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Why is iodine solution a very effective and with a broad spectrum, bactericide, fungicide and viricide?
What is the similar property in each that allows a solution of iodine to deactivate and destroy so many species even from different kingdoms?

What research have you done before asking it here?

None, any guidance where to start ?

I'd suggest you begin with Google, and use reliable sites like Wikipedia (its usually reliable) or research sites like NCBI, Nature, Wiley, etc.


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What is the difference between kingdoms protistae and protoctistae?
I understand that both kingdoms represent primitive eukaryotic organisms, and both contain both unicellular and multicellular organisms.
What are the points that distinguish one kingdom from the other?

source: Stack Exchange

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

sort: votes


text:
Can you say "screening for a" in English?
I know this is not a "Correct Use of English Forum" but I'm afraid that people from outside the field won't be able to properly answer my question.
Would it be correct to say "screening for a long peptide capable of killing Gram-positive bacteria"? Or you just have to turn the word "screening" into a noun like: "preparing a screening for a long peptide capable of killing Gram-positive bacteria"?
The last one doesn't seem right to me at all, but I'm not sure since I'm not a native speaker :(
Thank you for your time!

There's nothing evidently wrong with your first option. Your second option could read "preparing a screen for…"

"Screening" can be a verb here ("we screen for the long peptide") so your first sentence would be correct.
Even in this biological context this might still be a question better fit for the English/Learning English forums though.

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


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Phylogenetic Independent Contrasts with discrete traits
I understand that PICs are normally only used for continuous traits. However, on this how-to site (https://www.r-phylo.org/wiki/HowTo/Phylogenetic_Independent_Contrasts) there is mention of "Discrete traits can be coded as continuous variables (see ?contr.treatment) and analysed as usual, if they are independent (explanatory) variables."
However, I'm having trouble understanding the commands described in ?contr.treatment and how they relate at all to using discrete traits in PICs. I assume it is a way to transform discrete into continuous data (or at least the appearance of cont. data) so as to perform the PIC, but I don't know how to get there from that hint.
This would very much help analyze my data, which includes both continuous and discrete data. I've already performed a phylogenetic logistic regression, but I feel that PICs could help cement my case if possible to perform.

Assuming that by "discrete", you mean "discrete and ordinal" (like 2, 21, 7, 12) and not "discrete and nominal" (like red, blue, yellow, green), then it is really easy. It just mean you can just use your numbers. The contrast between lineage with average trait 6 and lineage with average trait 9, the contrast is therefore 3.
If your data are nominal, then there is no way to calculate a contrast.
Not however, that typically you might violate assumptions of the PIC model. Make sure to know those assumptions and have a feel of whether you seem to respect them.


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Why did evolution make people's skin dark?
Why do people living in the equator have dark skin?
I know that Melanin acts as a protective biological shield against ultraviolet radiation.
But doesn't black absorb all light in a way making the body more heated than the surroundings ?

It didn't, the basal condition for humans is dark skin, all other pigmentation patterns evolved from it. Additionally Dark skin is not monophyletic/homologous in humans,
 that is some darks skinned humans evolved from light skinned humans who in turn evolved from ancestral dark skinned humans, (Evolution made skin lighter then made it darker again in other regions). Skin dark/lightness is also well correlated with latitude (which is correlated with UV levels).

First it helps if you remember skin is translucent so even very light skin absorbs a great deal of light. Additionally black also radiated heat better than white its is a double edged sword so to speak, it absorbs heat better but also sheds it better.
But the current hypothesis about why light skin evolved is due to vitamin D. The skin absorbs some UV radiation to manufacture vitamin D. Dark skin blocks more of this radiation reducing vitamin D levels. As humans migrated into higher latitudes with less UV radiation they needed lighter skin to harvest more of it. If your skin is too light you have issues with sunburn, skin cancer, and folic acid destruction darker skin protects from these. Now in modern humans clothing and diet completely swamps these effects, so studying it is difficult. the use of clothing in humans moving into colder climates may have exacerbated this effect. The later evolution of lactase persistence could further confuse the effect.
Note that this hypothesis is controversial and only weakly supported because it is extremely difficult to test and the the multiple confounding factors.
http://evolution.berkeley.edu/evolibrary/news/140305_skincolor
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3024016/
https://www.ncbi.nlm.nih.gov/pubmed/16766240
https://dl.dropboxusercontent.com/u/38568440/admixture/shriver01.pdf
https://en.wikipedia.org/wiki/Human_skin_color

Thanks for shedding light on how skin types evolved. But  the question asks why black ? Why did people from hot parts of the earth have black skin when we know that black absorbs heat making it uncomfortable. Why did evolution occur this way? http://scienceline.ucsb.edu/getkey.php?key=3873

@nishanthmenon maybe you are forgetting that its (comparatively) easier for our body to deal with heat than to deal with skin cancer. So which one is on high priority in our preventions list?

@another'Homosapien' maybe you should read the question properly. I know that it saves and protects us from UV rays, but the question is why Melanin causes the skin to become darker and not lighter thereby solving both the issues at once.

@NishanthMenon Melanin is a brown-black pigment. How would it make the skin become lighter?

@nishanthmenon in a way, that'd be asking why chlorophyll is green, hemoglobin is red or why water is colorless. Thats nothing about biology, but about the optical properties of the compound. Melanin makes the skin darker becuase melanin itself is dark. BTW your question's first line says, "Why do people living in the equator have dark skin?" No offence but...

@NishanthMenon dark skin does absorb heat better, but it also sheds heat better, so it warms up faster but also cools down faster, but really since skin is translucent and not opaque it really doesn't matter much the color has a much weaker effect on temperature in a translucent media .

@GerardoFurtado It can also refer to a group defined by a feature, but your right homologous would be better.


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Why only honey bee collects & store honey?
In Insects, most of flying insects like butterfly etc, diet is sucking honey from flowers. none of them store honey except honey bee. Why so ?

Nectar: sugary goodness in a flower. Honey: vitamin enriched food processed from nectar.

Also honeypot ants are not a single species but a group of ant species who have developed honey storing behaviour.

Many different bees also make honey, not just honey bees (Apis species). There are carpenter bees, bumblebees and as Geraldo said, there's honey pot ants.
Only honey bees make any great quantity of honey. The other species make far less and it's a different consistency. Honey bees live in large colonies and honey is stored to feed developing larvae as well as feeding workers and the queen through winter. Other bees are solitary except for a few bumblebee species but their colonies are much smaller - usually less than 50. Bumblebees make far less honey. There's no need to store honey for winter as the queen and workers die in late fall. Only a newly hatched and fertilized queen will survive, hibernating through winter underground. Hence, storing more than the immediate needs of queen, larvae and workers would be pointless.
You mentioned butterflies sipping nectar. A butterfly's lifespan is very brief and only sips nectar to provide energy for fertilization and egg laying. Then, generally, they die. Larvae have been provided for already since the eggs hatch on the appropriate plant leaves as their food.

Its a symbiotic relationship nature has established between honeybees and the vast hundreds and millions of plants that depend on them for pollination.  Honeybees do almost all of the pollination.  You cannot compare the vast proportion of pollination performed by honeybees with all the rest of the pollinating insects combined.
Because of this pollination dependency, nature has provided honeybees with robustness of colony sustainability, survival, and reproduction.  The energy density of honey is very high and it has all the nutrients the bee larvae need to grow into healthy robust adult bees.  The honey is also a great insulator to help prevent the hive from getting too cold in the winter.  Honeybees are the earliest pollinating insects in the spring, right on time for the earliest blooming flowers.  Their communal collaboration and communication teamwork in gathering nectar is astonishing, unique, and well documented.
Without honeybees, we would have to do without fruits and vegetables, which is why scientists are working around the clock to figure out colony collapse disorder.


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Which scientific names designate eyespots?
I've found that names containing ocellata and ocellatus designate species that feature eyespots. Are there other words in the scientific names that designate eyespots?
The problem I need to solve is: I want to fill the category Eye shapes in nature, therefore any method for finding such species is welcomed.

Eyespot is a scientific name. Other names: false eyes, fake eyes.

Octopus bimaculoides ; Raja binoculata; You might want to do a regular expression search on .*oc[ue]l.*, e.g. Oligosoma lineoocellatum


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Frog in Akaka / Loango Région Gabon
I was recently in Gabon, and I did some long and serious treks with Pygmées into some forest mostly to see Chimps and Gorilla around the Akaka area in Loango national park.
During a trek in forest I took a picture of this frog, it's been a little while now I can't find the exact species of it.
Any ideas guys ?

https://ibb.co/eU4ROk Full sized picture here

I'm not completely sure as it's very difficult to determine frog species with just one picture taken from the side.
Morphology-wise it looks like this is a Afrixalis dorsalis, although it's colour doesn't comply with the most comomon pattern. You can find pictures of this species with specimen looking exactly the same or very similar.
Colour deviations occur in several frog species...
interesting article about frog species in Gabon
AmphibiaWeb Afrixalis dorsalis (this also mentions differences in patterns and light coloured populations)

Source: Wikimedia Commons

Source: http://calphotos.berkeley.edu

Common colours and pattern
Source: http://calphotos.berkeley.edu

Thanks for your answer, true the morphology looks like afrixalis dorsalis, might be it ! Just could not find that pattern with the black strip from the eyes to the nose and also that little shiny yellow on the top of the eye. Could be a variation.


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How does a gene "know" what to change to?
Excuse my ignorance but I've always been curious about this...
For example, a frog is red, but it starts living in a green forest. Over time the frog becomes green to camouflage. But a gene can't see and I'm sure there's no mechanism for color info to be transmitted to individual genes from the brain. So how does a gene know to pick green over, say, blue?

Colour adaptation does not involve changes in genes. Why you would assume this I really don't know but it makes nonsense of your question. If you want to know how colour adaptation works rephrase your question accordingly. But please never ask questions applying the word "know" to insentient objects. Take the trouble to express yourself in a scientific manner.

@David: you say the question is "nonsense", yet it has a number of upvotes, and very good answers, five of them at the moment of writing. I would also like to know what it means to "express yourself in a scientific manner"; and, is that a requisite to ask a question?

@David - just saying thanks for being ever vigilant and for your efforts in trying to keep the site's overall quality in check. Having said that, I also wish to share that your comments here are receiving flags [general tone, rude, offensive, yadiya, you know...].

@MartinArgerami - the high number of upvotes, as well as the high number of answers is more related to the fact that the question made it into the hot questions list than because of its quality. In fact,  the question has been downvoted 4 times too. The fact that some folks (like Remi) know very well how to generate excellent answers, doesn't take away the fact that the question itself testifies of a certain lack of scientificness.

@MartinArgerami — Please read what I wrote, which was that talking about "genes knowing" makes nonsense of the question. As genes are not sentient beings, this phrase is nonsense, and if you have a question (which may have some merit) including nonsensical expressions invalidates or "makes nonsense of" it. This is avoided if the idea that the poster wishes to express is framed in a scientific manner. I am not clear what the poster means, but an example of scientific expression might be "Is there a way in which electrical signals from the brain can cause genes to mutate in a particular way?".

As it is written, the question asks about change in colour over the course of an individuals life, but the highest voted answer discusses change in colour of a population due to evolution. The question should be closed as unclear until the asker clarifies it.

@canadianer - I totally agree, but vow against mod-closure :) The top answer now basically states - your question is based on the incorrect assumption that a gene has a brain

The pedantry here is absurd.  OP obviously knows "know" isn't the correct word, that's why they put it in quotes.  Not knowing how to refer to it or how mutation works is why they're here.  "You're ignorant and write nonsense" is not an appropriate response to someone trying to learn.  And a Q&A site is probably not the best place for those users who are interested in neither questions nor answers.

Is punctuated equilibrium relevant here? I'm surprised nobody mentioned it... but I'm not a biologist either, so...

I asked the original question (system doesn't let me post in the comment section.) I can't believe how quickly this devolved into an argument about the semantics of the question. If you are versed in science and esp. biology isn't obvious that gene's know know anything? Even I know that, and I'm not a scientist. I very clearly stated that i am ignorant on the subject, hence the question. If we knew how to ask all the right questions in the right way then we'd be much more advanced as a species. Anyway, I appreciate everyone who put semantics aside and answered the question. Thank you, it is mu

Using your example, the gene doesn't know anything. Mutations cause some of the offspring of the red frog to turn green, some to turn blue, some to turn fluorescent yellow, and some stay red. Birds can't see the green ones as well as the others, so more green frogs survive and make more green frogs. The red frogs, the fluorescent yellow ones, the blue ones, mostly get eaten. After a few generations, almost all the frogs are green -- not because the gene knew anything, not because the mutations went in any direction, but because all the other changes were counterproductive and got eaten.
The gene doesn't know anything. It's just a bunch of chemicals that randomly react with cosmic rays, chance, whatever. Most of the changes are irrelevant or actively bad, and the frog that's carrying those particular chemicals doesn't survive. But sometimes the change benefits the frog carrying the particular chemicals and then the frog sends those chemicals down to its progeny.
Obviously this is hugely over-simplified. A short and simple intro to the basics of evolution is Understanding Evolution, by UC Berkeley.

This is a good answer but I just want to add that this process is called "natural selection", and is fueled by "selection pressures".

@immibis: Not necessarily. The green gene could be recessive and initially rare. It wouldn't even require mutations, it simply would be a matter of the dominant red genes disappearing due to predation.

Unless female frogs prefer to mate with red frogs, then green frogs are out of luck, and frogs will more likely become extinct than "evolve" to become green.

@Peter: ...although those female frogs that don't prefer red mates so much will have greener offspring on average, and so more of their female offspring will survive to mate again. So the female preferences will tend to change over time, too, unless of course the frogs go extinct first. (But near-extinction events do tend to accelerate selection, since the last few frogs to survive are likely to be the greenest ones.) A bigger potential issue is that if there's a steady supply of red frogs migrating in from another habitat, that'll make it hard for a green subpopulation to get established.

Honestly, I'm not really sure this answers the question. When was the last time anyone saw, say, a green deer? If colors change randomly and it's just a matter of survival, then surely someone should spot randomly colored animals occasionally. The closest I've ever seen is white giraffes, which simply lack pigments. So it's easy not to believe natural selection as a layman. I think if you want this answer to be convincing, you should give some numbers as to how often you'd expect to see weird mutations if you are to be likely to observe a change that can be selected for over a span of N years.

Second @Mehrdad, plus: what about chameleons?

But fluorescent frogs don't get eaten because the birds assume they are poisonous...

This is the theory of evolution through randomness. It doesn't explain changes that require 2-3 major simultaneous changes for the survival of the mutated animals. Then one starts to think whether evolution really happens on a random basis.

@akostadinov if you genuinely don't understand this simple concept, ask another question and someone will explain it to you.  The comments are not  the right place to ask new questions (or to make old and long-debunked claims)

@iayork, I don't see a question in my comment. I was trying to point out a weak spot in your answer. Or maybe whatever in your answer is the thing much harder to explain.

@akostadinov (or to make old and long-debunked claims) - I was giving you the benefit of the doubt and assuming you might be genuinely ignorant, but since you first parroted the long-debunked creationist talking point and then responded with classic creationist obfuscation, I'll just point out (in case newcomers are fooled) that this "weak spot" is nothing of the kind and is a well understood concept, even though creationists constantly try to lie about it.

@iayork, as long as you don't provide evidence, your position is just an opinion or a belief. While some naive forms of "creationism" have been proven wrong, this didn't prove the "random" evolution theory in any way. The "random" theory in my opinion is equally naive as some "creationism" theories and has never been proved scientifically. I'm not going to write anything more. Anybody that can think and read can go on investigate and think for him/her-self.

Another fun example is a certain type of moth that used to live in Western Germany ("Ruhrpott") and other areas during the Industrialisation. Its main habitat are birch trees, i.e. mainly white tree barks. So the animal used to be white with a few black spots.
Sometime in the past, the Ruhrpott had an awful lot of coal production, and in some areas the birch trees actually went and turned black from all the pollution in the air. Lo and behold, after some time, the moth also turned black with white spots.
As has been mentioned, obviously this is just basic evolution. What is nice about your and mine example is that this is a very direct, clear connection. If the animal is clearly sticking out due to its color, it will be frequently killed. It is not the other way 'round, where a slightly positive bias gets slightly more offspring, but a clear-cut, straight "be red (or white) and get caught" fact.
The effect of this is that this kind of evolution works really fast. It may have a tremendous effect after only one or two generations (obviously). So, with such drastic changes of the environment, after a handful of generations there may literally be no white moths left, the dark ones then have the whole habitat for their own (i.e., lots of food/nesting places, whatever moths do to reproduce). Hence this kind of evolution is - in contrast to other developments, which may take hundreds or thousands of years - very visible to humans.
Another fun fact: after the Industrialisation, our air turned clear, the birches turned white, and the moths got eradicated again until they were white again. Poor animals...
Source: Peppered moth evolution. Interesting read; all of this was not "obvious" to people back then, and there is criticism to be found as well.

Of course, as you know, a gene does not have any conscious, a gene does not know anything. It is all just a bunch of chemical reactions.
Central dilemma
First, you have to understand that a gene is a piece of DNA that will be transcribed in mRNA and the mRNA will be translated into a protein (this is a bit of an oversimplification). The protein is the molecule that is causing an action. The concentration of proteins in the cell is key in causing a phenotypic effect.
Regulatory mechanisms
The concentration of proteins can be affected by many regulatory mechanisms.
Gene expression regulation

Regulation of gene expression includes a wide range of mechanisms that are used by cells to increase or decrease the production of specific gene products (protein or RNA), and is informally termed gene regulation. Sophisticated programs of gene expression are widely observed in biology, for example to trigger developmental pathways, respond to environmental stimuli, or adapt to new food sources. Virtually any step of gene expression can be modulated, from transcriptional initiation, to RNA processing, and to the post-translational modification of a protein. Often, one gene regulator controls another, and so on, in a gene regulatory network.

Post-transcriptional regulation

Post-transcriptional regulation is the control of gene expression at the RNA level, therefore between the transcription and the translation of the gene.1 It contributes substantially to gene expression regulation across human tissues.

These include mechanisms such as

capping
splicing
Addition of poly(A) tail
RNA editing
mRNA Stability

Post-translational regulation

Post-translational regulation refers to the control of the levels of active protein.[..] It is performed either by means of reversible events (posttranslational modifications, such as phosphorylation or sequestration) or by means of irreversible events (proteolysis).

Skin colour changes in frogs
One such regulatory mechanism must be involved.
I really don't know much about physiology and molecular biology but I could find a large number of papers (including Taylor and Hadley 1969 and Fernandez and Bagnara 1991) showing that the colour change is mediated via production of the Melanophore Stimulating Hormone (MSH) produced by the hypophysis. Maybe a better physiologist / molecular biologist could give you a better answer.
If you are interested in the particular case of color change, you might also want to have a look at Neri and Castrucci 1997 and Skold et al. 2012.

Still doesn't explain why the mRNA transcribes one piece of DNA rather than another.

The mRNA is the result of transcription but it does not transcribe. 2) yes, it does (see gene expression regulation). There would be a lot to say about gene expression regulation, so for more information just have a look at the wikipedia page or at an intro course such as those by Khan Academy for example

Each offspring's color is a bit different from its parents.  Some colors help the frog survive, other colors tend to get it killed before it reproduces.  Over time, the species tends toward a color that improves survival because those that fit their environment better will reproduce and those that fit their environment worse don't reproduce at quite the same rate.

How does this answer a question that is clearly concerned with molecular mechanisms, even though it makes wrongheaded assumptions?  All you are saying is "it happens".

@David I don't think the question is concerned with molecular mechanisms, I think the questioner is just confused about how evolution works, in particular the genetic variation/mutations side of things.

@BryanKrause — Who knows? But the answer is terrible whatever the question. The question is clearly unclear and should be closed unless someone edits it. Don't you think?

I think this answer is just fine. It isn't perfect, and I think @iayork's answer is more precise in wording, but this one benefits from being short and to the point and accessible to someone truly new to evolution, like the OP appears to be. It's much better than your comment "Colour adaptation does not involve changes in genes" which is clearly wrong, of course adaptation involves changes in genes, just not in the manner the OP was thinking.

And although the original question shows a poor understanding, I'm not convinced it's actually a terrible question. I think there is almost certainly a duplicate someplace to close it with, but the OP's thinking and logic are clearly displayed, and they aren't asking for an answer that would be too broad or in-depth for this site.

The change in colour may be caused by new mutations or by epigenetic changes (e.g. changing the diet of a pregnant rodent may change coat color of pups, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC165709/). If the change is epigenetic, it means that the blueprint for producing the new colour was already present in the animal's genes before the colour change was triggered in its offspring by a change in the environment. In the case of the frogs, it could have been that the red frogs had some green ancestors that evolved the ability to toggle their colour between green and red in response to an environmental factor (like the availability of some specific food).
I don't know what the commenter David means with his comment "Colour adaptation does not involve changes in genes.", though. Even if the change is epigenetic, it still affects the functioning of genes.

Intro
There are actually at least three ways in which the colour of a frog might change to adapt to the colour of its environment. I will layout briefly how the three work, because from some of the comments there seems to be some confusion between the three, and also because the question mixes up changes within the lifetime of an individual frog with changes to the genome of the frog. These three categories can be more broadly applied to the question of how animals adapt to the environment.
Evolution

Occurs over multiple frog lifetimes
Involves changes to the genes
Is inherited by the offspring

Evolution occurs through natural selection. Other answers such as @iayork's answer have explained this mechanism.
Gene Expression

Occurs within a frog's lifetime
The genome of the frog is not changed, and the changes are not inherited
The way a gene is interpreted changes

While the genes of an organism don't change over the course of their lifetime, the way they are expressed can. This can lead to changes in skin colour based on environmental changes. This is explained in Environmental Influences on Gene Expression.
This would be a pre-existing response to a particular set of conditions; thus they 'know' what to change to because the response to the environmental change is pre-determined by their genes.
How the gene expression is influenced by the environment would depend on the particular trait in question. The mechanisms for this are not well understood, at least for some traits, as seen in The effect of light on gene expression and podophyllotoxin biosynthesis in Linum album cell culture from Plant Physiology and Biochemistry Volume 56 (July 2012, Pages 41-46)
Background adaptation

Does not involve the genes of the animal except in as much as every biological mechanism is encoded in the genes
can occur rapidly

Background adaptation is the approach used by Chameleons, but some frog species, as well as various fish and crustaceans also have this ability. In essence the distribution of pigments in specialised structures in the skin can be changed to modify the colour of the animal.
In at least some species this process relies on the animals ability of sight, so it seems likely the information on which colour to take is transmitted through the nervous system. The Wikipedia article on Chromatophores gives more information in the section on Background Adaptation
Conclusion
The kind of change described in the example could not be through genetic change, as this occurs over many generations, rather than one lifetime. To understand how animals adapt to the environment it is important to separate this kind of adaptation from the longer term adaptation through natural selection.
In these more rapid changes the colours to which the animal can change are already encoded in its genes. One mechanism by which the changes to the environment can be conveyed to bring about physical adaptations is through the nervous system.
TLDR:

Changes to the genome of an animal don't happen over the lifetime of an individual, but natural selection combined with random mutations can cause changes over multiple generations.
Immediate changes in response to the environment like the changes in Chameleons (and to a lesser degree in frogs) are not caused by changes to gene expression, but by mechanisms inbuilt in the animal in question.
Over the lifetime of an animal the way genes are interpreted can change in response to the environment, but this is also an inbuilt mechanism and the changes are not inherited.

DNA contains if-then statements that direct the mRNA to transcribe one piece rather than the other. I'm no microbiologist so I'm glossing here, but the transcription-mechanism is what allows proteins to be build which are then somehow assembled into hormones, tissues and various fluids such as mucus, gall, etc.
The question is really, what triggers one branch of the if-then over the other? Temperature appears to be one: deer, for example, are sexually active only in the autumn. When the temperatures drop, they start producing high-levels of sex-hormones, which cause the males to grow antlers and fight each other.
Color perception must be another: chameleons and certain species of squid are very dramatic examples. Eyes contain various cells, which are sensitive to certain wavelengths (https://en.wikipedia.org/wiki/Color_vision). The cells transmit signals to the brain, which must somehow result in the production of hormones that in turn trigger the skin-cells.
Some chemical reaches the mRNA in the relevant cells that sets the variables seasonIsAutumn or environmentIsGreen to true and the deer start growing antlers and the frogs, chameleons and squid turn green.
Of course, these signals, of temperature or color, will only have effect on those species, subspecies and genders whose DNA contains a relevant if-then statement. Deer obviously do not possess a switchColor function, just as frogs or does do not possess a growBigAntlers function.


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Supercomputer Vs Human Brain
With supercomputers doing calculation in petaflops ($10^{15}$ Calculations per Second), have we crossed the speed of Human Brain?

Related question on Cognitive Sciences: Why do scientists say brains are faster than computers?

Did you ask this question and then immediately answer it yourself... and then accept your own answer? This doesn't suit a biology forum either, it's information theory really.

@Louis: Will it be down voted if I say, yes? :)

There's a very big difference between doing the calculations needed to simulate the human brain (or any animal brain - we can do a fairly decent job on C. elegans), and doing computations.  While a basic leaky integrate & fire model is fairly simple, to accurately simulate a single neuron in real time takes a pretty fast computer.  See e.g. these links for more, http://www.neuron.yale.edu/neuron/,  http://bluebrain.epfl.ch/ http://www.artificialbrains.com/darpa-synapse-program.
Brains do well what computers do poorly, and vice versa.  The HP12C calculator on my desk, made in the early '80s, can do many sorts of mathematical calculations faster than I can, because brains aren't really optimized for doing, for example, compound interest calculations.  But my brain, or my dog's brain for that matter, can do all the 'calculations' needed to process a stream of images, recognize that they show a ball, predict its path, and catch it - while simultaneously processing visual, auditory, olfactory, and kinesthetic inputs for obstacle avoidance and threat recognition, and (in my case, anyway) perhaps thinking about how to solve complex programming problems.
Maybe I should add that there are basically three different things that a computer can do in this context:

Complex calculations, whether compound interest, weather modeling, seismic tomography or whatever.
Simulating the actual behavior of a brain, or some subset of one, starting from a single neuron.
Trying to replicate what a brain does through algorithms, or Artificial Intelligence.

(1) is what we mostly use computers for, and they're way better at it than human brains.  (2) is a special case of (1), which we do because we don't have much of an idea how to do (3), and having a simulated brain we can alter at will might help in learning how real brains do what they do.

In my opinion this is a much better answer than Devashish Das (OP)'s answer which got 15 up votes and is chosen as an answer at the moment.

Yes, I like this one too.

It is kind of meaningless to compare an analog device with a digital one to begin with.

I will just show the statistics of last attempt to mimic the brain process.
In 2011 fastest computer in Japan was launched:
K computer OR SPARC64 VIIIfx 2.0GHz
Features:

Manufacturer:    Fujitsu
Cores:   705,024
Linpack Performance (Rmax)   10,510 TFlop/s
Theoretical Peak (Rpeak) 11,280.4 TFlop/s
Power:   12,659.89 kW
Memory:  1,410,048 GB (16GB RAM per CPU)
Processor:   SPARC64 VIIIfx 8C 2GHz (88,128 CPUs, 8-core each)
Operating System:    Linux

It's currently world's 4th fastest supercomputer.
Source: Top 500 Supercoputers

Image Source: http://wondergressive.com/wp-content/uploads/2014/01/WG-k-computer.jpg
Now,

An 83,000-Processor Supercomputer Can Only Match 1% of Your Brain
...The most accurate simulation of the human brain to date has been
  carried out in a Japanese supercomputer, with a single second’s worth
  of activity from just one per cent of the complex organ taking one of
  the world’s most powerful supercomputers 40 minutes to calculate.
  Researchers used the K computer in Japan, currently the fourth most
  powerful in the world, to simulate human brain activity. The computer
  has 705,024 processor cores and 1.4 million GB of RAM, but still took
  40 minutes to crunch the data for just one second of brain activity...
Source: http://gizmodo.com/an-83-000-processor-supercomputer-only-matched-one-perc-1045026757

Human Brain:

Do we have brain to spare?
by David A. Drachman, MD
Within the liter and a half of human brain, stereologic studies
  estimate that there are approximately 20 billion neocortical neurons,
  with an average of 7,000 synaptic connections each.1 The cerebral
  cortex has about 0.15 quadrillion synapses—or about a trillion
  synapses per cubic centimeter of cortex. The white matter of the brain
  contains approximately 150,000 to 180,000 km of myelinated nerve
  fibers at age 20, connecting all these neuronal elements. Despite the
  monumental number of components in the brain, Szentagothai estimated
  that each neuron is able to contact any other neuron with no more than
  six interneuronal connections—“six degrees of separation.”

Image Source: http://www.nature.com/polopoly_fs/7.2933.1329907514!/image/far-to-go.jpg_gen/derivatives/fullsize/far-to-go.jpg
Why Brain beats Supercomputer?

Why is it so hard for computers to reproduce what your grey matter
  does as a matter of course? Volume. The human brain consists of about
  200 billion nerve cells (neurons) that are linked together by
  trillions of connections called synapses. As the tiny electrical
  impulses shoot across each neuron, they have to travel through these
  synapses, each of which contains about 1000 different switches that
  route that electrical impulse. In total, one human brain could contain
  hundreds of trillions of these neural pathways. It's like a Choose
  Your Own Adventure book that stretches from here to Jupiter.

This is a great answer!

It is not just processing speed that affects the speed of calculation. Algorithms also play a great role. I am very sure that electrical circuits have a much much faster response than the ion-current based neuronal circuits. Speed of information flow is not the sole criteria.

@WYSIWYG: They have used open-source Neural Simulation Technology (NEST) = http://www.nest-initiative.org/

Fuzzy mathematics and neural networks can play vital role in up bringing  computer science to higher grounds of Artificial Intelligence. But only considering the computational and memory speed couldn't be a right criteria in the development. While we increase the computational power and memory of a computer finally it is the quality of the software that decides what we achieved.

I don't think that difficulty of simulation is good measure for such comparison.

What this simulation is doing is basically hardware emulation, which is always slow (try compared the speed of a video game on native hardware with an emulator, even on a faster computer).  By this logic, weather has much greater processing power than a supercomputer, because a supercomputer cannot accurately simulate weather.

Computers work very different from brains.  Douglas Hofstaedter wrote an excellent essay to explain this:  http://themindi.blogspot.dk/2007/02/chapter-11-prelude-ant-fugue.html

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Is there any completely Computation Drug ever launched in market?
I am working in bioinformatics(part of it in Drug Designing) for years, still if I have no idea about it. As it is too hard to prove (Pass all Clinical trials) and get FDA Approvals.
So, My question is there a drug available in market, which is actually designed computationally?

Yes, there are a few. Mostly they are designed in combination with X-ray crystallography of the target which should be inhibited. Then molecules are designed which fit specifically into these targets.
The oldest example I could find is Dorzolamide which acts as a carbonic anhydrase inhibitor. See here: "Application of the three-dimensional structures of protein target molecules in structure-based drug design."
Some more examples are names in the Wikipedia article on drug design.
While looking for an example, I found these articles, which also look interesting:

Molecular Modeling and Computer Aided Drug Design. Examples of their
Applications in Medicinal Chemistry
Computer-based de novo design of drug-like molecules
Recent advances in computer-aided drug design

I am also not sure, to what extent the modern small molecule inhibitors like Vemurafenib (PLX4032) and others are designed using computers. At least to some extent this should be true.

Thanks Chris, this was the question which almost stopped getting my current job!!(Though I got it finally). Still there are 4-5 drugs as per my boss. So, if you find them, sure add to the list.

Have a look at the Wikipedia page I linked. There are some more examples listed (although I haven't checked all of them).


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Facultative Cannibalism?
I heard about Larger cats eating the cubs. Is it some kind of facultative cannibalism or they can eat there own kind like that?
What are the facultative cannibalism present in animal kingdom?
What is the genetic origin?

+1 Spawned a related question on Pets Will neutering a male cat stop it from killing kittens?

Lions
Lions are a classic example of cannibalism. To understand why this occurs we have to understand their mating system.
Males have a harem of females and males fight in order to access a harem (Note: females may also take part in the battle depending on which male they prefer). When a male takes over a new harem, he kills the young ones of the previous male if these young ones are still dependent on their mother. The reasons are:

The mother is not fertile while she is taking care of a young baby while the male would appreciate that the female is ready to raise his own kids.
The mother needs to invest quite a lot of energy to feed/milk their young while the new male would prefer this energy to be invested in his own offspring.

In short, a male kills the young ones when he takes over a new harem because these young ones do not carry his genes and prevent this new male to optimally pass on his own genes as the offsprings of the previous male consume time and energy from the females of the harem.
And well… once the offsprings are killed, it would be a shame to waste all this good and fresh meat. Better to eat them!
In the cases of lions, cannibalism does not result from food shortage but from "not wasting food". I think that the "not wasting food" hypothesis is the most explanation for cannibalism (I am not sure though). I guess that most often the "not wasting food" occurs after death due to competition as it is the case in lions.
Other Examples
There are many cases of cannibalism in the animal kingdom. Chimpanzees eating other chimpanzees and bear eating other bears. In the tiger salamander, there are cannibal morph and normal morphs. In this species cannibalism is very frequent as in nature one offspring over 5 is eaten through cannibalism (if I am not mistaken). Cannibalism is very common in prairie dogs as well (Reference). In Dragonflies cannibalism represents 95% of the total mortality (Reference).
Sibling sharks eat each other in their mum's womb. Here is a video on the subject. This type of cannibalism is called siblicide.
In Praying mantis the female may eat her mate after copulation. This is referred to as sexual cannibalism. The subject is slightly controversial, please have a look to the wiki article for more info.
In many species (including the dragonflies example above) the old individuals eat the young. This is referred to size-structured cannibalism.
Fillial cannibalism is a type of cannibalism when the adults eat their own offsprings as it is the case in the prairie dogs example I cited above.
Have a look to the Wikipedia links for filial cannibalism, sexual cannibalism and siblicide, they go further than my answer.

Wow!! Can you add something about Siblicide too?

I don't know much about all that. I'd suggest you to have a look to the wiki articles I linked in my answer and eventually come up with a more accurate question on another post as this post was fairly broad.

My first thought of why siblicide may evolve in sharks is: It seems a good solution for the parents to make sure that the only offspring they want to produce will carry very good genes. It is like producing a "pre-selected" offspring. r-strategy species don't do that. They let selection act later. But that makes sense that siblicide occurs in sharks as they perform some parental care and they don't want to lose energy for unfit kids. according to my hypothesis the question might then be "Why don't everybody does that?" But I really don't know much. I just had fun formulating a hypothesis!

@Remi.b the video you linked says that the oldest embryo eats the young ones as soon as its teeth are sharp enough. So not that much selection going on, except for the possibility that an older embryo with retarded development could be eaten by a younger sibling with normal development. But there isn't a bunch of embryos hunting each other at once.

It's a dangerous strategy for the species. Some embryos might develop particularly fast and then be strong enough to kill/eat their fellow embryos. That doesn't say much about their fitness as adult sharks. E.g. imagine if all the geek kids got killed by their football-loving classmates? Who would run the Internet? Siblicide probably leads to fast evolution into a niche (more siblicide). Allowing the siblings to live longer and compete for mates and offspring probably leads to more stable/fitter/more adaptable outcomes, at the expense of slower evolution.

Cannibalism in praying mantises is not a required part of copulation, this is a myth, as they can successfully mate without the male dying. It is speculated that sexual cannibalism is due to other factors such as hunger, increased aggression in the female due to invasive observation at the time of copulation, or a few other factors.

@Remi.b Your comments makes it seem that you believe that a species has conscious control over evolution or that the mother shark has control or influence on this type of behavior of the embryonic sharks within her. This is just NOT how nature works.

Ha ha seems that I would have better to remain silence on possible explanation of the shark siblicide. I have to confess that it was a quick thought. @TecBrat No, I didn't any of these naïve mistake. I am just saying that the parents may want to make sure that their unique offspring is fit to carry the parents' gene further.

@rumtscho Indeed this is interesting and is a counter-argument to my hypothesis. However, developmental time might be a proxy for fitness. Similar mechanisms exist in bees. The first queen to hatch will usually be able to kill all the other before they even hatch.

@winterblood Ok, thanks for the comment. I edited my post to indicate that it seems to be a myth. If you have a reference, the answer could be definitive. Thanks

The wikipedia article you linked for the praying mantis covers most of this in the first two paragraphs of the  Reproduction and life history section.

@winterblood Thanks! Seems indeed that the subject is controversial. Feel free to edit my answer if you want to improve it.

@winterblood Making any generalisation about cannibalism (other than that it often happens) in praying mantis copulation isn't currently scientific. Research has only been carried out on a few species.


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What would actually be the ecological impact of deep sea mining?
In the last few months I have read a number of articles with increasing alarm concerning the potential of many countries soon engaging in deep sea mining. The idea is that in order to produce numerous technologies key to moving green, such as batteries, industry needs a good supply of metals that are currently rather rare, such as manganese or cobalt, and there are so-called polymetallic nodules covering various parts of the sea floor (for example the Clarion-Clipperton Zone) believed to be rich in these materials.
As covered in numerous places, for example here, the International Seabed Authority was supposed to draft some kind of agreement on what kind of mining like this is acceptable but the deadline has passed for it to set down laws so currently we're in a kind of "wild west" scenario where many companies can mine down there potentially with little regulation.
My question is: what will be the ecological impact of this kind of mining?
In some sense, there are obvious arguments as to why we shouldn't do something like this. One would be that it is a relatively untouched part of the world (in terms of human influence) and that fact inherently gives the idea of leaving it alone value to me. However, this could be applied to absolutely anywhere and we do probably have to occasionally conduct mining, farming etc. activities somewhere so what makes this different?
Let's imagine two counterfactuals:
One is that instead of deep sea mining, the recent events had concerned mining in the Amazon rainforest or the Great Barrier Reef. I have chosen these places as being ones I know are widely accepted to be extremely biodiverse and home to numerous unique species. Clearly this would be horrific for life on earth and I would hope most people on this site would be against it unless there really was no other option.
Another is that instead of deep sea mining, recent events had concerned mining in the middle of some deserts, say the Gobi. In this case, there is wildlife in the desert which is of intrinsic interest (for example, they give plentiful examples of extremophiles) but broadly speaking there's barely anything there. Arguably it would be difficult to find a better place to conduct mining if you want to minimise ecological impact! Thus I can't imagine many biologists being as concerned beyond the fact that these are again relatively untouched and thus hold intrinsic value.
I am interested in where the deep sea mining lies between these two extremes. My (admittedly fairly lay person) perspective is that on the sea bed it was definitely a surprise by biologists to find complex life but that, broadly speaking, there still isn't much going on. Furthermore, the Clarion-Clipperton Zone (the major area of interest) varies in depth between 4-5.5km deep. If we say it's on average 4.75km deep that's around 11 Empire State Buildings end-to-end stacked on top of each other! The point is that at such a depth, can life down there or activities down there really affect or be affected by things happening above, say at the surface?
As I understand, there is such a separation between life down there and above that creatures share very few similarities at the bottom to surface dwellers (if you need a specific example of how this distance can affect lifeforms, consider deep sea gigantism and we're looking even deeper!). Surely then even major activities down there will have little effect on the rest of the biosphere?

I just want to give a postscript to this question that I do not support mining in untouched areas of the world. This question is not supposed to advocate for deep sea mining but purely to understand better what is currently going on by asking experts.

In 10, or 5, years time we will be able to look back on the evidence.

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How many Watt-hours can an electric eel produce in a day?
Electric eels are cited as being about to produce about 860 watts of energy. But I haven't been able to find information on how long they can sustain their charge.
https://www.youtube.com/watch?v=y9wktSQdyaE
In another question, it was shown that they can continually power a Christmas tree, albeit the lights flicker, just when it's hanging about and doesn't appear to be defensive. This suggests that it has some ability to sustain a low level of current... so I'd be surprised if there is no study that has measured the potential Wh. Sadly, I cannot find it.
Does anyone know any estimates for the energy an electric eel can produce over the course of a day?

I don't understand why this question has been downvoted. There is a common curiosity about the power of electric eels, and potential utility for that power.

Someone thinks that eels are not funny :)

@aliential I quote like electric eels, and find them quite funny, because they're some sort of catfish. And I'm pretty sure it was a kind of catfish that climbed onto the side of a boat, and accepted beer from the occupants. Quite an intelligent fish, they show fish possess higher brain activity than they're given credit for, just in my opinion.

I found some information on how much energy an electric eel can theoretically produce for an hour, but not per day. Thanks to this excellent answer from dtrades and my own research.
Apparently, electric eels can produce up to 860 watts, at up to 1 amp, with 1ms pulses and up to 500hz, with older/longer eels being able to produce a more stable output. That would theoretically make for a 50% duty cycle, with square waves, but will be something more like a 25% duty cycle when we average the pulses (if I'm not mistaken).
River Monsters S03E06 Electric Executioner claims they can produce a shock for "over an hour," I'd like to find more definitive data on their potential length of shocks. I did see a video of an electric eel being bitten by a reasonably sized gator, and shocking into into unconsciousness or death after 40~45 seconds, so I would believe they could keep it up for an hour, especially since they can still shock even eight hours after death.
Conclusion
So, all that together, suggests that an electric eel could theoretically produce 215 Wh, after one hour. It might be too exhausted to keep that up.
Of course, that is the most ideal result for one hour. What the average eel will manage, averaged over a day, is much harder to say. Still, I'm skeptical they are only capable of less than 1 Wh, and I'd figure a result in excess of 215 Whs would be more likely, under ideal conditions.
Containment
They also, as an aside, have to be careful to not electrocute themselves and stop their own hearts, and they have to take care not to electrocute each other. The father will keep his fry in his mouth, and signal them as to where they should go to be safe, when he performs a shock.
For those reasons, if you did use electric eels for power, you'd have to be careful how you contained them, so they had enough space to not electrocute themselves or each other.

This research states that an eel whose size is 90 cm can provide 6.05 mW, which is 145 mWh every day. They say you'd need 165 eels to be able to read for 24 hours using a 1W lightbulb like the one on a phone.
An electric eel should be able to flash a 0.6W L.E.D. light for 10 milliseconds at full power every second, which would be very visible in daylight, and would light up the room.

Thanks, I'll check out the paper! It's interesting that they got such a small wattage out of the eel. They can apparently go up to 860 watts of charge. There's a video somewhere out there, where an eel electrocutes an aligator to death over 45 seconds (you can find it if you search). The gator was spasming from the shock, so I figure it can't be a few miliwatts. But then, the fish was fighting for its life. Notably, another report states that they can emit a shock even hours after their death, and Wikipedia claims they can maintain a charge for an hour (no source, sadly).

That video is evidence for 50w to 500w pulses for 40 seconds, if it's 1ms pulses of 500w to the caiman's gums, every pulse is 500w/60000 ms = 0.008 Wh. In total the eel exhausted perhaps 0.4Wh to stun the caiman. No evidence the eel and caiman actually died. Caimans do eat the eels sometimes. A small watch battery is also enough to cause death at 600v.


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Help me identify this spider from my garden
Found this in my garden today in Sydney, Australia (specifically Lane Cove). Can you tell me what it is?

Can you get a close up shot of the top?

I believe it is a Garden Orb Weaver spider. The Australian garden orb weaver, Eriophora transmarina, has a strikingly similar body

Haha, yours is WAY closer than mine! You have to cut me a break though, this is my first attempted species-identification. Perhaps I should delete my answer to spare myself the humiliation... all the same, great job. +1

@CDB thanks. Species identification can be difficult but it is fun to play detective.

It looks like Neoscona Crucifera to me, but I could be wrong.
Here is a picture of her:

Another one, only this is more of the web:

wrong continent for Neoscona crucifera, which is found in the US and Mexico.


text:
Help me identify this... plant? fungus?
Today I found several of these in my back garden in Sydney NSW, Australia (specifically the north shore). They seem like flowers, except I don't see any attached plant and they have a weird brown goo around the mouth. I've never seen anything like this. Any ideas?

That's absolutely an Aseroe stinkhorn. The way stinkhorns disperse their spores is rather interesting - rather than producing powdery wind-dispersed spores like most fungi, stinkhorns make flies do the disposal by placing the spores in a foul-smelling gel called gleba(the brown slime visible on your specimen). Flies pick up the stench, and land in it and eat it, thereby spreading the fungus to any suitable patch of soil that the fly lands on.

After some Googling, it seems maybe this is a stinkhorn fungus, specifically Aseroe rubra.


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From where can I download the database created by Hsu et al for MORFs?
I am working on an independent research project for which I require access to the MORF database created by Hsu et al. From where can I download the database of MORFs of IDPs and their binding partners that was created by Hsu et al.?
I would appreciate a link to that page. I have searched a lot of keywords on Google but I could not come up with it. I might have, but I'm not too certain of it. I have already wasted 3 days searching for it.

In the future, it would be really helpful if you at least included a link to the paper by "Hsu et al." We can't read your mind. Secondly, the contact information for the corresponding author is included in the paper for a reason. If a careful reading of the paper and all referenced supplemental material doesn't answer your question, then contact the author directly. Most scientists I know are very happy to talk about their research and answer any non-trivial questions you may have.

I'm voting to close this question as off-topic because it is not about biology.

@MattDMo I got access to the database about a few hours after asking this question but I forgot to come and close this question. As for the question details, yes I completely agree with you. I made quite a few errors due to haste in typing the question. I'll make sure I do not do that again

I'm assuming you're looking for the dataset that was used to train MorfPred from this paper? http://www.ncbi.nlm.nih.gov/pubmed/22689782
There's a link to it on this page: http://biomine-ws.ece.ualberta.ca/MoRFpred/index.html
If you're referring to another paper, it is likely they used the same data set. The best way to find the supplementary data, is to read the paper thoroughly - this is a better approach than a Google search! Keep in mind though, that sometimes the data set is not publicly available and you must e-mail the researcher in question to request it.


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Is it possible to knock out a gene in adults?
gene knockout is mainly used in creating newborn animals... right? Well can you do it to already-adult animals or humans so that they themselves would experience change in their body and not just their off springs?

To do so would be considered gene therapy. It is possible, but obviously far more difficult due to the number of cells involved.

To knock out a gene in an adult animal requires knocking out the gene in each individual cell. Could we do it? We have the technology to do it in a single cell. Will anyone do it to all 3.7 trillion cells in the human body? Definitely not anytime soon.

a conditional KO would make more sense, and that's actually what gene therapy tries to achieve. But basic mechanisms between KO and gene therapy are very different.( except for Crispr, I think)

Woa yea thats a lot of cells! Can a conditional KO mean KO in limited area(s)? Like just in the spinal cord, brain or another organ or something. Sounds easier than 3.7 trillion cells

Even gene knockout in newborn animals is extremely difficult. Your only chance to get a complete knockout in all cells is probably at the single celled zygote stage. Knocking out, or down, expression in certain cells in an adult is possible, but gene delivery is still pretty difficult and results aren't guaranteed.

you can try KO in subset of cells. Why bother with all $10^{10}$ cells if you are curing liver or something. Also lower chance of propagation some unwanted, off-target genetical effect down the family tree.

Another option for adults is a gene knockdown instead of a knockout.  Knockdowns involve changes at the RNA level instead of the DNA changes of a knockout.  The challenge is to get the reagent used to cause a knockdown into the cells of an adult organism (this is an active area of research).  Knockdown reagents include siRNA, PNAs, phosphorothioate oligos and Morpholino oligos.  Some are in clinical trials now.

Actually, Cas9 system might be a possible method to achieve your aim in the future, research teams are trying to utilize cas9 in vivo, which means maybe someday we can doing some genetic modification in body cell precisely. However, this is only a future direction and we still can not say its fit for a knockout.(Patrick D. Hsu, Eric S. Lander, and Feng Zhang, (2014) Development and Applications of CRISPR-Cas9 for Genome Engineering. Cell 14(6): 1262-1278)
And for editing some cell gene in a limited area, some research are on going for therapeutic purpose (Liqun Zhang et al.CFTR Delivery to 25% of Surface Epithelial Cells Restores Normal Rates of Mucus Transport to Human Cystic Fibrosis Airway Epithelium), but haven't seen research are trying to built KO cell in vivo.

thats all true, albeit speculative. Current Cas9/CRISPR efficiency is very low. around 10% for creating indels/knock-outs and around 0.1% for targeted genome integrations. In vitro you can get away with it because you don't inject/transfect single animal/cell. But in adult there should be some shotgun-like transfection with following selection. Which is very risky endeavor.

@aandreev Newer approaches increased the efficiency quite substantially, look at this post. It's again in vitro and I hardly see how that can be translated in vivo as such but I am confident this will greatly improve in the future. Also off targeting is still an issue for using CRISPR as a clinical treatment. A lot of work is being done in finding the best ways to predict the best sgRNAs for both efficiency and specificity. In essence I agree but I have good hopes.

i do have good hopes. However, paper you cite (NHEJ inhibition etc) seems to me like a novel way to screen: instead on neomycin authors rely on fact that cells with non-repairable NHEJ will most likely die. Hence increase in efficiency.

@aandreev. Nope, NHEJ and HR are two competing DNA repair mechanisms and it's not due to cell dying but rather HR being favored hence increased efficiency.

@cagliari2005 isn't it trinity: cell death/severe mutations, HR, NHEJ? sorry for off-topic, just to wrap up

@aandreev. CRISPR induces nicks in the DNA (to which extend this can be lethal depends on the guide RNA and where nicks are created). Gene, or DNA region, deletion/insertion is achieved exploiting homologous recombination. NHEJ will simply repair the nick without any modifications of the DNA therefore by disfavoring NHEJ an higher efficiency of genetic modification is achieved as now the cell is "forced" to use HR to repair the DNA. The 1st figure in the post shows that cells lacking CRISPR complexes survived (2nd lane)  to the Src7 treatment but are of course not modified.


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Do sodium channels keep renewing themselves with new subunits made by genes?
genes make alpha beta gamma subunits (proteins) to be used in making sodium channels... If I understand correctly? And so, since the genes keep making those subunits, does that mean new sodium channels are continuously being made with those proteins till you die?
In other words, if those genes suddenly stop making the subunits in your 50's or something, your sodium channels will disappear or stop working? (Probably unrealistic, but theoretically...)

This is your second question about sodium channels that seems to show some misunderstandings about genetics, gene expression, and protein expression. So far, you've just used the term "sodium channel", I suggest you read the wiki page, then ask about a specific sodium channel, or at least offer more details. I am also having trouble understanding what you're asking. Are you asking if 1 gene makes multiple copies of the protein it codes for (it does) or are you asking if 3 individual protein subunits make multiple proteins (they don't).

Please do some research on protein turnover. Sodium channels, or any other protein or protein complex, are not just created early in life, then stay where they are until the organism dies. Cells are constantly dying and being replaced, and within a single cell proteins are constantly being degraded and new ones made. For some proteins the half-life is seconds or minutes, for others it can be hours, days, or longer, but eventually it all gets renewed. I suggest you do some more background reading on cell biology - Molecular Biology of the Cell is a good start.

You should really study the basics before asking specifics about a particular protein. I am not voting to close the question, however.
DNA catalyses the formation mRNA (transcription) which in turn catalyses the formation of a polypeptide (translation); RNA polymerase and ribosome are co-catalysts respectively.
A functional protein may have many polypeptide chains as in the case of Sodium channel (or even haemoglobin). The function of the protein complex may be compromised if:

The polypeptides chains are not formed
The polypeptide chains are not associating properly

The former can result either because of a block in translation or a block in the transcription. These blocks can also arise because of active regulation in response to a certain condition; this is a temporary change.
Mutations can lead to loss of function by either causing transcription/translation blocks or abolishing interaction between different polypeptides.
In a cell all biomolecules are continuously formed and degraded. The rate at which they are degraded is called the turnover. If a steady level has to be maintained then turnover rate should be balanced by the formation rate.
When formation is abolished then different biomolecules will disappear at a speed proportional to their degradation rates.
If the mutation causes a loss of association of polypeptides then non-functional proteins will replace the functional ones with rate proportional to the degradation rate. (NOTE: Formation rate of a protein is proportional to the available mRNA).
Most intracellular and membrane proteins have high turnover. Extracellular structural proteins such as collagen have a relatively low turnover. So if sodium channel gene stops transcribing the effects would be felt very soon.

You are asking about two different processes: turnover (degradation) of mRNA and turnover of proteins.  In a typical mammalian cell the mRNA half-lives of stable messages approach the length of the cell cycle (e.g. 24 hr). One mRNA could be translated around the clock if needed. The resulting proteins will also have a measurable half-life, and that will vary with the protein and the cellular conditions. If a cell ran out of protein and its mRNA there is often a feedback loop that activates transcription of the structural gene back in the nucleus.

Feedbacks are not essentially always present.


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Why is it easy to separate the cotton wool from the roots of young plants grown in cotton?
In my book it is said that if we grow Maize and Gram seeds in wet cotton, after the seeds are sprouted it is easy to separate the cotton wool from the roots of young plants.
My question is why is it comparatively harder to separate roots from soil while it is easy for cotton wool?


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Horizontal gene transfer versus convergent evolution
There are several often noted examples of convergent evolution (eyes, bat/bird wing evolution etc.)  How do we rule out horizontal gene transfer in these cases?

You know that bat wings are modified hands, while bird wings are modified arms.  And human eyes and insect eyes are very different.

Without any molecular evidence you could infer convergent evolution if the species being compared shared a common ancestor that lacked the trait in question.
With genomic and developmental data you would measure the degree of similarity shared between the relative factors in each species. Little or no similarity indicates convergent evolution.
Horizontal gene transfer is predominantly found in bacteria. Although there are examples of limited gene transfer in eukaryotes, the donor is almost always bacteria. And there are currently no known cases of multi-gene transmission of complex networks.
It is interesting to contemplate how a full network might be transmitted horizontally. Horizontal Network Transfer would first require a mechanism for segregating the relevant genes from the rest of the genome. It would also require invasive machinery that allows the large amount of foreign genetic material to bypass the host's defense systems. Furthermore, integration of a foreign network is increasingly more difficult with the more genes you transmit due to positional and regulatory effects of the host genome. And on top of that, it is highly unlikely that a full complement of genes involved in a complex developmental process would function in any way resembling eye or wing development. These networks have been coevolving within massively complex genomic environments for hundreds of millions of years. Expressing a large network in a foreign cell would likely prove toxic.
A looser definition of HGT might include bioengineering, specifically stable transgene integration.

A small comment on the use of the term homology. Homology is an absolute state, i.e. genes (for instance) are either homologous or not homologous. Referring to degrees of homology is misusing the term. Genes can be identical to a certain degree which not necessarily means that they are homologous.

@RickardSjogren you're right. I've edited the answer to use the correct term. Thanks!


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Verifying Protein Folds
I have recently begun using Folding@Home and I am curious how people are prevented from cheating the system. It seems to me that unless the final result is easily verifiable users could submit bogus folds in order to quickly gain credits. Is it in fact the case that the final results of calculating a protein fold are easily verifiable?

What I think might be happening is the same set of sequences is sent to multiple computers, and the incoming results are compared a number of times before they're declared valid. So, for example, the same sequence could be sent to 50 computers, and a certain threshold need to match (say, 20 of them) before they're marked as valid. Then, if any other computer submits a different result, it's marked as invalid and not counted.


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Is this pCAMBIA co-transformation possible?
I would like to know whether the pCAMBIA1200 and pCAMBIA0380 be used for co-transformation of rice using Agrobacterium LBA4404.They probably have the same ori site so they belong to the same incompatibility group.So will they co-exist in one Agrobacterium strain and be transferred to the rice plant?
Please let me know.

It would be good if you include the plasmid map.

Please check and tell me and how do I go about the co-transformation of rice using Agrobacterium starting from E.coli


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Bohr effect in respiration
Would I be correct in saying that the Bohr effect is ONLY related to the concentration of [H+] in the tissues.
Obviously the concentration of carbon-dioxide can contribute to this concentration by producing protons (through carbonic anhydrase) but it isn't directly involved in the effect?

Would I be correct in saying that the Bohr effect is ONLY related to the concentration of [H+] in the tissues.

I would say no. Because oxygen binding affinity is inversely related to both [1]:

high $[H^+]$ concentration and
$CO_2$ increase (which is can be a consequence of the first)

$CO_2$ is involved in the Bohr effect:

The biological significance of the negative influence of the carbon dioxide pressure on the oxygen binding of blood is obviously very big. [...] During the bloods movement through the body the oxygen-pressure will decrease to a relatively low value, whereas at the same time the carbon dioxide-pressure rises. This will greatly support the oxygen release from the blood, resulting in an improved efficiency in oxygen usage [2].

References:

Wikipedia contributors, "Bohr effect," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Bohr_effect&oldid=618215597 (accessed August 4, 2014).
Chr. Bohr, K. Hasselbalch, and August Krogh. Concerning a Biologically Important Relationship - The Influence of the Carbon Dioxide Content of Blood on its Oxygen Binding. Available from http://www.udel.edu/chem/white/C342/Bohr%281904%29.html (accessed 04.08.2014)

In a strict sense, I think you are correct that [H$^+$] contributes directly to the Bohr effect. A paper by Perutz et al. (1980) identified at least two amino acid residues in hemoglobin that account for the Bohr effect by interacting directly with H$^+$. CO$_2$ is not directly involved. Further, the Bohr effect (and the Root effect) are defined in terms of pH.
You and @Cornelius are correct that CO$_2$ contributes to the Bohr effect but speaking strictly it is a contributor and not the proximal cause. CO$_2$ dissolved in water produces H$_2$CO$_3$ which dissociates to release H$^+$, decreasing pH. But, lactic acid (for example) can also contribute to the Bohr effect again through the release of H$^+$.
While CO$_2$ and lactic acid contribute to the Bohr effect through the release of H$^+$, the H$^+$ is the actual cause through interaction with amino acids in the hemoglobin.

Perutz, M.F., et al. 1980. Identification of residues contributing
to the Bohr effect of human haemoglobin. J. Molecular Biology 138:
649-668.
Root, R.W. and L. Irving. 1943. The effect of carbon dioxide and
lactic acid on the oxygen-combining power of whole and hemolyzed
blood of the marine fish Tautoga onitis (Linn.). Biological
Bulletin 84: 207-212.


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Enzyme Assay, absorbance change to concentration change
I have a few issues with this question.
An enzyme assay is performed and the kinetic data graphed. The y-intercept of a Lineweaver-Burk plot is 0.6 min/ΔA. The substrate being assayed has a molar absorbance coefficient (ε) of 4500 L/mol.cm.
What is the V max of the enzyme in mmol/L.min?
My working:
Vmax = 1 / 0.6min/ΔA = 1.66ΔA/min (the units switch back I believe?)
And then 1.66ΔA/min / 4.5L/mmol.cm to get 0.37 mmol/L.min?

This looks correct to me, although it odd not to relate the activity to the amount of enzyme that was added to the reaction - the Vmax that you have calculated is a property of the exact assay conditions used.

see here.
y-intercept = $\frac{1}{V_{max}}$
To convert absorbance to concentration, plot the standard curve and get the linear relationship between the two quantities. Make sure that the line that you fit (for standard curve) passes through origin.

No need for a standard curve if you have an extinction coefficient, as in this case.


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How is photosynthesis observed?
How is photosynthesis observed?

Say I have plants A and B, and I want to find how fast they are able to turn carbon dioxide into oxygen. How would I experiment this?
Say I have one plant A, which has two kinds of leafs B and C. I hypothesize the B-leafs produce oxygen faster than the C-leafs. What kind of experiment could I set up to test this?

Is that a homework question?

No, I'm just interested. Anyway, if the question is too simple for this site, I would be happy with a good reference alone.

No, that's fine. I am just asking.

What do you want to measure- $CO_2$ consumption/carbon fixation, $O_2$ production or $ATP$ production ?
All rates need not be the same..

You can try isolating the leaf/bunch of leaves (in a transparent cellophane paper or something similar), and then pass the air content inside the isolated region after a while, through solutions such as $KOH$ or alkaline pyrogallol. $KOH$  dissolves $CO_2$, whereas pyrogallol dissolves $O_2$. The reduction in the total gas volume will be equal to the amount of the particular gas. You should normalize this with the total surface area of the leaves.
This is just my guess for a homework type experiment. I am sure complex equipments exist.

Not sure, this what you need, but here you can find a detailed description of how photosynthesis efficiency can be measured in the field, with a list of modern devices. In short, it's about measuring the uptake of CO2 and release of H2O of individual leaves.

Hydrogen carbonate is an indicator commonly used for testing photosynthesis. It shows changes in carbon dioxide concentration in the air. You would set up the plant in a sealed system next to a tray of hydrogen carbonate indicator solution and observe the colour change.


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Machine learning for light microscopy -- problems to solve?
I would like solve some biological problems that would improve the state-of-the-art of biology or bioinformatics. In particular, I want to apply machine learning on light microscopic images. The equipment and experience I have are:

Bright-field, dark-field, and phase-contrast microscopy
Modern laptop
56-core super-computer with >100 GB of memory (on request)
Intricate knowledge of machine learning algorithms and signal processing
PhD-level research skills
Programming skills that would get me to work at Google
Limited knowledge about biology, bioinformatics, and microscopy (yet)

I want to do some publishable research free from all academic hassle. I will do this solely on my own time, without hurry to publish, in an attempt to do something good for the mankind. I can throw a few hundred dollars on the project every two months (or abour 1000 USD per year).
Much of the biological research published in Science, Nature, PNAS, Cell, etc. are so specialized that I find it difficult to detect important problems I could have a good chance of solving given my skill set. Thus, I am asking your help:

What kind of software you always wanted for light microscopic research, but did not know how to build?
What are some important biological problems you would like to get solved? (For machine learning, problems with a binary decision task are particular well suited -- e.g. "does this person have malaria or not"?)
What are some recent, high quality reviews on open problems in biology?
Something else?

While my question is a bit broad, I think this goes under the "good intention" (or whatever it is called) SE policy.

Neat question, but I'm, afraid there isn't one answer to accept and this one might get voted off... while it's up, though, how about pollen identification? There are ecology, paleoecology, forensics, health, and food safety implications, it's a challenging computer vision problem, and there should be plenty of imagery online to train an expert system with.

This is a great question and should not be voted closed since it is attempting to address an important issue, which (if solved) can have great implications in automation of imaging and data flow and the type of data obtained! Surely biology stack exchange is designed to help with questions such as this!! Kudos to you @days_of_good. One great place you can start is looking at fiji image-J (image analysis software) and look at its plugins. Most are open-source and it would be great if they could be incorporated in microscope imaging softwares and perform instructive commands to the microscope!

@days_of_good is there a scope for your work to cover fluorescence microscopy such as confocal or snapshot widefield and deconvolution microscopy of z-stacked images? a very very large portion of microscopy in the current scientific landscape uses fluorescence techniques to detect molecules or structures at cellular level, mainly using either fluorescing molecules GFP, RFP, YFP, etc attached to the molecule of interest or antibodies which detect a molecule and they themselves are detected by fluorescing secondary antibodies. The main problem in the field of microscopy is the noise-to-signal.

@Bez No, unfortunately I do not have access to fluorescence microscopy. Is there need for deconvolution methods applied to light microscopic images? I know some blind deconvolution methods, which could maybe used to pass the diffraction limit (kind of super-resolution).

@Oreotrephes Do you know any good recent review about pollen identification? The problem sounds like it could be solved using some supervised multi-class machine learning algorithm.

@days_of_good it should be possible (though never done it for visible light) since you are still dealing with light waves/particles except the wavelength is different to fluorescence. SoftWoRx software (Applied Precision) in my opinion produces one of the best deconvolution images using iterations, which comes with delta vision core microscope. I'm confident if you contact your nearest university and discuss what you would like to do, they will be more than happy to put their equipment at your disposal and they even provide help! I know may PIs that are desperate for such talent and enthusiasm

@days_of_good I know for example people use light microscopy to assess embryo phenotype to predict its development. Although I can't access this article but I assume they use light microscopy and look at the overall shape (phenotype of the embryo for the study) so deconvolution would be very handy for this (http://www.fertstert.org/article/S0015-0282(14)00203-9/pdf)

@days_of_good This might be a good starting point for pollen-ID http://tinyurl.com/p44loza

Unfortunately exactly that :/ This question fits several of the "what not to ask" examples in the FAQ. (http://biology.stackexchange.com/help/dont-ask) You can of course bring these sort of things to chat! (link at the bottom of the page)

This is a great and thought provoking question. If it were in chat I would never even have seen it. Many years ago I worked with a scientist at Kodak's research division in Harrow, London. The work was to count the number of photons required for activation of silver halide grains (interpolated from silver nuclei). The bulk of the counting was done on a Cambridge Instruments Image Analyser hooked up to a microscope with a TV camera attached. Not much call for it these days but I could envisage the equipment discussed being used for counting particulates in polluted water and other such tasks.

I know this question is going to close. But, if you want to work something you can work on:
Cryo super-resolution fluorescence imaging

Highlights

CryoFM allows imaging of vitrified biological samples with fluorescence microscopy.
There are significant challenges to achieve high-resolution cryoFM imaging.
Fluorophore characteristics at low temperature offer additional advantages.
Cryo super-resolution fluorescence imaging will give dramatic resolution improvement.

Source: Fluorescence cryo-microscopy: current challenges and prospects.

RE: What kind of software you always wanted for light microscopic
  research, but did not know how to build?

I research fruit flies and in this field (and many other insect ecology model systems like beetles, moths, butterflies) we use a lot of visually scored data, e.g. body size, wing size, wing morphology, eye colours, bristle numbers, genital morphology, sex comb morphology... the list is huge! One program used is WingMachine - though the link to the software seems to be broken - which can measure morphology aspects of a fly wing.
Something I'd like to be able to do is put a vial of food under a scope and have it quickly count the number of eggs on the surface of the food. I asked a question about it a while back.. This would be very useful, many labs have to count eggs (to make the number of eggs constant in each vial, variation here can have serious effects on the adult fly so control is important in ecology studies) and it is a slow, difficult and highly inaccurate, particularly variable between people. If there was some way of putting the vial under the scope, hitting a button and getting an approximation of the number it would be great!
A colleague counts dead beetles at the moment, I'm sure he'd appreciate a similar kind of program where he could image and have the software count automatically. I think both of these problems would be easy to solve with very similar software. Making software that is easy to "teach" how to recognize individuals is the key.
A slightly more complex bit of machine learning might be getting it to count different phenotypes in one image. Fitness assays in flies often use a wild type fly with dark bodied (ebony) competitors, the body of the wild type is comparatively more yellow. The fitness of the focal wild type fly is then the number of wild type offspring among the total (the dark body phenotype is recessive, therefore when the focal wild type mates with an ebony it produces wild type flies, if two ebonies mate we get a dark body offspring). Here the machine would have to be able to tell the difference and count both.
I'll attach a proper picture from under the scope later, the picture in my previous question was taken with a digital camera, not via a scope but it gives an idea of what it looks like.

You might be interested in reading the article "Machine learning in cell biology – teaching computers to recognize phenotypes" (http://jcs.biologists.org/content/126/24/5529.long)

Please summarize the relevant aspects of the link in your answer. See the 'provide context for links' section of the Help Center.

One of my colleagues does lots of histological work, staining and identifying tissue at the microscopic level. Software that could be helpful to that discipline might be the ability to distinguish among the different types of tissues present, and perhaps calculate the "area" occupied by each tissue type as well as empty space. This would not be unlike a GIS type problem, but I don't know if it fits well with a Yes/No binary decision framework. I don't know if it could be trained to learn to identify specific types of tissue, but perhaps it could recognize each distinct area of a cross section as different from other such areas.  Here are a few cross sections to show you what I mean:
Colon:

Source
Smooth muscle:

Source
Seminiferous tubules from testes:

Source
Notice the different tissue types in each cross section, plus the white space. Each tissue type has different light transmission patterns, which may allow a computer to learn to distinguish among the different tissue types.


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Is DNA replication a serial or parallel process?
This video entertainingly supplements this 3d animation of DNA strand replication. Does this process happen serially from the beginning to the end of a DNA strand (like having to unzip a six foot long zipper - example A below) or does the strand get chopped up into chunks, unzipped individually, replicated then brought back together (example B)?

I suspect the answer is case A. If so, is any phase of replication done in a parallel fashion? I would think something has to be (since it happens so fast and serial anything is typically very slow in comparison).

The DNA isn't cleaved, but replication can be initiated at multiple points on a chromosome and proceed in both directions. I'll elaborate on this later and post an answer in the future if no one else has. This paper estimates that there are 10,000 to 100,000 replication origins in a human cell. This means that the average leading strand would be approximately 60,000 to 600,000 bp long.

It's like having a zipper with multiple "pulls" along its length.

My personal opinion is that videos of this type and 3D animations are scientific poison. OK, for popularising science, but not a useful source of serious information. Rather than speculation, however intelligent, I suggest you consult text books that have been carefully written by experts, professionally illustrated, and edited by other experts. You can get access to older editions of some of these on NCBI Bookshelf: https://www.ncbi.nlm.nih.gov/books/. If you search there for DNA replication you will find clear and comprehensive accounts to answer your question.

@canadianer, you're picture is perfect! That's the answer!

@David, thank you for the link. I'd like to add that popularizing science is good for science (which is antithetical to poison). Science without much interest or support doesn't get very far

@AlwaysConfused Which one? They both work for me.

I think I made a mistake with my math. Should be 30,000 to 300,000?

@AlwaysConfused I didn't post that… and I can access it fine.


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Are enzyme inhibitors only a possibility?
I take 3 medications that metabolize by the same liver enzyme cyp2d6. A drug interaction checker told me that on or two of the medications i take may slow metabolism of another by altering drug metabolism. Ive had no side effects or interactions from this combination of drugs. Ive also read of people being on the same combination of drugs with no problems. If a drug is considered an enzyme inhibitor, is it a definite that it will slow metabolism and raise blood levels of another drug, or is this just a possibility?
Thanks for any feedback

The interaction checker is flagging those drugs for a physician/pharmacist to monitor and make a treatment decision on. It does not mean "people that take these two drugs will die immediately." It might mean "people that take these two drugs together are more likely to see rare side effects" or "people that take these two drugs together might have a lower blood pressure on average" - without more information you can't know.

It is unlikely that any of the drugs are enzyme inhibitors.  Generally the drugs can interact by competing for the use of the CYP2D6 enzymes for the period needed for enzymatic activity (usually quite short for each molecule of a drug or other compound, other than inhibitors).

My main question is that the interaction checker states that two drugs i take may or can alter the metabolism of a third drug i take. To me this means only a possibility, and won't necessarily happen. Hence, using the words may and can. Is this the way others here understand this?


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Grasshopper identification
I found this grasshopper (although I'm not sure if it was really one) near a lake in Bangalore, back in mid April. This is the only picture i could get and since it's so well camouflaged I would like to point out that it's right in the middle. It had those very conspicuous green bands on either half of the dorsal side with longitudinal white pinstripes. It was around 10 cms in length. Can i get an ID please?

What's meaning of get an ID?


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Pest on fenugreek
I need help identifying this pest on a fenugreek leaf. It is very common Maharashtra and Karnataka (India), and probably other states as well. Some of the leaves in the fenugreek bunches bought in the market have this kind of a distinct pattern. I am not able to pinpoint the exact orientation and shape/size of this organism on the leaf so I'll be glad to accept any help for that as well.

It is some kind of leaf miner, which should narrow the search. I am not sure what species.


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What exact characters determine an animal's Genus?
I do know that if two animals cannot naturally reproduce, they are said to be of two different species. But what determines the genus?
Just for example, the African elephant belongs Loxodonta but the Indian counterpart belongs to Elephas , despite the fact that they are so similar, as opposed to say, the fact that, the Bengal Tiger and the Snow leopard despite being so different , are placed in one genus, Panthera ?

I don't think there is any non-arbitrary concept being used to tell whether two species belong to the same genus or not. The same goes on with any other taxonomic rank. Systematicists build some intuition within each clade about what a genus could mean and use it to argue what is the most strategic grouping but the concept of genus may well vary a lot from clade to clade (from spiders, to mammals or to flowering plants, ...).
Note that even the concept of species is not as nicely defined as you may think. Have a look at How could humans have interbred with Neanderthals if we're a different species? for discussion on the concept of species.

What also SciShow forgot to mention is that, by the very definition of evolution, taxonomy is just a handy way that we invented to simplify our life (or complicate, if you ask me). As they pointed out, categorizing and identifying appeals to our brain. But it's just a photo of a runner; if you snap it a few seconds (or geological eras) apart then you get the runner in a different position.
Reminds me of a riddle I was told some time ago: "where was the men when he jumped off the bridge?". If your answer is "in the air", well that's AFTER he jumped... likewise "on the bridge" is BEFORE he jumped.
So what we today identify as a specific species or genus might very well change in the future decades or even years and taxonomy is full of cases in which species where "relocated" and renamed. Sometimes changing the parameter on which you build the taxonomy (mostly now is gene based, before it was morphology based) might completely turn the tree upside down from the roots. Plant taxonomy (being a botanist that's what I'm familiar with but I suppose it happened also with animals) was revised multiple times because some clades would change position depending which gene was used as reference.


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Red bug with white tips on antennae
These red bugs can be found in hundreds in our locality in Bangalore, India.
They are just about 3.5 cm and have these white (or maybe pale yellow) tips on their antennae.

Can someone identify them and suggest a link where I can find substantial information on their morphology and general behaviour?

What's That Bug? (https://www.whatsthatbug.com/) is another great place to ask for bug identifications.

I think they are called "Red Bugs" (really), otherwise known as Antilochus conquebertii (aka Antilochus coquebertii).

The black coloring changes from location to location. These were found in India. They were even described by the querent as eating black seeds.
Viet Nam Red Bugs are pretty as well:

The family Pyrrhocoridae is commonly called the Red Bug family, and the family includes the Cotton Stainers as well as the Firebugs, so Red Bugs is the more general family name that includes the other genera and species.

Thank you for the answer but I think it's A.conquebertii, with a double 'i' . Also where can I find some information on them?

@AdDate, Google is your friend.

I didn't find much though. I want some more details.

Antilochus is a sister clade of Pyrrhocoris which we call "fire bugs" (or "gendarme" in french). You'll easily find more info for Pyrrhocoris.

@AdDate Note by the way, that it is more polite to say "I would like" than "I want".

@BumptiousQBangwhistle - Thanks so much! That is a great help. I'll edit that into my answer.


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Are Raf, MEK, and ERK MAP kinases?
I am trying to make sense of this diagram.  Can Ras activate RAF or MAPKKK, or is RAF a MAPKKK, making MEK a MAPKK, and ERK a MAPK?

Mitogen-activated protein kinase (MAPK) is a generic name for a family of different but related enzymes involved in this specific signalling cascade. RAF is a MAPKKK, MEK is a MAPKK and ERK is a MAPK. This is evident in the Nature article from which your image is apparently adapted:

Activated RAS triggers the activation of the MAPKKK RAF. Activated RAF then phosphorylates the MAPKK MEK (MAPK and ERK kinase) on serine residues leading to its activation. Subsequently, activated MEK catalyses the dual phosphorylation of the MAPK ERK.


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Transfering Odds Ratios to another SNP with high LD?
I have the Odds Ratios (OR) for a particular risk allele in a SNP (I'll call it SNP1).  That SNP was unfortunately not genotyped in my data, but I don't want to throw it away.  I have looked up the SNP on LDLink and another SNP (I'll call it SNP2) is in high linkage disequilibrium with SNP1 (R2=0.94).
How do I transfer the OR from the SNP1 allele to the corresponding SNP2 allele?
I know it is something similar to log(OR)*sqrt(R2) but I'm not entirely sure.  Could somone please clarify if this is the correct formula?


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Why does rotational cleavage take place in mammels like humans. What is its significance?
What is the actual reason behind the rotational cleavage that takes place in humans? Why does it happen? If it doesn't occur, what will happen


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Assessing carrier Risk
susan has been found to be a carrier of Tay Sachs. what is the risk that her maternal aunt is also a carrier if we don't know her parents status?

I believe it should be 1/2 since her mom is also 1/2. I just want to know if I am right.

First you have to know that Tay–Sachs disease is an autosomal recessive genetic disorder. Below we will assume that the mutation is at low frequency in the population.
Probability that Susan's maternal grandparents carry the mutation
The probability that Susan's mother carry the mutation is $\frac{1}{2}$. The probability that the mutation is present the Susan's maternal grandparents is therefore also $\frac{1}{2}$.
Probability that Susan's aunt received the mutation if her parents where carrying it
Now, if the mutation is present in Susan's maternal grandparents in a single copy (which is a consequence of the assumption of the mutation being at low frequency in the population), then the probability that the sister of Susan's mother received this allele is $\frac{1}{2}$ too.
Putting these two probabilities together
Putting these together. $\frac{1}{2} \frac{1}{2} = \frac{1}{4}$. The probability is $\frac{1}{4}$.