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Current understanding of abiogenesis
I am trying to understand the current work on abiogenesis in biology, e.g. primordial soup, the Miller-Urey experiment, etc.
How has our understanding of abiogenesis been revised since the Miller-Urey 'primordial soup' hypothesis?

Start with the references in the Wikipedia page, do some targeted googling, and work from there.

@MattDMo I realize I can do this. However, this is an academic discussion forum. I would like to hear from academic biologists for the state of the field.
That's distinctly different than just googling. I can read biology textbooks too, but the point of this question is to hear from academic biologists.

This is not a discussion forum, it's a question and answer site. Not everything goes. Matt's comment is very appropriate; not possible when I was studying molecular biology (I read Oparin's The Origin of Life.) But for the history and an intro to where we are now, the references given in Wikipedia are a fine start. You can always ask more specific questions then. Please see the site tour and the help sections for more information about the site, particularly what kinds of questions are on topic here. Thanks!

@anongoodnurse I think "who is currently at the forefront of the field" is a fairly specific question. Also, I don't think it's helpful for learning to close down/vote down such questions because they are borderline discussion questions---this is a bit too pedantic. Stack Exchange was set up for learning, and that's exactly what I'm trying to achieve.

While your question might be specific, based on the fact that academics are humans its answer will be primarily opinion-based and thus out of scope for this site anyway. Person X might think, they are on the top of the field and their area of expertise is one of the major research topics, but their favourite academic competitor Y might disagree and instead bring herself and her topic in the discussion. And now it is a discussion. Unless there is a publication (from a field like sociology?) which studied the "academics of abiogenesis" there is no scientific answer to your question.

@skymningen Ok, how would you prefer I rephrase this question: "How has our understanding of abiogenesis been revised since the Miller-Urey 'primordial soup' hypothesis?" That is also strictly speaking not an objective scientific question, but it has educational merit. That is the point of Stack Exchange. Not all questions should be homework-esque questions.
Also, where else would you suggest I post this question in order to reach academic biologists, if not here?

@ShanZhengYang The question you pose in your comment is answerable in a way where one can cite the most important (published in high impact factor journals and/or highly accessed/cited) publications. Then maybe you sort them in a timeline and there you have a development. It might not picture everybody's opinion on it, but it will picture how this scientifically developed and the answer can have a objective approach.

@skymningen OK, that sounds reasonable. I've edited above. You are welcome to edit as well. Thank you :)

My "answer" to this question may interest you: http://biology.stackexchange.com/questions/19316/first-rna-polymerase-mrna/19737#19737

Our understanding of how life began on earth has indeed advanced substantially since Haldane, Oparin, Miller, and Urey. To learn about the latest ideas, I can't think of a better place to start than this excellent video series with Nobel Laureate Jack Szostack, who is currently doing some of the leading work on the subject.


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Biologically, does life and death matter?
(Sorry that I'm on mobile, so I can't make a good formated question (no links). I will add them later. Just can't resist the urge to ask)
In the recent hot question about whether mitochondrial is alive or dead (it's technically dead), the top answers don't only explain whether it is dead or not, but also further explain why it doesn't matter: they just do what they need to do. This provokes me a question:
Q: Biologically, do life and death matter? Is the functionality of something the only thing that life cares?
We human are scare of death. Because of that, we tend to apply that idea into everything we can observe, even if it's meaningless. But why is death scary? Isn't it because when you die, you stop function anymore? So ultimately, isn't what we really mean when discussing whether something is dead or not the functionality of that?
Not only that, "there is no consensus regarding the answer to the question as to when does life begin". If we approach this in a different way: the time when an individual function begins to work, will there be a consensus? I mean, just don't think if an organism is alive or not, just think that how much functions of it have started to work.
If we are the combination of the numerous of selfish genes, would "humanity" be a collection of functions?

" Isn't it because when you die, you stop function anymore? "       Your body still has use after you die, Bacteria and fungi can decompose you and recycle your elements like Nitrogen to put it back into the Cycles that exist. Like the Nitrogen Cycle. I also feel like your question is still vague, since you haven't really set a definition to use for "life" or "death". A "function" is a bit vague too, since as I stated before, there can be the concept of recycling to allow for various functions, whether the source is living or dead.

The "death" definition is taken from the discussed question which I haven't linked to this. A "function", well yeah, it isn't defined well. But I would define it like a mathematic function: output = f(inputs). (Thinking a while). Ahh, what I mean is the metabolism.

I feel like your question answers itself almost. I mean I feel this topic is becoming more philosphy than biology, but could there be something biologicaly existing without a function? If not then I suppose functionality would be important. And I personaly can not think of some object(s) that are biological and that lack a function. Maybe that is just my lack of imagination though.

Then we have to define what is "biologically existing", or specifically, "biological". I think we will lead to the point that there is no such thing "biological". Anyway, why the downvote?

Well there is a limit to defintions, which is why I think the topic is better suited to philispohy. If I was vague though, I guess I meant " something that's living or dead ".

On a very different note, I feel that this particular question has hardly any relevance in biology. This question is a philosophical which is not really the same as science.  Many will argue that biology is the study of life itself, I strongly disagree, biology is a field in science aimed towards the study of aspects which can lead to better human wellbeing/welfare/health. The study of science itself is ofcourse the sating of one's curiosity. Philosophy has no place in science.

@KoustavPal would this be on topic on Philosophy? (Though I think it would be a dup there)

I feel so, and I think the mods will agree with me on this. I went over there and searched once or twice, they have certainly many questions discussing different philosophical aspects of death. So certainly you will get a much better answer to your question which discusses; if the question of what is life or death is even worth discussing, over there than here.

Man fear death because he does not know what happens after that. No one knows if we really cease to exist or if there is a life after death as many claim. Biologically the concept of life after death can't be researched as of now, I mean with our current level of technology. It is mostly a fear of unknown.

We human are scare of death. Because of that, we tend to apply that idea into everything we can observe, even if it's meaningless. But why is death scary? Isn't it because when you die, you stop function anymore?

Fear of death is hard-wired into our nervous systems. A thirsty wildebeest will approach crocodile-infested water very, very reluctantly. The wildebeest isn't thinking about the selfish gene or the loss of his function in the world; he's hardwired to be afraid of the situation. The same is true for any prey animal: fawn, rabbit, gazelle, mouse. The difference (maybe; simplifying for convenience) is that we are rational, and like all of our primitive fears (e.g., of the dark, when there really were sharp-toothed predators with better night vision than ourselves), we try to rationalize them. We also rationalize our existence.

Is the functionality of something the only thing that life cares?

Nature is red in tooth and claw. If you want to anthropomorphize Nature, then sure, we matter (we're destroying the earth at unprecedented speeds). If you believe in a spirit, we matter. But if you believe in none of it, the only purpose we serve is to propagate ourselves, and when the last of our species is gone, Nature will not care a whit. Just as it doesn't care that dinosaurs, wooly mammoths, passenger pigeons, tasmanian tigers or baiji river dolphin are gone.
It can be argued that in the grand scheme of things (and here I'm speaking of the entire Universe), biological life doesn't matter at all.

Then the sun, the earth and everything else don't matter at all. Sorry, I think my question is not clear. "Is the functionality of something the only thing that life cares?" should be read as "Is the functionality of something the only thing that we should care at all?". I don't intend to anthropomorphize nature.

@Ooker - That's a very different question! The answer to that, I think, is very, very different. I can't answer that because of the words "functionality" (who gets to define that?) and "should". Should, to me, implies a moral perspective. I believe we "should" treat life in and of itself as precious. If everyone agreed with my moral perspective, there would be no starving people in the world, livestock would be raised much more humanely, etc. etc. Clearly, everyone does not.

Nice comment! @anongoodnurse

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Finding a reaction from a KEGG map
I have come across a map and a part of it looks like this:

Now I have not been able to locate the reaction that converts alpha D-Glucose to Glucono-1,5-lactone but was successfully able to locate the reaction that converts alpha D-glucose Glucose to Glucose-6P. Since an arrow exist from alpha D-Glucose to Glucono-1,5-lactone, i am assuming that such a reaction exist. But could not locate it. I clicked on the arrow marked in blue in the picture, but could not find the desired reaction.(alpha D glucose and beta D glucose are different compounds)  What is the reaction and how is it possible to find the reaction from the map?
NB: The arrows are clickable so are the circles that denote the compound.

It was a simple search. You could have easily searched for glucose oxidase in KEGG, and you would have got this reaction.
In fact if you had clicked the link for glucunolactone's compound page, you would have got a list of many different reactions that convert glucose to glucunolactone.
You can even click the arrow which opens the KEGG-ORTHOLOGY page. You can find a field called RN in the section called "Other DBs". The links corresponding to this field would give you the exact reactions, that the pathway uses.

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Chimeric Gene vs Fusion Gene?
According to wikipedia on chimeric genes:

These mutations are distinct from fusion genes which merge whole gene
  sequences into a single reading frame and often retain their original
  functions.

I am not totally sure I understand the statement. My interpretation is that a fusion gene is caused by a translocation of DNA in a single gene; therefore, it "retains their original functions". This is different from a chimeric gene where DNA from two or more different genes are translocated to a new location to form a completely new gene.
Is my interpretation correct?

A chimeric gene is formed from fragments of other genes whereas a fusion gene is formed from the entirety of other genes. Often in the literature you'll see the term fusion gene used for both cases.


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What Chemical Trigger Causes Ectomycorrhiza To Change From Asexual To Sexual?
I want to know the trigger behind the change of asexual to sexual ectomycorrhiza when symbiosis with a tree root is formed. As ectomycorrhiza attaches itself to a root, it forms a relationship wherein phosphorous to the tree/plant is exchanged for glucose to the fungus. When this symbiosis occurs, the fungus, which is normally asexual, becomes sexual(male/female components) and buds form as a result. Thus I could hypothesize that if glucose is the catalyst, I could saturate the soil and cause this reaction. However, I am not sure what the actual chemical signal is, or if there is an unforeseen factor causing this change. Does anyone have any knowledge on the subject of what the aforementioned catalyst would be?


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Why would a plant evolve to produce an addictive chemical?
It seems kind of anti-productive in terms of survival for a plant to produce an addictive chemical as that plant will constantly be sought after by animals that ingest it. In this instance, I'm looking for a possible general & inclusive answer here that would describe most plants that make this. Not a specific instance (although if provided as an example would be a plus).
To appreciate the scope of this is terms of number of plants producing potentially addictive compounds - see this compendium:
compendium of botanicals reported to produce toxic, physchoactive or addictive compounds

Which addictive chemical?.. Can you add some examples and references?

Compounds like nicotine and caffeine are poisonous, especially to insects.

@WYSIWYG I'm trying to keep this general, but I know this question is borderline-maybe a little too open ended.

The supposed addictive properties easily could be random side effects, unrelated to whatever function the chemical performs in the plant.  Remember that evolution does not plan ahead.

@canadianer There was an article in science magazine some months back which said that bees develop a stronger memory of flowers that contain caffeine in their nectars.

@WYSIWYG That's quite interesting. I was also thinking that such compounds, being addicting, could aid in seed dispersal by higher animals.

@canadianer Found the article... I added that as an answer..

Well, see. Coca or tobacco plantages house billions and billions of plants. That's a huge success in terms of Darwin!

They didn't really "Evolve the trait of addictiveness"

@WYSIWYG didn't think about seed dispersal! You come up with that yourself? Nice one

Besides smoking a truck load of banana peels what fruits have addictive compounds? Interesting.

Good compendium http://www.efsa.europa.eu/en/scdocs/doc/280rax1.pdf

@WYSIWYG: Which suggests that caffeine is good for bees - as it is for humans.  I suspect bees would also have better memories for flowers with more/more nutritious nectars, while the plants would have pressure to evolve (through selection of random variations, not intent) nectars that "taste good" but are not so energy-intensive to produce.

How do you define "addictiveness" in the general case (i.e. not only for humans)? Would you e.g. consider nectar an addictive compound for nectar-feeding insects? How do you separate addictive compounds from simply preferred compounds, substrates or foods. Does the compound have to be detrimental or toxic to some extent for the species feeding on it (many examples normally labelled as "addictive chemicals" in humans are considered detrimental)?

Just this morning I've read about a caterpillar that produce a sugary substance addictive for ant. The ants will spend the rest of their lives acting as bodyguards for the caterpillar. Plants could develop a similar defence mechanism, doping other organism to act as its defence.

@algiogia symbiotic relationship

It's a matter of perspective. Most of the chemicals that are addictive to us humans (particularly alkaloids), and may be addictive for some other animals as well, are also insecticides. Lots of plants that we consider poisonous are good food for other species, and lots of plants that insects would consider poisonous are treats for us.
This is a great example of the aimless nature of evolution. The plants that could successfully defend themselves against insects stabilize on a solution that happens to be bad for them in certain ways. Although, you would be hard pressed to find a better way to guarantee reproduction than being addictive to humans.
Background reference

Plant-insect coevolution and inhibition of acetylcholinesterase
The defensive role of alkaloids in insects and plants
Exploration of nature's chemodiversity: the role of secondary metabolites as leads in drug development

Also of interest

Bees prefer foods containing neonicotinoid pesticides

Good answer, gonna keep this open for a couple more but I like this

No addictive products produced by plants can be found to have exclusively detrimental effects on the plant, they all have mostly positive effects, and plants can minimize or maximize a single chemical at their disposal, over some dozens of generations, because it's only a single chemical. Chemical changes are the most usefual and evolutionarily cheap method for plants to ward off or attract animals, easier to adjust than color, shape, hairiness, stinging cells, size, and so on.

Indeed. Even if they are generally toxic to the plant's system, they simply store them in vacuoles.

1 for "Although, you would be hard pressed to find a better way to guarantee reproduction than being addictive to humans."

Add to that most plants are not nearly so addictive in their natural forms as they are when processed.  So, the problem probably self regulates to an extent until such time as we decide to break out of the natural system and cultivate it.

Being attractive to humans may promote distribution, but "good for us" hardly matches "good for the species" (our plantains (bananas) would die quickly if care ceased), and we are careless (Silphium was possibly harvested into extinction).

As someone commented earlier, chemicals such as nicotine and morphine were products of evolution meant to repel animals. It is explained in more details in this article here.

Evolutionary biologists studying plant–herbivore interactions have convincingly argued that many plant secondary metabolites, including alkaloids such as nicotine, morphine and cocaine, are potent neurotoxins that evolved to deter consumption by herbivores.

But it seems that those same chemicals produce adverse effects to what they were originally intended for:

For example, one or more plant alkaloids have been identified that interfere with nearly every step in neural signalling. Targets include neurotransmitter synthesis, storage, release, binding, deactivation and reuptake, ion channel activation and function, and key enzymes involved in signal transduction.
Paradoxically, the same properties invoked to explain why common drugs like caffeine, nicotine and cocaine are toxic are also those invoked to explain why these compounds are rewarding. It is therefore important to stress that these and other addictive drugs appear to have evolved only because they successfully deterred, not rewarded or reinforced, plant consumption.

For example, let's take a closer look at nicotine. This compound is not present at all times in the plant, instead it is produced as a reaction to a trigger.

Nicotiana attenuata is an important model species for the analysis of plant–herbivore interactions involving nicotine. It is a domesticated North American tobacco plant that is attacked by over 20 different herbivores, ranging from mammalian browsers to intracellular-feeding insects. These attacks elicit a battery of defensive responses, including nicotine production.
Nicotiana has therefore evolved to allocate chemical defences strategically by concentrating them in the most valuable parts of the plant, such as young leaves, stems and reproductive organs, and by modulating its production according to the type of herbivore and extent of leaf damage.

This last example concentrates on nicotine, but it makes it easier to grasp how plants might use the production of such a chemical as a mean of protection.
Also, depending on the substance and the creature which consumes the plant, one might witness different outcomes. I found interesting information in this less detailed text here:

Defensive compounds from plants, like nicotine and cocaine, usually target nervous system components in insects. These components include proteins that have important roles on the insect’s physiology, which may include specific receptors, ion channels, enzymes, etc. In most cases, the defensive chemical kills the insect by interfering with one or more of these proteins; in other cases, the chemicals just make the plant distasteful for the insect, and therefore, the bug will leave the plant alone.

I am providing an example which somewhat contradicts the points mentioned in the other answers regarding toxicity of alkaloids to insects.
Caffeine is a stimulant and is toxic at high doses (also for humans) but at low doses it has a stimulating pharmacological effect on the organism. The same principle applies to insects as well. A study by Wright et. al (2013) has revealed that caffeine in the nectar of some flowers, enhances the bee's memory of that flower (a reward, in general).
They have also mentioned that:

Two caffeine-producing plant genera, Citrus and Coffea, have large
floral displays with strong scents and produce more fruits and seeds
when pollinated by bees (8, 9)

However, caffeine tastes bitter and bees would reject nectar (sugar solutions) containing high levels of caffeine (>1mM).

Arguably, caffeine acts as a stimulant at all doses, which is why it is toxic at high doses.

It's also arguable that everything is toxic at high doses - including oxygen and water.

Caffeine has an overall positive effect? That's not what I heard:  New research from Johns Hopkins Medical School shows that performance increases due to caffeine intake are the result of caffeine drinkers experiencing a short-term reversal of caffeine withdrawal. By controlling for caffeine use in study participants, John Hopkins researchers found that caffeine-related performance improvement is nonexistent without caffeine withdrawal. (found at https://www.linkedin.com/pulse/20140908162020-50578967-caffeine-the-silent-killer-of-success )

As for bees developing a preference for addictive drugs, that's actually turning into one of the great tragedies of our age: part of the reason honeybees are dying off so catastrophically in the last few years is because of the introduction of new pesticides derived from nicotine, which, in addition to being highly toxic to bees, is also highly addictive, so they just keep on coming back for more until it kills them.  Entire colonies worth of them.

@MasonWheeler Caffeine and Nicotine has been existing for several thousands of years.

@WYSIWYG: Sure, but what does that have to do with what I wrote in comments?

@MasonWheeler That question was asked on Cognitive Sciences if you're interested.

I don't think this contradicts the other answers, just adds a potential second reason why plants might have evolved to produce certain drugs.

Short answer
The appearance of psychoactive compounds in plants has nothing to do with their addictiveness in man.
Background
Psychoactive plants were there long before humans. The question therefore should be: "Why would humans evolve brains that exhibit addictive propensity to poisonous compounds abundantly available in nature"? The answer is: because our brain evolved in the absence of addictive substances.
One has to realize that addictive compounds are grown and processed. When humanoids evolved over millions of years, for the larger part there were no means to grow, harvest and process coffee beans, tobacco and coca leaves. Moreover, the most addictive drugs like injectable heroin and smokable cocaine (crack) are chemically purified. Methamphetamine and many addictive opiates are purely synthetic. In their native form, coca leaves and poppies are far less addictive, because in the raw form they lack the dopamine rush. Instead, the chewing of raw plant materials like coca leaves produces a mild high with a slow onset, and a mild offset. The sudden dopamine rush is what evokes the blissful euphoric state chased by heroin, crack and meth addicts, while the dreadful crash associated by these purified drugs is one of the strong motivators to seek for another hit. Also note that tobacco is heavily processed through a curing process before it is sold. The raw, woody tobacco products are far less likely to cause addiction.
Moreover, note that many of the addictive stuff originates from the Americas (coca) and Asia (opiates). Humans came from Africa. Africa is one of the continents with very, very few drug containing plants (Qat being the exception - a mild drug).

It's a good response but not what I'm looking into. It's pretty obvious that purifying cocaine and heroine make a much more addictive version. And the disease model of addiction...another topic. I was trying to question a natural selective process in which these compounds have apparently developed a survival niche in a sense

@rhill45 - and that line of thought is exactly what I counter here. I understand it is not what you want to hear, but I deemed it appropriate to share my view. Others have explained why plants produce drugs, I explain why the appearance of those plant-based drugs have nothing to with addictiveness in man.


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Is there a good analogy that illustrates the difference between early DNA sequencing techniques and shotgun sequencing?
My first university biology classes begin in September. In preparation, but increasingly out of curiosity, I've been studying some basic biology. Saying that to say, I know as much about DNA replication as the Khan Academy videos teach.
Presently, I'm reading about the two efforts to sequence the genome. From what I've read, Collins' project used "polymerase catalysis and nucleotide labeling"; whereas, Venter's project used "shotgun sequencing". I didn't know enough to understand the article I read on "shotgun sequencing" and couldn't find one that described the other technique.
I suspect that, in order to comprehend a concise description of the two techniques, I'd need to learn more than I could learn from an answer to this question. That said, it'd still be nice to have a very rough idea of what each process involves and how they differ from each other. A crude analogy to something concrete would be great.

You should read about chain-termination (aka Sanger) sequencing; it was used by both projects. Shotgunning is a technique used to assemble an entire genome out of the many short reads from the sequencer. The private project used whole genome shotgunning whereas the public project used the clone contig approach. This looks like a good read for you: http://www.ncbi.nlm.nih.gov/books/NBK21117/#!po=29.2373

The public effort, led by Collins, relied on a physical map of each chromosome.  Very large pieces of genomic DNA were sub cloned into cloning vectors and used to create genomic libraries in cosmids, BACs and YACs.  The sub clones are ordered using hybridization probes from either known genes, or RFLP genetic markers. In this way a physical map of each chromosome was built up, and then the project would march down the ordered clones, sequencing the sub clones.  If the physical map is good then you have a very good idea of where the sequence comes from.
Shotgun sequencing, in contrast, involves randomly fragmenting the entire genome into small fragments (using sonication, for example), sub cloning those pieces and sequencing everything.
In the first method each base is sequenced a minimal number of times, whereas in the second approach each base ends up being sequenced many times (on average).
For a whole genome, shotgun sequencing requires an excellent computer algorithm to "assemble" the resulting data into overlapping contigs.

What information informs the 'decisions' of the algorithm, and what sort of decisions is it making?

Good answer, though I'm not sure how useful it will be for someone just starting biology ;)

I don't think I have the expertise to compare and contrast the pros and cons of the competing approaches.  Have you read the Wikipedia entry on the Human Genome Sequence? There are many good references there. If you are interested in Venter & Gene Myers' algorithm you may find Michael Ashburner's short book about sequencing the Drosophila genome helpful. That was essentially a dry run for the Human effort, and they developed the tools then.  Matt Ridley's book "Genome" has a good description of the shotgun approach, as I recall.

PCR (polymeraze chain reaction) and shotgun sequencing are two somewhat complimentary approaches to sequencing. In the former case one uses chemical reaction to create multiple copies of the genome of interest, which allows to reduce the error in sequencing this genome. The latter is done by sequencing the data directly, i.e., without any genome multiplication.
PCR is more suitable when we are studying a particular genome or a few genomes, e.g., when sequencing the genome of a particular person or a particular type of organism. However, when some very different genomes are present, the amplification might be very uneven, and in fact introduce additional errors. This is why in some situations one prefers shotgun sequencing, e.g., when studying microbiome, containing many different types of bacteria, archaea, viruses, etc.
Both terms refer to the so-called High-Throughput Sequencing (HTS). You could learn a bit more about sequencing technologies from this popular science article.

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Spider Identification Michigan
This was taken in Ann Arbor, MI.  It looks a bit different from the wolf and grass spiders I'm used to seeing.  Anyone know  what this might be?
edit: Per request, I've uploaded a better picture.  Actually, it's the same picture, but I postprocessed the first image quite a bit to ease identification.  The second one is not post processed but (hopefully) clearer.
Processed image:

Unprocessed image:

the camera focused on the trash instead of the spider. Do you happen to have a better image?

Unfortunately stack overflow optimizes it a lot when I upload, and the quality suffers.  Let me try Dropbox.  Just a moment

Also consider switching your camera to a non-lossy format for future use, if possible.

@jzx - Can this be done on the iPhone 6 - do you know?

What was the real color of the leg's stripes?

@Ilan:  I don't know if you can see it on your screen - but the actual image color of the non-processed image is pretty close.  Something like a medium-to-light brown.

I am not an expert by any stretch of the imagination, but I think  the lighting is pretty different in my examples. There are about 70 kinds of spiders generally in the U.S. The shapes are important, as are the habitat, the  presence or absence of a web (fishing spiders don't usually make webs), an egg sack, etc.  Narrowing things down significantly, this is my best guess . The eye pattern would help a lot.

I can't tell how big your spider is. :( But I agree, it's probably not a wolf spider. (The fourth pair of legs is the longest in the wolf spider
I think it might be a fishing spider (Dolomedes tenebrosus). They do hang out in man made structures and are the most common fishing spiders found.

Fishing spiders are similar to the larger wolf spiders in size, shape, and coloration. Species in the genus Dolomedes are called fishing spiders because most live near water and have been reported to catch small fishes and aquatic insects from the water as they walk on the surface. The species Dolomedes tenebrosus is more frequently associated with wooded areas (it would be more accurately classified as a tree-dwelling spider) and is a common household invader in these locations. It occurs from New England and Canada south to Florida and Texas.

The stripes on the legs are characteristic, the shape and size ratio of the thorax and abdomen are right, and they are smaller than their giant cousins that catch minnows (!). The coloration on the abdomen can vary. The females are 1.5 to 2.6 cm *about an inch) in length; males are smaller. The legs of both male and female are banded with alternating brown/black, scalloped rings on the femurs and reddish-brown/black rings on the tibia. Seeing an eye pattern and/or a good side view would help.

This is a great answer.  Unfortunately - he has been released into the world, so I can't get any better pictures.  The only thing that makes me question (not disagree) whether this is the  right guy (or gal) is lightness of the hair on your guy.  There are a million different reasons that that could explain that  that are unrelated to anything biological, but it seems to me, mine is quite a bit darker.  I'm certainly no expert, so I'd definitely defer to your wisdom here.  Thoughts?


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How did evolution support sports, fun, entertainment etc
We know that many animals entertain themselves by playing games. But sports actually increases risks of death,or at least accidents. So why did evolution choose it? And why did evolution decide to make us look for entertainment every now and then?

not moving and sitting behind a desk all day probably poses more risks.

Evolution didn't "make" us do anything, it created a brain which can choose to do or not do them.  As for games and participant sports, think of them as practice for the various challenges of life - the old "use it or lose it", with a rider that if you lose it, you're lunch for something.  The existence of pectator sports, though, leaves me completely baffled :-)

I would advise that you read up some basics of evolution. Evolution does not decide; it is stochastic. Most sports are basically a kind of simulation of war, hunting or other essential physical activities that ensure fitness of the individual or the community.

@WYSIWYG. Talking about evolution as 'deciding' is a cruder way to describe evolution than describing it as 'stochastic', but it isn't strictly wrong in so far as it describes what evolution produces as contingent on the relevant facts of the world - just as what an agent decides to do is contingent on the relevant facts.

If you're asking about entertainment generally, I think music and dancing are pretty obviously related to reproductive fitness. The evidence says so anyway. In fact, there's a pretty strong correlation between the amount of the right sex hormones in a person (i.e. testosterone in men, estrogen in women), fertility, physical sexiness, and singing and dancing ability. In short - we find fertile people hot, and signs of fertility are found in physical appearance, singing, and dancing. Kind of neat.

@Hal but an agent can still decide in long term. Evolutionary process does not "think" long term. It is Markovian and not a decision process.

@WYSIWYG Fair enough. I don't regard 'decide' as entailing (or precluding) long term planning. E.g. When given two appealing options, sometimes my dog just reacts to one instead of the other. Sometimes he seems to think about it. However, I don't think he ever thinks long term, it's always an immediate response to what's happening. in any case, I don't mean to defend the analogy. It's far from perfect. I just mean to say that it's not dead wrong.

@WYSIWYG What are your thoughts on the use of game theory (the study of multi-move - i.e. long term - decision) in modeling evolution. From what I've heard, it often models evolution well. Although, I really don't know.

@Hal though it may not be dead wrong, it instills a doubt and as such most people do not understand evolution properly. Therefore it is always good to be explicitly clear. Game theory also just predicts long term consequences (simulation of steady state) and ignores any possibility of an event that may cause a change of scenario. It is possible to model and predict the outcome of stochastic processes.

@WYSIWYG Thanks for the info.
"It is always good to be explicitly clear" +1

This answer can be from many different perspectives! I'll try to blend them all together as much as possible.
First of all evolution did not choose to make us love sports. Evolution made us social animals. And sports is just one of the tools we use for that purpose. Think about it, because if evolution gave us sports, then you will play sports, your kids will inherit that bit of experience from you and they would be that much better than you. But no, we all start from level 0 when we try to play any games or sports. This is because, sports is primarily a motor memory
So why are we social?
This study back in 2014 was one of the first to suggest that memory can be heritable. It generated a lot of attention and the authors themselves suggested that their findings were standing on a very capricious footing and required further validation.
This point is valid because evolutionary forces require mechanisms by which features/mechanism which bestow advantages towards the survival of the species are positively reinforced. In this case social behaviour is the function.
Do not go googling the word Social behaviour, for some reason the wiki article looks only at dogs and cats. That is unpragmatic, because we also have the same function.
I will broadly breakdown social behaviour into

Accommodation of non-aggressive behaviour from individuals in neutral territory.
A means to communicate

But, you may ask how does social behaviour benefit you? Well the answer is simple, increased survival capacity, and better chances of propagation.
Such studies exist in crows, which have studied social behaviour. Indeed, if you start to consider studies in behavioural biology, you would find that there are instances where female mosquitoes do not just mate with any male mosquitoes, even in this case you can call it a very rudimentary form of socialising.
So in your case sports is a tool which allows us to accommodate and communicate with others in neutral territory.
You can take a look at this which better explains the social aspects of sports

You should avoid usage of statements like So why did evolution choose to make us social? .. Evolution does not decide.


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How to identify the age of a "living" person?
An Indian old man claims he is [180 years old] now.
We are not able to tell he is 180 or 181 probably. But can we tell he is 90, 120, 100 or 150?
Different people may age differently.
A 60-year old person may appear to be 80, while somebody else could appear younger than their mathematical age. Some other people may have progeria.
What is the most accurate way to identify a living person's age nowadays?
Are there reliable parameters to measure?
C-14 needs a long time base line. Hence, it is suitable for the bone of dead people.
What kind of method can guarantee it can distinguish a 30y and a 80y old person?  What's the error bar of that method?

Cut off a limb and count the rings

possible duplicate of Can we determine a person's age by dating methods or other means?

Birth certificate, I presume :P

@WYSIWYG: Assuming that you a) Have one (and only one); and b) Haven't done some creative editing on it.

@WYSIWYG By the way, a person celebrates his/her birthday on the correct day only for (max) 4 years after his/her birth.

We can tell he isn't 150. People just don't live that long. He almost certainly isn't 120, and very likely isn't 100. The unusual thing about people who lie about their age is not their age. It is that they lie about their age.

@mmesser314  You mean biologically we are not able to tell he is 80 or 180?

@questionhang Scientifically no, we'd have no standard of comparison since people don't live that long.  If there is something that happens to the body post 120 years, we'd have no idea.

@questionhang - Or more realistically, yes. If he was 180, he would have been dead for 60 years at the very least.

@Mercury - A person is a year older when the Earth has gone around the Sun exactly once. This takes about 365 1/4 calendar days. Most calendar years have 365 days. So every 4 years we add a day. This keeps the calendar birthday happening at the right time. Every 100 and 400 years, there are additional leap year adjustments to account for the "about" in about 365 1/4 days.

You have the wrong impression about carbon-14 dating, the long time horizon doesn't have anything to do with not being able to use it to date the age of a living organism. Living things are constantly replenishing the very limited supply of carbon-14 while they are alive. It is only after the organism dies that the carbon-14 clock starts to tick. A dead organism no longer replenishes its supply of carbon-14 and the carbon-14 it did have begins to decay into nitrogen-14. We can then measure the percentage of carbon-14 left in the remains and date them to when they died.

The most accurate method known so far may be Horvath's methylation dating algorithm, which uses 353 CpG sites (Genome Biology research article, Nature news article).
From the Nature article, this method was validated with at least one population.

[After the publication in Genome Biology] Marco Boks at the University Medical Centre Utrecht in the Netherlands applied [the algorithm] to blood samples collected from 96 Dutch veterans of the war in Afghanistan aged between 18 and 53. The correlation between predicted and actual ages was 99.7%, with a median error measured in months.

However, I did not read the original research article and it seems that the dating method works poorly on cancer patients.

DNA methylation is susceptible to environmental factors.

Good article. This may replace teeth as the gold standard.

@anongoodnurse, I was actually hoping someone would argue that dating using teeth would be the best way to estimate the age, since I'm not familiar with this literature.

@Jonathan - See the possible duplicate. I think it's close. I almost posted an answer, but the Nature article surprised me. Plus, you don't need to pull a tooth.

My question is about the error bar in fact. Look at the boldface sentence please.

@anongoodnurse - Besides, a 180 year old man probably doesn't have any teeth left to pull.


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Why are female clones more often produced
As a student of biology when ever I come by artificial cloning, I always find examples of females being cloned - Dolly the sheep, CopyCat, Daisy, etc. The only male I could see was Fibro mouse and a few more. What is the reason behind this? Is the male genome more difficult to be cloned? I am specifically looking for genetic reasons or other complications.

It might just be a case of they take the sample from the same animal they are using the eggs from for ease of access.

@SolarLunix I dont think this can be the reason. By the way, thank you.

What exactly do you mean by "cloning"? Somatic cell nuclear transfer? Making transgenics/knockouts/other genetically-modified organisms? Please [edit] your question to add additional information, as well as some literature citations supporting your observations, as currently this just appears to be anecdotal evidence. There is no difference between the male and female genomes, obviously excepting the sex chromosomes.

No there is no problem as such. However, a female can produce her own clone but a male cannot.

I mentioned this below but to be more clear: Rarely (ever?) does or can a female produce her own clone.  It still takes large numbers to get viable offspring, so at least dozens of surrogates will be used.

Female can be inseminated

@rhill45 Do you think it has any link with artificial cloning? What can be its benefit?

You can maintain some of the genetic traits in progeny if you clone a female, since it, as a female, can give birth. A male would be a more difficult model to work with if you were studying genetics. If anything, because females have more genetic content (x is bigger than y), the success rate of the micro injections for females I would be willing to bet are a little less successful. But I'm just guessing here in all honesty about my last statement. @RehanUllah

@rhill45 Wow! thats really a good point for industrial or educational cloning!!

They aren't, anymore.  It was a fair guess at the time, but first I think we should define what cloning in this context mean.
Our own cloning tag says:

The process in nature or in the lab by which a new organism is created that is genetically identical to its predecessor.

For animals - I'm going to use Dolly as an example since you do as well - when we say "cloning" we usually mean somatic cell nuclear transfer.   This image from Wikipedia sums up the process:

Basically, you take the nucleus of your to-be-cloned animal and put it inside the egg cell from another animal.  Dolly was not produced by one animal but by two - a donor and and a surrogate.  She was made using mammary tissue (another good image here) from the donor, which is important to note.
Dolly was the only one out of 277 egg cells that made it.  This is a hard technique, and we still don't understand a lot of it.  With even less information at the time, some prevailing ideas were:

Maybe there's something special about reproductive-based tissue
Maybe there's something special about female tissues

Even when using a different technique (e.g. Cumulina), early cloning attempts hedged their bets with those same tissues. That's why Fibro, the first male cloned (from tail), was a big deal - he showed that any tissue could be used, and that reproductive or female tissue wasn't inherently special.  You still need an egg and a surrogate, but if you can get the nucleus right it's just as doable.

I'd also make the case that, where the XY sex system is in place, anything genetic with a Y chromosome is inherently less stable.  But that's my opinion.

Nice explanation. Thank you for the valuable images.

@Amory A nitpick - If I understand correctly, the image from Wikipedia is somewhat misleading, as the whole somatic cell is fused with the enucleated egg (i.e., we don't use solely the nucleus of the somatic cell). See another question.


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Doubling the concentration of extracellular calcium hyperpolarizes a neuron. Why?
I was doing some back of the envelope calculations to try to answer this question in more mathematical terms. Essentially the question states: Why does increasing the extracellular potassium concentration depolarize a neuron, while increasing the extracellular calcium concentration hyperpolarize the neuron?
My initial thought was that there is a change in the equilibrium potential for each ion. Working this out however I realized I was wrong in my reasoning; my math proved me wrong.
Doubling the concentration of extracellular potassium makes the equilibrium potential of potassium 17.8 mV more positive. For calcium, it increases the driving force by 8.9 mV (based on room 300 K temperature). What this means to me is that both will cause the resting potential of the neuron to become slightly more positive, though calcium less so.
This is indeed obvious: adding more positive ions to the outside of the cell increases the driving force for that ion, and assuming there is any conductance (albeit small) then there will be some depolarization of the neuron.
This makes me think that this is not a phenomena explained by a neuron at rest. Some other mechanism is responsible for increased extracellular calcium causing the neuron to hyperpolarize.
My possible guesses:

If the calcium concentration is doubled, then the driving force for calcium increases, so there is more influx of calcium and thus the internal calcium concentration will increase. Because the concentration of calcium ions on the inside was previously near zero, now that internal concentration will rise to be some significant number, thereby hyperpolarizing the neuron.
The internal concentration of calcium rises slightly, but instead of (or perhaps in conjunction with) lowering the resting potential directly, there is more activation of calcium-activated potassium channels, thus raising the conductance of potassium ions, and thus ultimately hyperpolarizing the neuron.

Am I on the right track or am I missing something?

I edited this to clean up some of the misuses of terminology. One quick suggestion: the names of these ions are not capitalized ("Potassium", etc.). In fact, more often you will just see K+, Ca++, Na+, and Cl-, which is more convenient to write. Also, there is no such thing as the resting potential for an ion, just for the whole neuron; for the ion, it is the equilibrium potential or reversal potential. Etc.

"This makes me think that this is not a phenomena explained by a neuron at rest." Why not? If the neuron is not spiking--which it is not in your example--it is at rest.

This paper and this paper supports the second possibility I hypothesized. That is a increase in external Calcium concentration leads to an increase in conductance of Potassium.
While the increasing the external Potassium concentration can be shown to depolarize the cell with by calculating the Nernst potential for the Ion, the Calcium Ion has a non-intuitive effect. This means if one increases the outside concentration of Calcium Ions then inevitably there will be a small increase in the internal concentration of Calcium ions on the inside. This will slightly bias the Calcium Activated Potassium Ions to be a little more open. Thus raising the conductance of Potassium. This will mean there is a net hyperpolarizing current keeping the cell less excitable.


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Is Mutation Theory still "valid" for complex organisms?
I'm afraid like most people I suffer from having learned "A History of Evolution" in school, rather than cutting to the chase and learning the actual "up to date" version of the subject. (Imagine if programming classes did the same thing and you were forced to learn FORTRAN and BASIC before learning JavaScript) So please help me fill in some gaps:
From what I have been taught, Natural Selection (or even Artificial Selection) is great for panning favorable genes from a species and bringing them to the fore, however, it does not introduce new genetic changes.
It is possible to introduce new genetic changes through mutations. When asexually reproducing organisms receive a mutation, they pass that mutation on to their offspring. Mutations are somewhat rare, and beneficial mutations even less so, but happen frequently enough to make a dent over a long period of time.
The problem I don't understand is with larger organisms, aren't those already rare mutations only passed onto offspring if they occur in the short-lived sperm or egg cells of one of the parents*? At the very low probability of a beneficial mutation occurring in a single cell of a male's leg, not only is it unlikely he would benefit by this mutation, but even if the male reproduced, this mutation wouldn't be passed on, and would die with the male.
Are mutations viable methods to introduce new variations in more "complex" organisms that reproduce sexually? Or is there another theory or system that bridges Natural Selection and Mutation Theory in larger organisms?

* And as far as I know, there is no species known with mating habits that involve strapping uranium to their genitals.

I think mutations are more common than you think.

Your programming analogy is broken.  It's more like learning Newton's laws of motion before learning General Relativity.  Newton's laws of motion are not old or wrong, per se, but rather a much simplified version applicable to the scales of a human being.  In the same way, Natural Selection 101 is a simplified version of the complex process we know know as Evolution.

"programming classes did the same thing and you were forced to learn FORTRAN and BASIC before learning JavaScript"  people would be better software engineers.   Better analogy would be to learn Smalltalk and Self before Javascript.

" of a beneficial mutation occurring in a single cell of a male's leg, not only is it unlikely he would benefit by this mutation" How is it beneficial if it is unlikely he has benefit of it? And if so he has no benefit of it it dies with him, thats all what this theory is about. Tough, the connection between my reasoning isn't that right, but anyway you dont have benefits of things that don't benefit you.

@JDługosz: People would be better software engineers if they didn't learn JavaScript. ;-)

People in good colleges do learn things like C first before moving to high level languages. Otherwise you produce "engineers" who create memory leaks in Java and have no idea what the difference is in heap and stack memory.

@IQAndreas additionally, Fortran is still very much in use today (just one example). Unfortunately, so is Visual Basic :)

@Zaibis If a single cell in a male's leg mutates beneficially, over months it may divide and replicate into a hundred thousand new cells with the modification, but the small group of cells is still overshadowed by the billions of other "original" cells in the male's leg.

@IQAndreas: Yeahr so thoose overshadowed cells are no benefit for the male's leg at all, thats what I was mentioning.

Change in genetic variance

From what I have been taught, Natural Selection (or even Artificial Selection) is great for panning favorable genes from a species and bringing them to the fore, however, it does not introduce new genetic changes.

Yes, you are pretty much right. In a given population, directional selection will ultimately reduce genetic variance (Natural Selection selects for a few variants letting the other variants disappear and therefore diminishing the genetic variance) while mutations bring variance back to the population on which further selection can occur.
To go slightly further (but without developing this part too much): Genetic drift decrease genetic variance (on average). Balancing selection (such as negative frequency-dependent selection or spatially heterogeneous selection for examples) help to retain variation (but never create more variation) in comparison to what genetic drift alone would do. Different kind of spatial population structure also affect patterns of genetic variation. The important point to understand is that in an isolated population, mutation is the only process that can create new variants.
Mutations in multicellular organisms - Somatic vs. Germaline mutations
You seem to call complex organism what we usually call multicellular organisms. You are very right that some mutations might be passed on while others won't.
As you said, a mutation occurring in the left leg will never be found in your gametes. We call such mutations that can't be passed on somatic mutations. On the other hand, mutations that can be passed on are called germline mutations. Of course, in unicellular individuals, all mutations are germline mutations.

[..] aren't those already rare mutations only passed onto offspring if they occur in the short-lived sperm or egg cells of one of the parents

Germline mutations are not only mutations that occur in the eggs or the spermatozoids (egg and spermatozoids are called gametes). Germline mutations are any mutation within the lineage of the gametes. For example, a mutation that occurs during mitosis during the morula phase on the right cell is also a germline mutation. A mutation that occurs in the testis during the division of a cell type Ad spermatogomium to give rise to another type Ad spermatogomium and a type Ap spermatogomium is also a germline mutation (see figure at the bottom of this answer and see the Age-specific mutation rate section). There are therefore tons of divisions during which germline mutations can occur in big multicellular organisms, while (germline) mutations can occur during only the single cellular division in unicellular organisms.
How many new mutations do humans passed on to their offsprings?
Generally speaking, the germline mutation rate per nucleotide is around $10^{-8} \text{or } 10^{-9}$ but don't consider this value too much as the per nucleotide mutation rate varies a lot between species and especially between different genomic regions. FYI, the haploid human genome (just to consider an example) consists of about 3 billion ($3\cdot 10^9$) base pairs.
The number of new mutations per offspring in humans is a Poisson distribution with mean and variance of about 100 mutations (this estimate might be quite inaccurate). This is maybe more mutations that you may have expected.
Age-specific mutation rate
There are typically a lot of cellular divisions happening in the testes in order to produce the very important number of spermatozoids a male produces in his lifetime (See figure at the bottom of this answer and see spermatogonium). Mutations also occur during those divisions and therefore we observe a correlation between the age of the father and the number of new mutations transmitted to the offspring. Hong et al. (2012) suggest using the following formula. The number of new mutations transmitted to the offspring by the father in humans is equal to $25 + 2(g-20)$, where $g$ is the age of the father. Of course, this is just a formula that matches quite well the observations but has no theoretical meaning. This formula applies only to males that are older than 20 years old.
Drake's rule
Empirical observations show that the higher is the number of base pairs $n$, the lower is the per-base-pair mutation rate $\mu$. This correlation between $n$ and $\mu$ is roughly linear with a slope of about 1. In other words, the genome-wide mutation rate $U = \mu \cdot n$ is more or less constant in all species. This correlation is referred to as Drake's rule and again, it is a rough approximation of a more complex reality.
Sexual reproduction vs Asexual reproduction
I am not exactly sure why you are talking about sexual reproduction in your post. Note that the mutation rate during meiosis (a process that occurs during sexual reproduction) is much higher than the mutation during mitosis.
Mutational effects
The mutation effect is the effect of a given new germline mutation. Of course, not all mutations have the same effect and there is, therefore, a distribution of mutational effects. Most recent studies (often mutation accumulation experiments) tend to show that a highly skewed gamma distribution (the negative exponential distribution is a special case of the gamma distribution) is a good fit to model the distribution of mutational effects of either beneficial or deleterious mutations. So the whole distribution of mutational effects is estimated to be best modeled by a gamma distribution for the beneficial mutations and a reversed gamma distribution for the deleterious mutations put side by side (where the density probability of having a perfectly neutral mutation is at the intersection of the two gamma distributions). The exact parameters for those distributions are likely to vary depending on the species but most likely depending on the exact stretch of DNA under consideration. Different papers offer different estimates (the work of P. Keightley on the subject is particularly influential). You might want to have a look at this answer for a summary of empirical data on mutational effects... The two gamma distributions need to be rescaled to make sure that the whole thing sums up to one and I don't know of any paper that suggest actual parameters for this rescaling.
Probability of fixation
Fixation is the event of a given allele (=variant of a gene) to reach a frequency of 1 in the population. In other, one allele is fixed, whenever at the locus (=genomic region of arbitrary size) under consideration is not polymorphic anymore in the population. The probability of fixation of a given mutation is a very important statistic. Let's call $s$ the mutation effect (if $s>0$, the mutation is beneficial). The probability of fixation of a neutral mutation given the population size is $P(s=0 | N) = \frac{1}{2N}$ (assuming a diplontic life-cycle) as it can be demonstrated from Coalescent theory, Wright-Fisher model of genetic drift or Moran (birth-death) model. The probability of fixation of a beneficial mutation is higher, while the probability of fixation of a deleterious mutation is lower. Those probabilities can be estimated with different techniques that use different assumptions: Haldane's technic (assuming that the number of offspring follows a Poisson distribution), Kimura's technic (using diffusion equations), Birth-death models, etc... Some methods assume small values of $s$, some others assume that $2Ns >> 1$, etc..
Number of new mutations in the population and rate of neutral substitution
If the genome-wide mutation rate for neutral mutations is $U_n$ and the population size is $N$, then there is a Poisson distribution of the number of new mutations at each generation with mean and variance $2 \cdot U_n \cdot N$ (assuming a diplontic life-cycle). Because each one of these mutations has a probability $\frac{1}{2N}$ to get fixed, the rate of neutral substitution in this population is $\frac{1}{2N}\cdot 2 U_n N = U_n$. Therefore, the rate of neutral substitution is a function of the genome-wide neutral mutation rate only. This classic result is used in estimating time since the last divergence between sister lineages (molecular clock)
Did you say Mutation Theory?
I have never heard of Mutation Theory. I am pretty sure Mutation Theory is NOT an existing concept (but the question is clear).
Spermatogonium figure

Empirical observations show that the number of base pairs is linearly correlated with the per-base pair mutation rate, so that the genome-wide mutation rate is more or less constant. Can you please expand on this a little more?

@tel answer edited. This paragraph is now a small "chapter" in itself called Drake's law. Is it better now? Thnks

re "Mutation Theory" -- I'm thinking ESL here so you might not want to have that portion of your answer up front with it's own Bold Header.  -- Also you might give a rough estimate of the proportion of neutral-to-good mutations over neutral-to-bad mutations (if there are 200 mutations/generation for a given species but 199 are neutral-to-bad, then that has serious consequences for the remaining neutral-to-good mutation - will it actually get passed on?... not likely).

@user23715 I moved the "Mutation Theory" bold header to the end of the answer. I also added a paragraph about the distribution of mutational effects, another one about probability of fixation and third one about how many mutations occur per generation and why the rate of neutral substitution is just 1. I feel like the answer gets slightly long, broad and off-topic if I keep adding stuff though. Let me know what you think. Thanks

Good fixes! Too bad s cannot be as easily determined as cases of  Un, for that really is central to the theory. -- iirc there were some studies done on actual-rate verses theoretical-rate but my Google-fu is failing me at the moment. David Raup isn't the one I was thinking of but it looks like his work indicates apparent actual rates of fixation to be well below theoretical. The theory needs work I guess.

Sounds like, the discussion will quickly  be of a much higher level than what should be present in this introductory post. But I am interesting to hear more about that. I would love if you could link a few papers (or send the links to me by email). Thanks

You're right that the mutation must be in a germ cell in order to be passed on. Most errors are introduced during DNA replication (at a rate of around 10-10), which occurs a number of times between the zygote stage and mature gametes. This book estimates that there are 24 divisions between zygote and egg and 23n+34 divisions between zygote and sperm, where n is the number of years past age 14. Given the haploid human genome is ~3.2∙109 base pairs, you would expect ~10 new mutations in an egg and ~90 in the sperm of a 25 year old male. This is a very rough calculation, but predicts about 100 mutations per generation.
This paper, based on actual empirical evidence, finds 175 mutations per generation.
The point is, mutations do occur appreciably in germ cells and are passed on to offspring.  Also, keep in mind that mutations aren't the only source of variation upon which selection acts. Variation is also created by homologous recombination and random mating.


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What is the latency between paired neuronal responses in the brain?
Is there any data on how long it takes for signals to propagate from one neuron to its neighbors in complex networks, such as the brain (particularly the neo-cortex)?
If not, is there any reasonable way to estimate at least the order of magnitude (for example by considering synaptic delay, which is in the order of 0.5 ms and the firing delay)?

do you mean what the latency is in a two-neuron network? In that case, the synaptic delay is definitely the most time consuming step because it's dependent on passive diffusion of neurotransmitter.

@AliceD What I am interested in is to get some idea about the (average/lowest/highest) latency between any two directly connected neurons in a network as complex as the brain.

Are you mainly interested in the synaptic delay or the propagation delay? The later depends a lot on whether the axon is myelinated and the length of the connection.  Are you mainly interested in delays within a cortical area or between cortical areas? Note that the the brain is NOT a dense network.

@Jonathan Ok, good to know. I'm a little shaky on terminology, but propagation delay sounds fitting, if it is the correct term for the time it takes for a "signal" to propagate from one neuron to the "next", i.e. the delay between the first neuron firing and the second neuron's potential being affected.

Short answer
A rough indication of the delay in monosynaptically connected cortical neurons is 6 - 14 ms.
Background
As @Jonathan correctly states, there are many variables involved in neuronal delays. However, because you ask for an estimate of the order of magnitude of the neuronal delay between two coupled neurons in the neocortex, I will suffice by providing the latencies reported form one study that seems to meet your demands very well. In this study the latency data on horizontally connected neurons in monkey prefrontal cortex in layer III were reported González-Burgos et al (2000).
The authors inserted stimulating electrodes to evoke action potentials and used distant recording electrodes to measure the responses in cells located distally from the stimulation site (Fig. 1).

Recording setup used in González-Burgos et al (2000).
They report that delays between monosynaptic connections range between 6 - 14 ms. Fig. 1 shows that these latency estimates depend on the position of the stimulating and recording electrodes, i.e., which part of the presynaptic cell is stimulated and which part of the postsynaptic cell is recorded. Most notably in the recording setup used, longer axon collaterals will have resulted in longer latencies. The authors conclude that the conduction velocity of the horizontal axon collaterals was 0.14 ± 0.04 m/s and the synaptic delay was estimated at 2.29 ± 0.49 ms.
Reference
- González-Burgos et al., Cereb Cortex (2000); 10(1): 82-92

The conduction velocity can vary by orders of magnitude based on many factors, so more information would be needed for a useful answer. Unmyelinated axon conduction velocities range from about 0.5 to 10 m/s, whereas myelinated axon conduction velocities can reach up to 150 m/s1.
I'm also not sure what you mean by "dense network". The brain is not a dense network and it sounds like you are including networks that are not brains.
[1]: Neuroscience (Purves D, Augustine GJ, Fitzpatrick D, et al., editors. Sunderland (MA): Sinauer Associates; 2001. 2nd edition).


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What causes tissues manifest the various forms that they do?
A heart (or any other organ) is comprised of a group of cells. To the best of my knowledge, the growth of a heart depends on cell division. However, cell division by itself doesn't seem to explain why heart cells collectively manifest the form of a heart.
What causes tissues to manifest the various forms that they do?

Are you asking about how heart or any other organ forms, including how it assumes its geometry? That question would be too broad. You should narrow down the question to a specific aspect.

@WYSIWYG It seems to me that if tissue grows by cell division, all tissue should form a blob (or maybe an approximation of a circle if it were growing on a flat surface). However, organs grow into specific forms, not just blobs. It seems to me that the cells would have to coordinate their positions with each other in order to do that, which seems absurd to me. Nevertheless, something must organize the cells. I mean to ask what organizes into the forms exhibited by (for example) organs? Is that a sufficiently determinate question?

Okay... so add these details to your question. Clarify that you are interested to know how the cells get arranged in a certain structure. Since this is a general question you should expect only a general answer.

This is a subject of active research. All the cells in the zygote are identical up to 8 cell stage. At the next division resulting in 16 cells formation it is called a morula.
The zygote has totipotent cells meaning each cell has the ability to develop into full organism by itself if it separates from the zygote (this is how identical twins are born).
Human zygotes are totipotent till at least 4 cell stage. In other primates experiments have demonstrated totipotency upto 16 cell stage.
The totipotent cells differentiate into pluripotent cells and then into various distinct cells belonging to different systems. This process is very complex and a lot of embryological factors and chemicals come into play.
The embryonic factors cause migration (called embryotaxis) and differentiation of the embryonic cells. Some of the factors are sonic hedgehog, wnt, insulin like growth factors, Hox, etc...
Different factors cause differentiation into different cell lines. These factors also cause the organs to attain specific shape and structure, thus the heart is shaped as a heart and the liver is shaped as a liver and so on.
Once the cells differentiate into a particular line, the stem cells of that region generally differentiate into that particular line due to the paracrine influence in that locus, even though these stem cells can differentiate into other cell lines when appropriately stimulated (thus demonstrating pluripotency). So intestinal stem cells would differentiate into goblet cells, surface epithelial cells, Enterochromaffin cells, etc... which are present in that locus.

For more see here:

http://www.sciencedirect.com/science/article/pii/S009286740800216X
http://www.embryology.ch/anglais/iperiodembry/controle01.html
https://www.bio.cmu.edu/labs/ettensohn/pdfs/dvg22746-2.pdf


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What tools can help me determine if a plant homologous protein interacts with an ncRNA in the same way?
First post here, so bare with me if I violate any etiquette or formatting rules.
Let's say I've got a protein in humans. When it interacts with an ncRNA found in humans, it does something that I'm very interested in.  I see a highly homologous (~85% AA identity) protein in plants, and it's widely conserved.  I'm interested in eliciting the same activity of this protein in plants.  Only problem is that there's no native plant-produced ncRNA to interact with my protein of interest in the same way.  So I had an idea:
What if I introduce a transcript to plants that addresses this problem?  If the plant version of this protein interacts with this (introduced) RNA in the same way it will be really cool.  I'd like to test this hypothesis with some synthesized constructs.  But before I plunk down thousands of dollars on a few constructs, I'd like to explore any predictive or analytical tools to strengthen the case.  I'm aware the odds are against me.
Thanks!

I can't think of any predictive tools, but I think you should simplify the system as much as possible first. Instead of trying to express the ncRNA in plant, get the purified plant protein and purified ncRNA, maybe by in vitro transcription. Mix the two together and see if you can use coprecipitation or crosslinking or something to look for binding. Fluorescent anisotropy might be cool if you have a fluoremeter with polarizers, you could label the RNA with a flourophore, then measure the tumbling rate, once it binds the protein the tumbling should slow down. Use the human protein as control.

The ncRNA sequence from human may bind to the plant protein in the plant cells, but so what? You may be able to say the plant protein works as RNA binding protein, but no more than that.
Another concern is that the plant protein may not recognize the same RNA sequence to the human protein.
There are several ways to find RNA partners of RNA binding proteins.
SELEX
This method is used to find consensus sequences that your protein recognizes in vitro. Once you find consensus sequences, you can search ncRNAs from the plant.
CLIP
This is similar to Chip assay. You could find real targets of your RNA binding proteins

With my experimental plan, I plan to use a reporter transcript.  I will be able to say more than "it's an RNA binding protein".  My primary concern is precisely that the "plant protein may not recognize the same RNA sequence to the human protein" if at all.  SELEX and CHIP will likely help me in my objective here.  Thank you for your suggestions.

I would be careful using SELEX to find endogenous RNAs that bind the protein, it would probably find an RNA aptamer that binds the protein well, but there is no guarantee that the resulting RNA would actually bind in a relevant manner, or just be a novel sequence that happens to bind well. Being able to make an RNA to bind almost anything is why SELEX is so useful.


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What is the lifetime of the vasopressin receptor V2?
I was looking at the production of vasopressin receptor 2, also known as V2R or ADH-R. What I found is that it is coded by the AVPR2 gene and degraded by the Alix protein (source).
But I did not get a sense of the timescale. After a receptor protein has been produced and embedded itself in the cell membrane, how long does it live? Is it days, weeks, months? Does it live until the cell dies or is it degraded before that?
Does the lifetime differ between each receptor, or on the cell type, or is it roughly the same for all G coupled receptors?

But where did you read about this particular example? Certainly we can find some additional information from that source. But in any case, the turnover of different GPCRs shouldn't be the same.. There is no strong reason to assume so.

@WYSIWYG This is the one study I found about V2R degradation, it is the one which concentrates on Alix.http://ajprenal.physiology.org/content/292/5/F1303 I don't remember where I got the info about the encoding gene, it was simply a table listing hypophyse hormones I found somewhere, and it had a column listing the gene.

Okay.. can you cite that article in the question?


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Are dogs affected by dwarfism?
My husband and I noticed a dog today that looked like a smaller version of a purebred Border Collie, although it didn't appear to be a puppy. It made us wonder if other animal species experience dwarfism.
Are dogs known to display a dwarfism gene?

What is a dwarfism gene? Just a gene that influence body size? Is the question "Do we know in other species (than dogs) genes (loci) that affect the body size?". If this is the question, the answer is yes. Dwarfism exist in humans for example. A lot of species are under directional of balance selection for body size. In general, insular population tend to be of smaller size (in response to selection, there is therefore a gene coding for body size), a phenomenon called insular dwarfism.

Canines can have pituitary problems just like people, but it's rare, just like in people.

The short answer is yes, other animals can experience dwarfism, including dogs, although it may not be what you are expecting.  Dogs are apparently particularly susceptible but they often are a special case.  We've so heavily bred dogs for whatever traits we desire, so now entire breeds are affected by dwarfism, such as dachshunds and corgis.
The reality is that dwarfism is a mosaic, with many types, and shouldn't be classified under one umbrella.  You're probably mainly thinking of Achondroplasia, which is just one of many causes.  You may also be aware of Hypothyroidism.  Not every case looks like others, so in animals it may not be what you except.  Other animals are susceptible, such as the sheep mentioned in the above articles, and horses, which are also a long-time target of selected breeding.


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Can I compare Shannon-Wiener diversity indices between plots of different sizes (area)?
Can I compare the Shannon-Wiener (a.k.a. Shannon-Weaver) Index of diversity ($H'$) of plots (communities) with varying sizes (areas)?
If not, what steps do I need to take and/or which tests should I use to compare the diversity of different-sized plots?
I also wonder if this is possible for Simpson's Index of diversity?
Shannon-Wiener Index:
$$H' = -\sum \limits_{i=1}^S p_i \ln p_i$$
Simpson Index:
$$D = 1 -\sum \limits_{i=1}^S {p_i}^2$$
Where $p_i$ is the proportion of species $i$, and $S$ is the number of species.

Welcome to Biology.SE. I am not an ecologist and I don't know the Shannon-Wiener index (and don't remember by heart the definition of the Simpson's index). However, if you were to include the definitions of those indices, I (and others) might be able to answer without having to search the literature for those definitions. When you say different-sized plot, do you mean different total number of individuals (total abundance) per plot?

Different sized plots strictly in terms of each plot having inconsistent physical AREA. For example, 1 plot might be 500m2, while another might be 1100m2.

Oh Shannon-wiener index is just what I would call the Shannon Index. This is why I did not recognize it at first place. Thanks for the edit +1

No problem. I think the science community needs to make up their minds about what to call it ha!

Theoretically the index for two habitats of different areas are not directly comparable. Consider the species area relationship. You see more species when you look over a larger area. So you will potentially see a different index just from considering a larger area, and not necessarily because there is something different about the habitats.
Borda-de-Agua et al tackle this head on. They use fractals to account for differences in area when comparing diversity indexes. It's complicated and I won't try to put the methods here because I don't understand them. Definietly worth looking at yourself though.
I would also consider using species abundance distribution (SAD) curves for comparison. They give information about diversity but don't sum it up in one nice number like indexes. I feel they are area invariant too. Since if you keep increasing the area of your sample, the total species will only increase from relatively few rare species, while abundances will increase mostly with the abundant species. This will not change the slope of the curve but just the intercept (My hypothesis, not sure if it's actually true). Checkout a good comparison of SAD's and diversity indexes in the intro to McGill et al.

References
Borda‐de‐Água, L., Hubbell, S. P., & McAllister, M. (2002). Species‐area curves, diversity indices, and species abundance distributions: a multifractal analysis. The American Naturalist, 159(2), 138-155. Link
McGill, B. J., Etienne, R. S., Gray, J. S., Alonso, D., Anderson, M. J., Benecha, H. K., Dornelas, M., Enquist, B. J., Green, J. L., He, F., Hurlbert, A. H., Magurran, A. E., Marquet, P. A., Maurer, B. A., Ostling, A., Soykan, C. U., Ugland, K. I. and White, E. P. (2007), Species abundance distributions: moving beyond single prediction theories to integration within an ecological framework. Ecology Letters, 10: 995–1015. Link


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Variance in Fst in the infinite island model
The most famous result in the study of structured populations come from Sewall Wright. He showed that in an island model, where each subpopulation is of size $N$ and the migration rate is $m$, then the pairwise $F_{ST}$ is
$$F_{ST} = \frac{1}{4Nm+1}$$
This equation gives the expected $F_{ST}$. Because populations are finite in size ($N$), genetic drift yield this value to vary.
What is the variance in $F_{ST}$ in the infinite island model?

References
evolution in mendelian population is the original paper who derived this result from Sewall Wright.
Indirect measures of gene flow and migration: FST≠$\frac{1}{4Nm+1}$ is an influential paper in the field.
GENE FLOW IN NATURAL POPULATIONS is a famous review as well.

Could you post a reference or two in which that equation is derived?

@tel See my edit. Note also that I reduced the Fst formula making the standard assumption that $m>>\mu$ (, where  $\mu$ is the mutation rate) just to make things easier. Thank you

Say @Remi.b, if I had two populations, and for each population I knew the genotypes of each individual (e.g. Aa, AA, aa, etc.) but for multiple loci (e.g. AABb) do you know of any simple ways of calculating the gene flow between these two populations? I used some R packages in the past but they were a bit fiddly. If you can recommend me a R/Python package and/or the breakdown of the maths I would be much obliged.

@hello_there_andy Is it good to hear from you again. You should make a new post for your question. I don't quite know the answer right now.

From Lewontin and Krakauer 1973, the ratio
$$\frac{F_{ST}(d-1)}{\bar F_{ST}}$$
approximatively follows $\chi^2$ distribution of degree $k=d-1$. Here $d$ is the number of demes (number of islands), $F_{ST}$ is the random variable of the $\chi^2$ distribution and $\bar F_{ST}$ is the average $F_{ST}$ that is $\bar F_{ST} = \frac{\sum F_{ST}}{n}$, where $n$ is the number of $F_{ST}$ values.
The variance of a $\chi^2$ distribution is $2k$, therefore
$$var\left(\frac{F_{ST}(d-1)}{\bar F_{ST}}\right) = 2d-2$$
Taking $\frac{d-1}{\bar F_{ST}}$ out of the ratio, the variance of $F_{ST}$ becomes
$$var(F_{ST})=\left(\frac{d-1}{\bar F_{ST}}\right)^2(2d-2)$$
, which simplifies into
$$var(F_{ST}) = \frac{2(d-1)^3}{\bar F_{ST}^2}$$

The above expression is probably the most interesting result but one could go further and express the variance independently from the mean (by replacing $\bar F_{ST}$ by Slatkin 1991 expectation for $\bar F_{ST}$ in a finite island. It yields to
$$var(F_{ST}) = \frac{2(d-1)^3}{\left(\frac{1}{1+4Nm(\frac{d}{d-1})^2}\right)^2}$$
, which again "simplifies" into
$$var(F_{ST}) = \frac{2 \left(4 d^2 m N+d^2-2 d+1\right)^2}{d-1}$$


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Did modern alligators and caimans come from prehistoric crocodiles?
I know that crocodilians have been here since the time of the dinosaurs. I also know that crocodiles came first. But alligators have been here for a good 37 million years. Did alligators come from crocodiles when the crocs swam into freshwater areas?
And since the alligators and caimans are 2 groups in alligatoridae did they have a common ancestor?
And also if alligators came from crocodiles (which might or might not be true), why isn't it more like this:
Crocodylidae $\rightarrow$ Alligatoridae $\rightarrow$ Alligatorinae $\rightarrow$  Alligator
for alligators and
Crocodylidae $\rightarrow$ Crocodylus
for crocodiles?

The tree of crocodilomorpha is here on wiki.

This is the phylogeny of the Crocodilia, as best as we currently know it:
The order Crocodilia is a monophyletic group including all living crocodile and alligator species. That means that all of these species share a common ancestor and all descendants of that ancestor are part of Crocodilia.
Within the Brevirostres, three superfamilies exist - the now extinct Borealosuchus, the Gavialoidea, within only two species not already extinct, and the Brevirostres.
The Brevirostres are the monophyletic group containing the crocodiles and alligators (that includes the caimans).

Did alligators come from crocodiles when the crocs swam into freshwater areas?

That very much depends on what you mean with "crocodile". If it's Crocodylidae, then no, these are sister groups. If it's only the true crocodiles (Crocodylids), no, those evolved after the split with alligators. If it's Crocodilia, then yes, alligators evolved from crocodiles.

And since the alligators and caimans are 2 groups in alligatoridae did they have a common ancestor?

Yes. However, saying that is rather boring - all life has a common ancestor. If you mean whether they have a common ancestor and all descendants of that ancestor are either alligators or caiman, then yes.
Additional source: Crocodilian phylogeny inferred from twelve mitochondrial protein-coding genes, with new complete mitochondrial genomic sequences for Crocodylus acutus and Crocodylus novaeguineae


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Why does our body exhibit bilateral symmetry?
Externally, we (humans) look symmetrical. However, internal organs don't show the same patterns of symmetry (heart being on the left side while the liver is on the right side, etc.). It is a bit counter-intuitive to me that the exterior of our body seems to be mainly symmetrical while the interior is asymmetrical.

What is the advantage of having bilateral symmetry in our body?
Why don't all of our organs exhibit bilateral symmetry?

Welcome to Biology.SE. One cannot believe (or not) in evolution, one can only understand (or not) evolutionary biology.

The question is interesting +1, I am just afraid that there are two questions in the same post...we'll see if it is an issue. I'd guess that bilateral symmetry was under positive selection for mobility purpose but it is just a guess.

I don't wan't to be a bummer but I think you can just skip the I understand/believe evolution part. And the last sentence as well. I edited your question, feel free to roll back if you preferred your version. There are probably a few other edits to improve the question.

That's fine, the question gets more clear after the edition. I am thinking that internal asymmetry has something to do with improving biological functions like metabolism and absorption and assimilation, but I have no idea for our external bilaterally symmetry.

also Why are humans and almost every species on earth symmetrical?


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Multiple transcripts encoding for one protein
Trying to get a better understanding of the process of DNA to proteins.
So when we have a gene, it is read from the 5' to 3' end, only translating the exons to mRNAs. A single gene can have multiple exons, and use alternative splicing to create different transcripts. A transcript may result in mRNA (not necessarily right? Also other kinds of RNA?) which is translated to amino acids. Finally folded to a functional protein.
My question here, are there different transcripts (say in different genes) that encode for the same protein?

Yes, they arise because of gene duplication but usually the protein is not exactly similar but quite similar. These genes are called paralogs.

yes, for example, if one gene came from you mother and another from your father, they might be different enough to cause disease (see sickle-cell anemia or cystic fibrosis).

As I understood it, a transcription is a combination of exons being used for, for instance, creation of proteins. I'm not referring to point mutations and such, because than another protein will be made by the transcript. Most probably not a protein which is created in another gene.

Gene duplication accounts for different the same proteins to be created in different parts of the chromosome, in an extreme case on a different chromosome. But in principle, the genes are the same, hence the transcript is the same. Are there, naturally (so we all have) different genes encoding for the same proteins

Any mutations in the 3' UTR of a transcript for a paralog would result in a different transcript which encodes for the same protein.

Just a point of clarification: you say "it is read from the 5' to 3' end, only reading the exons" but this is not the case. The cell's transcription machinery reads the entire gene until it comes to a "stop" sequence. The resulting pre-mRNA is then spliced to produce the actual mRNA(s) that are translated into proteins. It is during this splicing that introns are cleaved out.

@MattDMo you're right. I skipped some steps...

@TomD interesting links! :-)


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Colourful aquatic animal identification
Of what species is the following creature?

I expect it would be a Cephalopod living in not too deep water with a tropical climate (Brazil?). However, I can not find any information about what species it actually is.

This has already been answered, but from the fin in the upper left corner of the image, you can clearly tell that it is an Actinopterygii and not a cephalopod.

@MarchHo It would be great if you could write an answer with that and more hints that should've given it away.

This is the Sarcastic fringehead fish (Neoclinus blanchardi). [Source2]

Didn't see that one coming, completely different than I expected!

Here is a video of the fish performing its dominance display.

While Ilan's answer has already covered the identification, here are a couple of other techniques which can be used to identify such animals in the future (or at least narrow down the scope of possibilities):
1: The upper left hand corner of the image depicts a fin which has multiple bony protrusions. This is an identifying feature of the Actinopterygii, which all possess such fin structures.

2: The image was not taken by you, but found online. In these cases, reverse image searches can be helpful in identifying the animal, since such reposts are often accompanied with identifying information.

To do a Google image search, just visit the main Image Search page and click the camera icon at the right side of the search box (at least, that's where it is in Firefox, other browsers may vary). You can then enter an image's URL or upload it from your computer.

I did do a reverse image search, which got me a lot of Spanish sites. I did see the name Sarcastic Fringehead on one of those sites, but it looked like a nickname to me since the next picture I saw with that name didn't look similar enough. The photo in the question is an action photo which made comparison to a 'regular' photo difficult.

This is a most enlightening answer! Is this reverse image seeking why some folks seem to have a magic hat where they seem to extract any species identification from?

@AliceD It's a very useful tool for obtaining the sources of unsourced online images, for example in my second most highly voted answer on Skeptics. However, it is not helpful for photos which were taken by the asker, since they presumably would not have been posted elsewhere with identification.

Aha! Gotcha. So it may be indirectly helpful for species-identification, but more so for source-localization?


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where can I find microarray images?
I have investigated some of the links to known microarray databases, such as arrayTrack, omnibus (NCBI), TCGA. I find that when trying to get microarray images I either get an exotic file format (such as .sdf or .cel) or text base information. Does anybody know of publicly available microarray images (preferable with metadata too) in .svg, .png, .jpg or another well known image file format?

Welcome to Biology.SE I am not quite what exactly you want to be displayed on those images. If you just type microarray on GoogleImages, you'll get many pictures of these dots of colours on a black background. Is it what you're looking for?

yes, it is. But I would like them to be available through a database system so I may get a lot of them with description of which genes are on the array.

Oh ok. That makes sense. I would tend to guess that researchers rarely upload the pictures directly (as it is a very costly way of storing data) but only the results in a .txt (or other) file (I have never worked with this kind of data). Out of curiosity, why do you want a lot of those pictures?

I would like to analyse them on a GPU as I think they are the perfect for data based parallelism.

Microarray images (at least for Illumina arrays) will come in .tiff format and are huge compared to the summarized formats (.sdf/.cel). Most places will not archive the raw images (so you won't find them online) and even when you run the microarray, you will often times need to make a special request to output raw images. iirc .jpg images are useless due to compression artifacts.
You can use the proper bioconductor libraries to extract data from the 'exotic' file formats. There are many bioconductor workshops archived online that will go through the steps of microarray analysis.
http://www.bioconductor.org/packages/release/bioc/html/affy.html
http://www.bioconductor.org/packages/release/bioc/html/beadarray.html
http://master.bioconductor.org/help/course-materials/2007/BioC2007/labs/oligo/BioC2007-oligo.pdf

sad that its not possible to get raw pictures ..

@hotGopher You might to directly contact the authors but that's a pain and it takes time.


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Do you know what plant it is?
I saw this plant when I was on my trip to the Ukraine.
I wonder if those berries are edible.

I noticed you asked the answer writer how they knew what it was. Check out my post over on The Great Outdoors StackExchange (Plant identification methods) to get an idea of how to best go about IDing unknown plants using primarily the internet!  (And it just so happens that my post is also in reference to a Phytolacca plant!!!) 0.o

It is of Phytolacca genus plant which could be toxic for mammals, DO NOT eat as is - it should be cooked properly to be usable/edible (the older, the more toxic leaves are).
Phytolacca acinosa:

Thanks a lot! Is there some sort of plant dictionary which can help identify plant species? Or did you just know what it was?

@TeikoAbe It is easily traceable - you should learn what Inflorescence is - https://en.wikipedia.org/wiki/Inflorescence and what Venation is - https://en.wikipedia.org/wiki/Leaf#Venation_.28arrangement_of_the_veins.29, from there it is very simple to know any specific plant.

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


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What was the evolutionary reason for cross lateralization of the brain?
In the human brain the right hemisphere controls the left side of the body and the left hemisphere controls the right side of the body. What led to this development? Why doesn't the left side of the brain control the left side and vice-versa?

The theory developed by Cajal more than a hundred years ago hasn't been challenged, according to a recent article in Molecular Neuroscience. Making it simple:

At a certain point in the phylogeny, decussation is favored for the optical pathways. Since the images are inverted on the retina, the crossing is necessary in order to build a coherent and continuous image on the cortex.
Decussation of the motor pathways appears next, and it is supposed to make the flight response more efficient. If a danger is perceived visually at the left hand side of one's body, it is processed in the right hemisphere and the motor signal is sent to the left hand side muscles, which are the one that can propel the body to the right, thus escaping the danger. The efficiency resides in that the interpretation of the danger and the signal for the reaction happen in the same hemisphere.

Your DOI link is broken. Can you add a link to PubMed instead?

@MattDMo I changed the link to a PubMed one.


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What kind of bug/insect is this? photo attached
This morning (a few hours after sunrise) I saw this insect running over the blanket.
I'm thinking what it is, if it's a bed bug that missed feeding time and is out of schedule (as i thought that they come out just before sunrise). And I thought they were brown, too but upon research found that they could (colorwise) look similar to this one too. Also, I have not found another one of these and my wife and I both don't find any bite marks on our bodies.  Our matress is packed in a plastic hull to not allow bed bugs to start living in it. What might this be?
Thanks!

Doesn't look like a bed bug - they have these distinct small heads and this reddish brown oval-shaped abdomen. What it could be is a silverfish nymph (you could tell by the smooth connection between thorax and abdomen) or otherwise something from the order Zygentoma with its filaments missing.

Do you have any other pictures of the insect?

I googled pictures of silverfish and it does indeed look like one. The legs especially, both their orientation and count.

I have a doubt we can answer this question with a high level of accuracy: the sample image is very blurred, it is unclear if there are posterior/lower body elements like forceps as well as other significant features which could help with the identification.
My best guess it is baby of Earwig (2000 species): If I look at the posterior part of the body I can "see" the preliminary forceps as well as other similar features, but still the accuracy of the ID is limited.
Enhanced image:

Baby Earwig:

It's an old post that got bumped, but  this is almost definitively not an earwig. Also, FYI: many insects have cerci on their posterior ends...