneurons in your comment - for OP, if you are asking these questions because you are studying a textbook, you will simply have to familiarize yourself with how your textbook chooses to label things.

@BryanKrause It seems I am getting the picture. Although there is one thing that is bugging me. I have included that in the edited question.

@DeechitPoudel I'm guessing the 20% number is referring to inhibitory interneurons; 20% is definitely a reasonable number for inhibitory interneurons in cortex (including hippocampus). If you want to define 80% of cells as "interneurons" that probably defines interneurons to include cells that project neurons within whole regions of the brain, like neurons that project to distant areas within neocortex. I'd say that is a relatively unusual way to define interneurons, but as we have addressed already, the terminology varies by source.

Short answer
According to definitions, I can say 'yes' to all your statements.
Background

So what are sensory neurons? Are [] retinal neurons sensory?

Yes they are considered sensory neurons, because sensory neurons are defined as:

[] neurons [that] run from the various types of stimulus receptors, e.g., touch [receptors and the rods and cones in the retina] [] to the central nervous system (CNS), [i.e.], the brain and spinal cord.

Adapted from Kimball's Biology Pages and Khan Academy
Fig. 1 explains what a sensory neuron is. Note that the cell body of the sensory neuron is located in the dorsal root ganglion, just at the boundary of the peripheral nervous system. The relay neuron is located within the spinal cord, and is hence classified as an interneuron. Thus, sensory neurons are located in the peripheral nervous system.
.
Fig. 3. Sensory neurons are located in the peripheral nervous system. source: Tanya HL's pages

And, as soon as the neurons of optic nerve terminate in optic lobe, then are all the neurons in the optic lobe connected to the neurons of optic nerve called interneurons?

Per above definition, sensory neurons are located in the peripheral nervous system. Once they connect to the spinal cord (or the rhinal cortex in case of the olfactory system) they are per definition considered to be interneurons. Which answers your next question:

Are all the neurons of brain interneurons?

Yes.

Unlike the peripheral nervous system (PNS), the central nervous system, including the brain, contains many interneurons. In the neocortex (making up about 80% of the human brain), approximately 20-30% of neurons are interneurons.

All of the brain's neurons are interneurons, per the classification of neurons in sensory, motor and interneurons. As BrianKrause pointed out, often the term interneuron is reserved for inhibitory GABAergic cells, especially in the scientific literature (e.g., Markam et al., 2004).
Post scriptum
The classification in motor-, sensory and interneurons is rather a schoolbook way of explaining the types of neurons. It increases the understanding of the classification of the different neurons, but you will inevitably encounter shady areas where things fall apart; consider the fact that the retina is often regarded to be a part of the CNS, because of its embryonic development (Purves, 2002). So while I support the above answer, it's important to note that it comes down to a gross over-simplification of the nervous system. Such blunt definitions tend to fall apart when looked at more closely.
References
- Markam et al., Nature Rev Neurosci (2004); 5: 793-807
- Purves et al., Neuroscience, 2nd ed. Sunderland (MA: (2001)

I mostly like your answer, but from the perspective of someone that studies the brain (and cortex specifically), I would generalize to say that you are relying on definitions of interneurons that are used when describing the relationship of the brain to the periphery. For people focusing within brain structures, it is definitely not true that all cells of the brain are thought of as interneurons; it is also not true that interneurons are reserved for GABAergic cells, although this is common, because other cell types like spiny stellate cells in L4 of neocortex are also called interneurons.

Also by some definitions, the retina is special among sensory systems in that it actually develops from brain tissue and therefore is often considered part of the CNS. Based on that and the rest of your definitions, then, bipolar cells would not be considered "sensory" because they are already part of the CNS, so they are just as much interneurons as any of the relay neurons of the spinal cord.

@BryanKrause Considering your first comment, the question specifically relates to PNS vs CNS, so I think the approach of the answer is OK. Concerning your last comment please read the post scriptum

Oops, I should have expected better from you, I completely missed your PS. Sorry for that comment! However, "the question specifically relates to PNS vs CNS": is that true? It seems the question is about the retina, which, as your PS notes, is often considered part of the CNS. My suggestion, which of course is your decision to accept or reject, would be to amend at least your 'simple answer' to make clear up front the ambiguity or context-dependence of the term "interneuron."

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What is this insect with scary antennae?
I encountered with this insect on the wet floor in Sri Lanka. Is it dangerous?

I see you edited your question, incorporating the cerci of my answer, to address the fact that the antennae was not a antennae... but now the question's title is a bit contradictory!

Yes I did it with intention to help someone who will search with the real name of that thing. (At first I didn't know it's called cerci before your answer.) I understand now its not going well with your answer however.

Actually, the antennae of that insect are not scary at all!
In your image, the antennae are pointing down; those forceps-like structures pointing up are part of abdomen, and are called cerci.
That insect (probably a male) is an earwig, from the Order Dermaptera. In the image below, the antennae are at the left, while the abdomen and the cerci are at the right:

Narrowing down the the Genus of your specimen is more complicated, but here is a list of earwigs from Sri Lanka: https://en.wikipedia.org/wiki/List_of_Dermapterans_of_Sri_Lanka
Regarding the danger: earwigs are not dangerous. The cerci may be scary, but they normally are not capable of hurting a human. Also (and I hope you don't believe urban legends), they do not lay eggs in human ears: http://www.snopes.com/horrors/insects/bugear.asp