text:
Can cancer cells in the same person, organ, and origin have different DNA?
Is it possible for cells from the same tumor to have different genetic material, and if so, to what degree is it possible (how fast do they mutate) ?

Cancer cells and normal cells differ on the genetic basis but they share the same genetic background, so they have not different DNA in the sense of two different people. They have to be different, since cancer cells have to accumulate mutations on a number of genes to become a cancer cell, which can survive and will not be directed into apoptosis. These are genes which control the cell cycle, certain growth factors, tumor suppressor genes, cell signalling and so on. In all these genes there need to be either activating or deactivating mutations present. Most of these mutations are point mutations (single nucleotide polymorphisms, SNP), where only one base is altered to achieve a mutation. An example for such a mutation would be the mutation in the B-RAF kinase, which is involved in signaling and activating genes, where a point mutation exchanges Valine 600 to glutamic acid (V600E, for reference see here). These are relatively small differences between these two cells. The Cancer Genome Project aims to sequence cells from a cancer and also normal cells from the same individual and then do a comparison. Later stages tumors often tend to genetic instabilities where complete regions of the genome are duplicated, inverted or deleted, see here for a review.
A more basic overview is given by the Ebook "Essentials of Cell Biology" by the Nature Group, which has an overview of cancer cells.
Regarding the mutation rate, this is hard to estimate. There are a few papers available here, but they focus on the mutation rate in germ cells, so these are mutations that are transmitted to the next generation. The estimates there are between 70 and 100 mutations per generation per individual, depending on the research method. You can find a nicely explained blog article here, which gives a number of original references, too.
The mutation rate in cancer is a different thing, since this depends on which genes are mutated. The mutation rate for cancer has to be higher for the cancer cells to allow to collect the necessary transformations into a cancer cell, but these mutations seem to occur only in a few hotspot regions of the genome (Further references can be found in this article called "The causes and consequences of genetic heterogeneity in cancer evolution" and in this called "Emerging patterns of somatic mutations in cancer"). There are two article called "The mutation rate and cancer" which are interesting in this context. They can be found here and here. As always, if you have problems with getting the articles, let me know, I can help there.

Your answer is good but if I am not mistaken, the OP is asking "Is it possible that two cancer cells (which originate from the same cancer) to have different genetic material?" And more interestingly, "What is the mutation rate of the cancer cells? Is it alike other cells, lower or higher?" Could you develop your answer?

I worked on it now that I could reach the Pubmed again.

@ Chris & @Remi.b excellent "what I need exactly ", thank you very much.

A) It absolutely is very common for extensive genetic heterogeneity to exist in tumours, including between individual cells. Talha already posted links to some very good reviews from Charlie Swanton and colleagues so I will just add in a citation for single cell evidence here ( http://www.nature.com/onc/journal/v36/n20/full/onc2016438a.html )
B) As for mutation rates - they tend to markedly vary across cancers and across regions of the genome based on replication timing and chromatin boundaries. Given the variation in the total number of mutations accumulated and assuming that a similar number of cell divisions , given birth and death rates, are required to get to a typical clinically observable tumour there must be variation in the underlying mutation rate.
Such variability may have much to do not only with background rates of mutagenesis but also with deficient repair mechanisms coupled to it, and there are clear examples of aberrant repair contributing markedly to mutational burden, including mismatch repair ( http://www.nature.com/onc/journal/v36/n20/full/onc2016438a.html ) and homologous repair defects ( https://www.nature.com/ng/journal/vaop/ncurrent/full/ng.3934.html ) and mutational processes (UV-induced and smoking induced cancers have particularly high mutational burdens)
http://www.nature.com/ng/journal/v46/n8/fig_tab/ng.3006_SF1.html


text:
Are original x-ray diffraction data available
Is it customary for investigators to publish the original x-ray diffraction data used in macromolecular structural determination? If not, why not; and if so, is there an online database where these data may be downloaded?

In many cases they are available.  One of the establishing principles of the Protein Data Bank (PDB) was to store not only the models (atomic positions and identities) of macromolecules and proteins, but also the originating X-ray data, more recently in structure factors.
If the question is 'why are they giving only the structure factors and not the original data they took' - such a task would require a lot of curation effort for very little scientific benefit.   Scaling the individual sets of data from the detector used to be a bear of a task.  The original myoglobin structure would entail scanned films in an ancient format from the 50s.  Nobody would be able to use that now without hacking the image format, if it wasn't on paper tape or cards.  In fact in that case the structure factors are not available.  Scaling many or several data collections together was often done with custom tweaks into the 70s and then in the 90s data collection became more routine, but several generations of x-ray detectors became popular and then faded from the market.  Each had its own eccentricities and requirements for combining data sets from multiple reads.
The purpose of having structure factors available is to allow anyone to reconstruct the electron density and evaluate the interpretive act which is tracing a peptide through electron density.  Since that format is mainly independent of the detector and has been fairly consistent over the years, it delivers a significant amount of scientific bang for the buck.
If you want raw image data or detector-proprietary data before multiple data sets from different crystals before they were combined you will have to contact the authors, who would probably have to sift through a sea of DVDs to get to it.  In older cases it might be tapes.
So as far as Structure factors, which are essentially the square root value of the combined and scaled Intensity data, they are available and a part of every submission to the pdb:
Look on any X-ray Structure Page at RCSB.  For example this one.
There is a box called "Experimental Details" and you can download the structure factors there by clicking a link.
If you are looking for more than one at a time, there are bulk downloads available through their download page.  Check the "Structure Factors" box.  Raw intensity data should be available if you look around for it as well.
Further Suggestion:  I was thinking that if you look at the scaling software that comes with the X-ray detectors you might find some tutorials with unscaled raw data.  I found one example at Marresearch - hen egg white lysozyme.

let me misuse this comment to bring your attention to crystallography.SE proposal. We don't know if it will gather enough people to make it worth its own site, although such site could be helpful. Now some relevant questions are asked on biology, chemistry, physics, earth science and math, but most of people in this field prefer dedicated mailing lists or forums such as ccp4bb, rietveld, xrayforum.

sounds good @marcin - i'll do what i can to support it!  it would be great to have it all in once place.

source: Stack Exchange

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

sort: votes


text:
Why it is rare for person to get infected with two Pathogens?
Why is it rare for a person to have 2 (or more) infectious diseases (for example: Flu & Cold together at the same time)?
Although it's rare, it happens when the immune system is weak (e.g when patient has both AIDS and Kaposi's sarcoma).

This needs a reference - I'd imagine it to be quite the opposite, probably we are often infected with many pathogens (even when not sick) and multiple pathogens would cause more stress on the immune system

This happens more often than thought. Classic examples are secondary infections which get a problem, when the body is already battling one pathogen. This would be for example pneumonia or otitis after other infections like the flu.

Your example is actually quite bad because the “common cold” is often an infection by several strains of viruses (and even bacteria) simultaneously.

There are multiple issues here. 1) Is it really rare to be infected by multiple pathogens? 2) If it is rare, is it rarer than would be expected from the independent probabilities of getting infected by that organism within a given time period? 3) If both the above are true, I would speculate that could be because the body's non-specific immune mechanisms have already been activated by the first pathogen, making it harder for a new infection to take hold.

Because the product of two small probabilities is much smaller than either probability by itself?

OP should consider revising the Q or making a new one..the concept of Interference (interferon) between viral infections is pretty clear, if thats the main thrust.  But per other comments/answers bacterial infections frequently super-infect during other illnesses.

What makes you consider it is rare? It is not at all uncommon to be affected by two infections. Typically I agree we aren't as the number of infectious organisms that we are exposed to which cause a clinical manifestation (i.e. aren't controlled by the immune system) are low. Nevertheless, any chronic infections such as herpes viruses may often manifest when we are under stress with another infection, many bacterial pneumonias are more likely to occur when a viral infection is also present and of course the many immunosuppressed people. Arguably a lot of infections are by two or more causative agents as often if one is able to enter where it shouldn't, another may, but one is likely to be more dominant. Furthermore even our infections can get infections with bacteriophages infecting the bacteria we are infected with.

I like the "infections all the way down" comment.  Can you add refs to bacteriophage infecting bacteria that colonize humans?

Secondary infection is not rare at all. I mean consider babies. When they get the cold their immune system is weak and focused on the cold virus and they can get viral pneumonia from the flu very easily for example.
TB is another good example of a disease often weakening the immune system and raising the probability of a secondary infection and HIV is a viral one with the same weakening and higher probability of secondary infection.

Another example where coinfections are common is with tick-borne illnesses.
One 2006 review suggests that in some regions of North America the prevalence of Ixodes ticks carrying two pathogens may be up to 28% and that from 4-45% of humans with Lyme disease also appear to have ehrlichiosis or babesiosis(Coinfections Acquired from Ixodes Ticks).

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

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


text:
The arrangement of retinal cells?
The section of retina shows a layered arrangement of the various retinal cells. Starting from the inside (where the light strikes first) is the nerve fibre layer, ganglionic layer, amacrine cell layer, bipolar cell layer, horizontal cell layer and finally rods and cones (and that too in inverted position, i.e. the actual receptor portions are farther inwards).

Why is this stratification inverted? If the receptors would have been the innermost cells, they could have received the maximum
  quantity of unaltered light. Does this "inverted" arrangement, i.e.
  arrangement with the receptor cell behind a screen of several other
  layers not hinder the process of photoreception by blocking a lot of
  incident light and hence the formed image? What is, if any,
  advantage of this reverse arrangement?

I don't have an other explanation than pointing to evolution. It was obviously not a problem to evolve the way it did. One article I found (see "The Inverted Retina: Maladaptation or Pre-adaptation?") called it a sign of pre-adaptation, where forms exist before they get their final function.
Another pretty comprehensive review can be found here: "Evolution of Phototransduction, Vertebrate Photoreceptors and Retina."

Thank you. And great references, as usual.

There is most likely no advantage to this arrangement and it probably is the result of the evolutionary history of the eye. Evolution always work by means of small adjustments from something that works into something that works better. During the course of evolution of the vertebrate eye the orientation perhaps by chance, perhaps for some reason unrelated to vision itself, became fixed in the inverted way it is today and as it appears to work very well, even though it appears as an inefficient design, it is still there. The point is substantiated by looking at the cephalopod eye. Squids, octopuses and cuttlefish have eyes that are anatomically remarkably similar to vertebrates, yet their retina is oriented the 'right' way, with sensory cells pointing towards the light and not away from it. Both designs seems to work.
The inverse structure of the eye is a good example to illustrate that evolution does not 'seek' to develop optimal solutions. Natural selection will improve whatever already works, which sometimes leads to solutions that from a purely engineering point of view are sub-optimal. Other very good examples are our extremely fragile knee joints and the extremely dangerous arrangement where all food and drink has to pass over the wind pipe to get to the esophagus, with danger of suffocation every time we put something into our mouth.


text:
Why genes are assumed to follow multivariate normal?
I wonder why gene expression data are very frequently modeled by multivariate normal distributions. What is the reason for those strong assumptions that the genes follow multivariate gaussian? Are there any reasons specific for genetics other than the reasons for general gaussian assumptions (the ease of calculation, etc.)?

Usually if something is not expected to behave according to some scheme then the measured values for such a parameter are assumed to be normal. It is not just with gene expression but with all types of measurements like dimensions of an object, luminosity of an electric bulb, range of a bullet etc.
In any measurement, the random error is modeled using normal distribution. I don't have a very intuitive explanation for why random errors follow normal distribution but mathematically it comes from the central limit theorem.
Now each gene is a variable and measurement of each gene suffers some random error; so a multivariate normal distribution is used.
When we dismiss a null hypothesis in a t-test or z-test what we are actually doing is dismissing our parsimonious notion that a sample is drawn from a given normal distribution. This means two things:

The sample belongs to some other normal distribution (different $\mu$ and $\sigma$)
The sample follows some other distribution

But a t-test will never be able to point out the exact reason. All it tells you is that the sample is not from some given normal distribution.


text:
When does identical twinning happen?
What is the window during which division into twins is possible (for instance can it still happen after implantation in the uterus)?
Is one twin the "original" and the other its clone?

In the case of two healthy, viable identical twins, the separation generally occurs at the first division from one zygote to two cells. So they are equal partners in the split, not an original and a clone. During the first several cell divisions in the morula and blastula, there is no significant growth. So these divisions produce smaller and smaller cells. If one of these smaller cells is separated, it is very unlikely to be substantial enough to survive and implant in the uterus.

That answer is partly wrong so I gave another one. Twinning isn't about a single cell breaking off from the rest but about the whole structure (or relevant parts of it) splitting in two, so it isn't limited to the first division.

This page describes what happens pretty well:
http://discovery.lifemapsc.com/library/review-of-medical-embryology/chapter-30-multiple-pregnancies
Division into twins can apparently happen at several stages up to and including implantation, but not much after that. The later the division the worse the prognosis because the more the twins share. The article mentions three stages in particular: division at the 2-blastomere stage (i.e. when the original zygote is cleaving), which leads to two completely separate embryos that implant separately, division at the embryoblast stage which leads to the embryos sharing a chorionic cavity (i.e. placenta), and division at the embryonic disk stage, which happens after implantation and involves the fetuses sharing everything - apparently to the point that they rarely survive until birth because they get tangled in each other's umbilical cords. Later divisions, after the primitive streak starts forming (i.e. about two weeks after fertilization), can lead to conjoined twins, because the division happened when the cells have already started to differentiate into which part of the body they'll be.
In no case can one twin be considered "the original" and the other not. Twinning involves whatever stage we're at dividing into two; we can't talk about one being an offshoot of the other, anymore than if you pour cake batter into two molds instead of one you don't end up with an original cake and a copy, you just end up with two cakes. Whose batter happened to be in the same bowl until some point in the baking process.
Moreover the twinning events usually involve a symmetrical division, meaning we can't even talk of one twin having a claim to a higher percentage of the original embryonic material or whatever. An exception may be parasitic twins and other examples of asymmetrical twins, but I haven't been able to find a good source on what causes those - it's unclear whether it involves twins resulting from an unequal division, or whether later development made them unequal.


text:
Is there a limit to twinning?
Can developing twins further divide and subdivide and become identical quadruplets or octuplets or...?
Can twinning be induced, either in utero or in vitro?
Might it be possible to just keep harvesting a few cells off the original clump indefinitely and making an unending stream of identical embryos for implantation in a surrogate uterus?

Sequentially:
Yes. Up to the limit of what the mother's body can tolerate.  Of course, if the cells never aggregate, that suggests some sort of fundamental problem with the embryo's developmental process, and you will probably not get a viable organism.
Sort of and yes.  In utero, fertility drugs can cause multiple eggs to be released per cycle, which can cause fraternal twins when each egg is fertilized.  IVF can do the same thing, but you can also manually subdivide a single embryo into two (smaller) viable embryos, provided you perform the division before any cell differentiation occurs.
Yes, but good luck getting an ethics review board to approve that :D


text:
When do chimeras happen?
If one developing twin absorbs another, when does that happen?
Is it possible for an appendage or organ to develop and be the only remaining vestige of an absorbed twin, such as a hand or a mouth, or a heart?


text:
Identifying whether ELISA kits are authentic or fake
What methods can be used to determine whether they are authentic or fake?

You are getting this Elisa Kit spam from China, too? The only way I see, would be to use a known reference standard so you can titrate both the specificity and the sensitivity of the kit. Ideally you would compare it with a known and proven kit. If you have the reference available in the lab and the cheap kit is not too expensive you can give it a try. I would do it, since work time and reagents also cost money.

the problem is, one of the reasons these kits are so expensive (at least the ones from reputable companies) is because they spend time and money to make sure the kits actually work and give reproducible results. For me, if I don't trust the quality of the supplier, why would I even think of possibly compromising the integrity of my data with substandard reagents?

Its the same for me. I don't order from suppliers where I am not sure about the quality. We routinely test substances from cheaper companies but there we either get tipped by colleagues or the stuff is so much cheaper, that we can give it a try. I don't see this for Elisa kits. And even if one batch is ok it doesn't necessarily mean that the next is as well. From the known suppliers we can be sure.

Just a few direct ways can figure out whether Elisa Kits are authentic or not.

Proposing to visit their factory. Generally bait company does not agree with it.
Complete range of kits. If a company has every and each ELISA Kit, it is usually fake. Unless they are very large  and professional companies, such as abcam, cellsignal, sigma, sabbiotech and so on.
See the price. If prices are ridiculously low, but in the name of large companies such as import R&D raw materials packaging. This ridiculously low price can't even afford the raw materials, which company will sell at a loss?

This problem is rampant and has been plaguing the research community for a decade. I can explain how exactly do these companies make these fake kits, how to experimentally verify what I said is true, and how to spot them by just looking at their website. I can even point fingers and name a few known and notorious companies that do this malpractice. What I ask from anyone who reads this is to recognize that these companies are the bad apples in Chinese companies and you shall not generalize all Chinese biotech companies. Generalization, not a good thing, and I trust all the years of training in scientific critical thinking has taught you better :)
Now how do these companies make fake ELISA kits? Simple. They use a universally present protein target, initially TGF beta--I do not know what they have shifted to lately--to make one type of ELISA kit, and label it as anything and everything.
How to actually prove it? Run a western using a trusted third party antibody. If nothing shows up, you know the standard is not what they claim it is. Or you can also run a third party recombinant protein on the kit. Same core concept.
Do not want to bother with all that? Then just keep an eye out for this signature: one company that has thousands sometimes tens of thousands of ELISA kits, covering all kinds of species--sometimes ridiculous ones like whales, giraffes, tadpoles, sharks etc.--nothing against giraffes, they are awesome and all but seriously... These companies are literally like Noah's Ark. How can one company you never heard of come up with so many ELISA kits while established companies who have been making kits for decades are dangling on the level of hundreds or thousands?
Maybe, one thinks, that someone went hard core and just made them all, that maybe this is real? After all there are no other choices, they are the only ones selling this ELISA kit, wouldn't hurt too much to give it a try...??
And that is why these companies still exist today. That is why so many papers got pulled, and so many clinically promising indications turned out to be false. That is what cost millions of dollars of tax payers money.
At the end I want to point out that, if researchers did their due diligence, or if there are some more effective forms of media where researchers can get information like this, these companies would have died a decade ago. Instead they just keep coming up with different company names and pulling the same scam.
I want to put examples of these companies by directly referencing their names but I am not sure about the forum rules would allow it so for this post, I would not do so. The signature described above should be clear enough for you to spot these companies. Wish you all the luck in 2015.


text:
Dogs bark at familiar person in Santa costume. Why? Don't dogs trust smell over vision?
Last night 10 humans and 2 dogs spent Christmas together. At some point, one human dissappears for a few minutes and comes back wearing a full Santa outfit. Upon respawning, the dogs start barking aggressively until they are calmed down by non-Santa humans. They remained attentive of Santa until he left after a few more minutes.
Why is this? Did the dogs not recognize the human because of his fake full beard and altered body shape (pillow under coat for fattening)? The human didn't shower or put on perfume or anything. I'm stumped by this and I'd love to learn the reason for this odd behaviour.

Upon respawning, the dogs start barking aggressively until they are calmed down by non-Santa humans -  best sentence on the site

I like this question

I think this question would be a slightly better fit on pets.SE. Looking at the number of upvote and comments and answers of reputed users, it seems to also be on-topic here!

The dog was probably freaked out by the weird costume.  Humans do it all the time (I've been seeing Halloween decorations for sale since early August, which is terrifying) but we generally comprehend what's going on.  Dogs may not fully understand the idea of a costume, much as a human infant might be scared by masks or beards (or the sudden removal thereof).
Anyway, this 1997 article titled Canine fears and phobias; a regime for treatment without recourse to drugs is kind of a fun read and has some interesting tidbits about, go figure, canine fears and phobias.  One thing it discusses is the importance of the primary associations brought on by sight, smell, and hearing.

However with a fear of hot air balloons the dog will hear the propane burner and see the balloon but a primary (coming from the balloon), olfactory cue will be missing.

Missing out on that is enough to freak 'em out.  This research article from the 1950s is a little more exact/thorough and has what you want.  It's worth reading in more detail if this topic interests you, but the part that answers you is here (emphasis added):

Some at least of the test objects could not have been discriminated by smell, as with the bronze deer, or the mechanical turtle, and in the course of the work it was frequently clear that visual cues were affective before olfactory ones could have been. Vision also can dominate olfaction: fear of a modelled human head was observed although the model was completely wet with dog urine.*

Likely what happened was the dog saw a weird/scary/new person and, were upset that their vision and smell didn't match up, and continued being freaked out.
(*The urine experiment comes from this article out of 1944 Germany, in what is now known as Ethology, in case you feel like reading German.)

I think dogs experience something closer to a horror movie and a panic attack that the original person had died because this new individual smells of them but is not them.

Like how children freak out at the "ive got your nose" game.


text:
Why has evolution made neurons use spiking?
I'm going to be forward and say that I'm not a biologist.  I don't claim to fully understand the functionality of a neuron from an electrical/chemical perspective... I'm curiously gazing from the outside in as a computer programmer.
Now, the big new thing these days with artificial neural networks is simulating them with biological precision- that is, with spiking, actually placing the network in Euclidean space, and all sorts of other goodies (Check out the Human Brain Project; it's really cool.  Our own brains are computable, given a powerful enough computer.  Probably has a lot of fascinating and horrifying philosophical implications too.), but this isn't the only model that people have commonly used for neural networks.
In the past, multilayer perceptrons were the big thing; I'm not going to go deep into explaining them, but essentially, each neuron simply performs a mathematical function on its inputs and then outputs it.  There's no spiking in the sense similar to our neurons.  A neuron could be blasting its output at nearly 100% indefinitely and there isn't any objective difference between that and it being at 0% or anywhere else.
Now, I sort of went off on a tangent, but what I'm trying to understand is- why this behavior is not observed in the system of computation that evolution has produced over the many, many years?  Why do we use spiking neurons instead?  We have instead developed a strange system where spikes travel down chains of neurons in patterns we don't really understand yet to produce the behavior necessary for the creature to survive.  My question is, why has this been favored over something similar to multilayer perceptrons?  Is it more energy efficient to use a spiking model?  The brain does use a disproportionate amount of energy.  I wonder if it is more effective as a model for computation.

Just to be sure what you mean, you ask why the neurons get activated only in a "on or off" method and why there are no intermediate states?

Sorry, no; I'm asking why neurons that spike is what is consistently used by every creature with a brain; spiking at specific times rather than, for example, conveying 50% "signal" for a sustained period of time or any other pattern of behavior.  So, not necessarily binary as you describe, but spiking itself.  This is hard to describe without explaining multilayer perceptrons in detail...

Especially since you have a quantitative background already, the book Spikes addresses a lot of these issues from an Information Theoretic point of view.

You should read up on how neurons work. You admitted that you don’t know this, yet it directly answers your question.

One of the many advantage of an all-or-none system is that resources can be conserved for timing events that require synchronized collaboration between many cells (like locomotion).  Binary behavior may also partially be a side effect of speed and efficient long-distance information transfer (which is one of the great advantages of neurons as cells in the first place).
It should be noted, however, that neurons aren't universally binary.  It is more accurate to say that neurons have binary properties that allow neurons to behave in a binary manner (but not all neurons do).  On top of that, many continuous (i.e. non-binary) processes underlie the neuron's excitability threshold.

One thing I think you're missing: a perceptron model and a spiking model aren't mutually exclusive. In fact, in perceptrons, people usually use a sigmoid function. That's not a coincidence: it kind of simulates a spike. If you were to model an organism such as C. elegans, whose neurons aren't spiking (but use "graded action potentials"), you would use another type of activation function (by the way, if you like the Human Brain Project, you should also check the Openworm project, which is much more realistic and already gives some interesting outcomes).
So, back to the point. When you try to model learning and generation of memory, you often end up dealing with plasticity. Just a quick explanation: a neuron does fire an Action Potential (AP) when its transmembrane potential gets above a limit. The potential itself changes due to the inputs from other neurons. But all the inputs don't have the same weight. Let's say you look at neuron A, which gets synapses from neurons B, C, D... If B fires at the same time as C, it can be enough to create an AP from A. But, even in combination with B or C, D doesn't elicit enough transmembrane potential variation to create an AP; it has to fire exactly at the same time as E, F, G and H to get enough "firepower" to activate A.
However, if each time D fires, A gets an AP (because of the simultaneous activation of other incoming neurons), then you could say D is "useful" for A, and (depending on the type of neuron and other parameters) the weight of D can increase, so that, after a while, D is able to elicit an AP in A just by firing at the same time as any other incoming neuron. That's a plasticity phenomenon. Note that here, it is a really simple hypothetical example. And also that the idea that learning results from plasticity is more and more being challenged.
So, if you want to understand how learning and memory happen, you might be interested in the weights of the connections only, and how they evolve depending on the network's activity. In that case, a perceptron model is a good way to go.

Now, the big new thing these days with artificial neural networks is simulating them with biological precision- that is, with spiking

So, as you already mention in your question, this is a matter of choosing a model that you're going to use (as a researcher trying to understand the brain). This is not trying to give an accurate depiction of how the brain really is. If you're interested in the weights of the connections, you can use a neural networks approach (and this is not outdated), and you don't care about a single ion channel on the membrane of a neuron. But alternatively, you can also dedicate your life to understanding the structure of a single ion channel, and how simple details can determine the whole working of the brain.
Projects such as the Human Brain Project are trying to create a "biologically exact" model of the brain. So, it involves modeling the spikes, as well as the network organization, as well as single ion channels. So, in that case they don't need to use paradigms such as artificial neural networks, since the network's behavior should be a result of the single neurons' modeling: that would be an emergent response. However, they don't have anymore the simplifications brought by other models, so, they need huge computational power, and they also face new problems: for example they have to give values to all the individual parameters of their models, some of which are currently unknown, and could even not exist at all.
So, I think this gives answers your question, in the sense that it is not the brain which evolved to pick a model, but the scientists who try to modelize one particular aspect of the brain.
EDIT: I see in fact this question is quite old; sorry it was a suggestion on the right which brought me here. But I think my answer can still bring an aspect which wasn't already mentioned in the other answers. So I hope you will see it.

The use of spikes is a mixture of their computational advantages and the limitations of the biological substrate in which they are implemented:

They can travel long distances at high speeds because they can profit from the saltatory conduction which is much faster than diffusion and it can be maintained over long distances. A digital signal is less prone to noise which is also a reason why our computers operate digitally.
Spikes can be modulated using chemical synapses which are a) directional b) can amplify the signal c) can modulate the signal d) can even inhibit the signal. Analog voltages have to be transmitted through electrical junctions that do not allow modulation.
Frequency coding (signal lies in interspike interval) has a wider dynamic range than voltage coding.
The spike generation can serve as non-linearity in the transfer function
The spike can be used to code temporal signals more efficiently by reducing the redundancy (only signal change).

Btw. do not expect too much from the human brain project - it is a lot of talk and no results.

It would be great if you added some references to your response!

My answer is a mixture of textbook knowledge and common sense. There are very few papers broad enough to substantiate one of the reasons.

Neurons are binary, in that they either "fire" or "don't fire".  There is no intermediate, because neuronal firing (biochemically) is an avalanche process.  Excitatory triggers raise the membrane potential and inhibitory triggers lower it.  Once the "threshold voltage" is reached, the neuron lights up and fires.  This is how "decisions" are made by neurons: inputs from many inhibitory and excitatory neurons are summed, and if the sum is above the threshold voltage, the neuron in question fires.  To use computational language, a neuron is a logic AND gate with hundreds of inputs.
Read the wikipedia article on "action potentials" for a more in depth discussion.

But my question is, what exactly is the evolutionary fitness benefit of using this mechanism over some other mechanism more similar to "nondiscrete logic gates" such as what is seen in multilayer perceptrons? Is it simply because spiking was the easiest method to develop, and as brains became more complex, they continued to be dependent on this architecture?  I mostly understand how spiking neurons work, at least from a mathematical perspective, not an electrochemical one (I need to read up on that...), but I don't think that's within the scope of my question. Sorry for not being clear.


text:
Clownfishes and Sea anemones
Relation between clownfishes and sea anemones is a classic example of mutualism. I wanted to list the species of sea anemones that are involved in this mutualism but I got lost.. Could you help me with that?
How many species of sea anemones which host clownfishes are there? Could you list them?

I only found this two references, but these are only secondary sources at the moment.
Look here "Clown Fish Anemone" and here "Choosing Clownfish and Anemones for Your Aquarium". It seems that there are only around two handful of anemones capable of supporting clownfish.
Here are some primary sources which confirm the 10 anemone species: "The anemonefish symbiosis: What is known and what is not." and "Field guide to anemonefishes and their host sea anemones". The last two links point to PDFs which contain a lot more references.


text:
How should I put a large phylogeny into a scientific paper?
I've been trying to put a phylogeny tree into a scientific paper. This tree includes ~220 species, which is too too large for one page for journal articles (Letter or A4 size). But in my paper it is crucial to show the whole tree on which the among-species distribution of a characteristic is indicated. I have looked up some journal issues but so far haven't found any similarly large phylogeny in one article. How do people usually treat this kind of situation in scientific papers? Could anybody tell me how to do it, or show me examples? Thank you so much.

Which journal and article type are you thinking of? I'd probably suggest it would have to be a supplement if it's too large for a page - is it also possible to simplify the graphic you are trying to display, perhaps by grouping?

Have you tried contactating the editors about this problem? Usually they are helpful.

Also, don't forget that you can deposit your full tree in treebase. So you can show the collapsed tree in the paper, and give a link to the full tree somewhere in the text.

The simplest way of course is to add it to the supplementary materials. However, 220 species are not that many, you should be able to fit that into a page. You have not shown us your tree so it is kind of hard to give specific advice but I am guessing that you have a linear rather than circular tree. If you convert it to a circular tree you should be able to fit it on a single page.
Here are a few random examples of large circular trees I found on the internet:

If you update your question to show us the actual tree I might be able to give you more specific advice. For example, you could split the tree into smaller ones, each showing a specific order or class or whatever resolution you are working on. There are various tricks you can try but they all depend on the details.

A circular tree is basically the only way to fit a large number of species onto a single page. Obviously, there is a tradeoff between being able to read each of the species names and the number of species you have in your tree. If the big pattern is important, rather than individual names, then you should be fine. Just make the species names as small as they need to be to fit. You can also include an arbitrarily large PDF of your tree with legible names as a supplement.

It is not always essential to show a big tree.
My opinion might be biased but it seems to me that huge figures with illegible labels are just a gimmick to make the reader feel that it is a great analysis (another case is that of networks).
First of all it is important to decide what is that you really want to convey from your figure. For example if your comparing some species with different clades then you can show the last common ancestor instead of showing all members of the clade.
As far as 220 species are concerned it will be tough to fit all of them stacked. But if you split them into two stacks it would be possible to fit with all labels legible (Paper=A4, Fontsize=6pt).

Agreed about people just wanting to make it look fancy - I often see people making figures (using R they have been to me for help with coding) and once they've put a lot of effort in to a figure they realize it doesn't really show the point but have become to attached to it because it was so hard to make. Wish more would think, before starting to make the figure, about what they want their figure to show - would save a lot of time and hassle!

LOL @GriffinEvo "become too attached to it because it was so hard to make".. This can become a PhD comics strip :)


text:
Ka/Ks (dN/dS) analysis module for Python?
From this wiki article:

In genetics, the Ka/Ks ratio (or ω, dN/dS), is the ratio of the number
  of Nonsynonymous substitutions per non-synonymous site (Ka) to the
  number of synonymous substitutions per synonymous site (Ks), which can
  be used as an indicator of selective pressure acting on a
  protein-coding gene.

Question:
Are there any modules/packages available in Python for doing Ka/Ks analysis? I wish to carry out whole gene Ka/Ks analysis and then maybe "codon level" Ka/Ks analysis (i.e. within gene via sliding window).

Do you know about BioPython?
Here, on another website, someone already asked this question and a pretty nice answer was provided by Brad Chapman. He gives already written functions to perform this kind of analysis (I personally haven't tried the codes).
In Perl there is Bio::Align::DNAStatistics. You might adapt it to Python.
This might be useful as well.
I think there are plenty of possibilities that are offered to you. You can go through some others by doing google search with the keywords synonymous, non-synonymous and BioPython.

Cheers, i'll give this a go soon!

I've looked into BioPython, they have an output parser for PAML but that software is not recommended when you only have pairs of protein sequences. I ended up programming my own version which implements the approximate Nei-Gojobori algorithm.


text:
Stress regulation in mosquitoes
I was just trying to understand how in insects, specifically mosquitoes does the process of emergency responding, stress regulation take place? Or in simpler words how are flight, fright and fight situations handled?
I understand that insects have a ganglion system and they do, suitably, respond to external stimuli, but I would like to know if there is any chemical coordination that works specifically in emergency situations just as adrenalin and nor-adrenalin do in our case.

see this

Does this mean that besides inducing long term effects, as suggested in the article, dopamine also induces the same temporary effects (like flying with greater speed and trying to escape when in danger) in insects as adrenalin does in our case?


text:
Speciation and Phylogeny of Lactobacillus
The lactobacillus, also called Döderlein's bacillus is a genus of facultative aerobic bacteria. There are several species such as Lactobacillus acidophillus and Lactobacillus reuteri.
I have several questions, all linked, for the concern of speciation of bacteria species used for lactic fermentation by humans.

Are all species that are used for cheese and yoghurt fermentation part of the genus Lactobacillus?
Do all species used for cheese and yoghurt fermentation form a monophyletic clade?
Did the speciation of this clade occurr before or after the use of these bacteria by humans?
What was the ecological niche of the ancestor(s) before humans used them for cheese and yoghurt?

I deleted your first question since a 3 second search should give you the answer. See NCBI's taxonomy page for Lactobacillus for a list of the various species in the genus.

Isn't that the exact same link I posted in my previous comment?

generally, lactic acid bacteria (LAB) are the ones you should be looking at for milk-based fermentation products. although sometimes species like bifidobacterium are added, which is of a completely different phylum. also, for cheese production, or the Dutch variety I am familiar with anyway, you would need fungi as well.
the lactobacillales order is not monophyletic, as you can see on the wiki page there are at least two different clades.
the wikipedia page 'Yogurt' speculates on the ecological niche of LAB: "Analysis of the L. delbrueckii subsp. bulgaricus genome indicates that the bacterium may have originated on the surface of a plant. Milk may have become spontaneously and unintentionally infected through contact with plants, or bacteria may have been transferred via the udder of domestic milk-producing animals." (source)
EDIT: the LAB are an order, they have been around for quite some time before the humans showed up.


text:
Is lemon water an alkalizing agent in the body?
I was recently having a discussion with someone about whether lemon water actually increases the pH of your body (by which I assume they mean the blood); their claim was that once Citric acid was metabolised it results in an increase in pH due to the "anionic properties of citric acid".
I looked around on the internet at it would seem that this is a common claim circulating around health forums: Example 1, Example 2, etc.
Now to me this sounds like something which cannot possibly be true and appears to be a crazy health fad (they seem to spuriously appear and gain popularity now and again), and I cannot find any scientific papers or articles to support or refute their claim.
Can anyone provide a reliable scientific reference or provide a reasonable scientific explanation (preferably accessible to a layman with only A-level (college level) understanding of chemistry and biochemistry) which either supports or refute the claim that drinking lemon water (citric acid) increases the pH of the blood?
I have crossposted this to Chemistry.SE as well, as it is a crossover between chemistry and biochemistry.

The link in Chemistry.SE is unlinked

The blood pH is tightly controlled since variations are quite dangerous for us. Under normal circumstances the pH is 7.4 (with a normal range between 7.35 and 7.45). Below that we are talking about acidosis, above it about alkalosis. If the blood pH goes about 7.8 or below 6.8, death will occur. This pH is maintained by the Bicarbonate-buffering system, for details see here and here.
Food that we take up does not directly influence the blood pH (and there is also no reason for us to do so, since this is tightly controlled and regulated), so this is a health fad. Details that debunk this myth about it can be found here, here and here.

The website to which you linked states that Lemons have a "moderate to strong alkaline-forming effect"? How is it that something acidic can form this "alkaline-ash"?

Food gets metabolized in the body and molecules get modified in this process. If you think of the stomach, this is highly acidiy, while the duodenum is pretty alkalic. This gets often mixed up...

What about giving lemon jucice in someone already having metabolic alkalosis or acidosis?

Short Answer:
There was an interesting paper that dealt with the pH of urine when citric acid was consumed.
The summary was: There was no increase in urinary pH or total nitrogen in 24 hours collection of urine.
What This Means:
The food we take does not affect the blood pH directly. Acidic food will cause increased secretion of alkaline components into the digestive tract to neutralize the excess acid. This will cause a fall in the bicarbonate ions concentration (this being the major alkaline buffer) in the blood. This might cause acidosis (depending on how acidic the food is).
The body compensates the decrease in bicarbonate concentration by excreting H+ ions in the urine. Thus urine becomes more acidic when there is a relative state of metabolic acidity in the body. There is also hyperventilation and excretion of more CO2 as this will cause excretion of H+ ions.

HCO3- + H+ ----> H2O + CO2

Incase of alkaline foods, the stomach acid itself would be partly neutralized by the alkali present in food. Thus the body need spend only minimal bicarbonate ions to neutralize the remaining acid.
If there is severe alkalosis body compensates by decreasing the respiratory drive (conserving more H+ ions) and excreting more bicarbonate ions through kidneys.
Compare this with the data obtained from experiment
If consuming citric acid would lower blood pH levels then the urinary pH should increase. As the data shows this is not so, that would mean the citric acid does not contribute to the acidity of food in any significant way even when consumed in large quantities.

The paper no where mentions Urinary pH, and deals with excess Citric acid consumption. I dont think your answer is valid

The administration of the material to the other subjects caused slight variations in the citric acid excretion, in general paralleling changes in the urinary pH.
Kindly read through before commenting

Ingestion of citric acid in addition to a constant diet did not affect the pH or the total nitrogen of the 24 hour urine collection.  Last line of summary

Before summary they do mention, there was a dip in urinary pH, but nowhere they quantify it or tell how did they measure.

The excellent answers from Chris and One Face have already written about why the claim is wrong, so I'm going to add a hypothesis for how this sort of nonsense could even originate in the first place.
The reason why lemons are acidic is because they contain a lot of citric acid, so in a solution part of this citric acid ionizes to citrate which increases the concentration of H3O+, thus increasing pH. Now imagine some quackjob with poor knowledge of chemistry reading about this, and only picking up the word "citrate".
Citrate is of course a weak base (since 3rd pka of citric acid is 6.40 then pkb of citrate must be 7.60) so if we pour some kind of citrate salt into water we would get a basic solution.
So basically, I think that the originators of this fad forgot about or didn't know about the H3O+ ions, which of course do not magically disappear when we ingest lemon juice.

Also, note that there are a lot of quack treatments that center around supposedly being able to alter the pH of your blood.  I think that quackery is why anyone would be interested in altering one's PH deliberately.

"The reason why lemons are acidic is because they contain a lot of citric acid, so in a solution part of this citric acid ionizes to citrate which increases the concentration of H3O+, thus increasing pH. " - You mean lowering pH?


text:
Where are newly discovered medicines tested
When a medicine is prepared by a biologist,then where does he first test on? And how does he know that this is the exact combination for a disease to get cured? Does he test that medicine on a human or specific sample of blood? I'm an engineering student but still I'm curious to know.

This is a very broad question, so I won't attempt to answer it fully. Instead, I'd recommend starting out by reading the Drug Development and Drug Discovery articles on Wikipedia, and if you have more specific questions after that then feel free to ask them here.
Basically, new drugs (either small-molecule "chemicals" or large-molecule "biologicals") are discovered in myriad ways, from pure accidents (see Penicillin) to specifically-targeted research. Once a lead compound is identified, it is put through a series of biochemical assays to determine, for example, if it inhibits certain enzymes of interest. From there, it moves into testing by cell-based assays using both normal cells and disease-specific models. All the while, investigators are looking for high specific activity (potency), low toxicity, and minimal off-target effects.
If a compound or group of them looks promising in these in vitro assays, experiments then move into animal models. The goals are similar here - high activity, low toxicity, and few (if any) side effects. The experiments get progressively more complex, with different endpoints depending on the exact aspect being studied.
It is only after extensive animal testing that a compound will be tested in humans. There are different phases of testing, each with different criteria, dosing patterns, number of patients, and reporting rules. The link I just gave explains each phase briefly.

Hopefully this is enough to get you started. Like I said earlier, if you have more specific questions after reading through all the references, please let us know.

Just to put all of this in perspective: this whole process (when properly done) can take around 15-20 years and a few billion euros.


text:
Book recommendations for algorithms used in evolutionary biology
Do you have recommendations for a book that presents the different algorithm used in theoretical evolutionary biology?
I don't mean evolutionary or genetic algorithms (otherwise this question would not be a good fit for Biology.SE) but algorithms applied to evolutionary biology. I am not interested in statistical procedures and algorithms to reconstruct phylogenetic trees, to annotate DNA sequences or to find out synonymous changes by comparing sequences of closely related species. I am not interested in introductory book on programming.
I am interested to computational modeling applied population genetics, kin selection, game theory, population range expansion, simulating sexual reproduction, selection for different sex determination system, evolution for robustness/evolvability, evolution of codon usage, evolution of genetic code, evolution of cognition, evolution of multicellularity, …
I don't quite know if one book that encompass all these subjects exist. If not, I wold welcome suggestions of book that present the algorithmic used in some but not all of these subjects.
Searching a bit in amazon, I easily found tons of book but don't quite know if they fit my expectations. Below are some examples
Evolution as computation
Individual based modeling and ecology
Models and algorithm for genome evolution
modelling for field biologists
Practical computing for biologist
Evolution as computation
Genetic and evolutionary computation
Genetic algorithms+ data structures = evolution programs
The missing algorith
Cellular Model: Mathematical and theoretical biology, Algorithm, Data structure, Bioinformatics, Computational biology, Artificial life, Computer simulation
Natural-Artificial-Models-Computation-Biology
An-Introduction-Genetic-Algorithms-Paper

Derek Roffs modelling evolution and another book I'm trying to think of (maybe by Otto) touch on some of these subjects.

Rather than asking people to click 10 links, can you add the titles as a list (with links)?

I have to agree, I didn't bother to check them all (because I'm reading on an iPhone)

@GriffinEvo I don't think Sarah Otto ever wrote a book about algorithmic. She wrote this book which is about mathematical modeling. The equivalent of this book but with the tools of algorithmic rather than mathematics would be a good answer to my question.

What you are describing usually falls under the category of computational biology or just mathematical biology. Unfortunately, the biggest part of this field is bioinformatics, or the application of statistical and/or dynamical programming techniques to sequence data. You exclude this in your question, and I would agree with you that it is a "boring" topic from a theoretical biologist's perspective, because it mostly uses computer science in a very standard way as a tool for experimental biologists.
As you noticed, it is also standard to use computational models in theory papers as a way of simulating things. I think this is the sort of resources you are asking for. Unfortunately, specific algorithms are seldom standardized or reused in this area. Typically, each paper (or sequence of related papers) uses their own models.[1] As you read a lot of papers, you will find some common themes, but these are just standard ideas of theoretical biology expressed as simulation. I doubt that comprehensive books exist, and even if some do their utility is not clear to me due to a lack of specific algorithm (re)use.[2] However, the most commonly used techniques are to either to solve differential equations numerically (which most would classify as mathematical modeling) or run agent-based or population-based models. General resources on these exist, and here are some discussions for the latter other SEs:

Simulation modeling of diseases.
Sources for Algorithmic Evolutionary Game Theory.
Canonical reference on agent-based computing.

Finally, do not confuse 'computational modeling in theoretical biology' with 'algorithmic biology'. Algorithmic biology is a new field that views ecological and evolutionary dynamics as computatioanl proccesses. Instead of using mathematical tools borrowed from physics (as is standard with the dynamic systems approaches to mathematical biology), it uses the tool of theoretical computer science (note that this is a type of math that has very little to do with programming the laptop infront of you). I know of only two books in this field:

Gregory Chaitin "Proving Darwin: Making biology mathematical" - Although Chaitin had contributed significant and original thoughts to computer science in the past, I would strongly advice against this book because it misses the point from both the biological and computer science point of view.

Leslie Valiant "Probably Approximately Correct: Nature's algorithms for learning and prospering in a complex World" - in this book (based on earlier papers), Valiant recasts evolution as a type of machine learning. This is very interesting from a mathematical point of view, although it might not connect directly enough to biologically relevant questions (see also some of the discussion in Kaznatcheev (2013) and Kaznatcheev (2019)) and misses the computational power of frequency-dependent selection (see Kaznatcheev (2020)). But I would recommend reading this book.

Notes

In general, I consider these sort of models as heuristics and I am skeptical of their usefulleness beyond rhetorical devices/examples.
I think that literature reviews would be interesting computational modeling in specific subfields. In fact some colleagues and I have wanted to do this for the smaller area of evolutionary game theory (This answer can serve as a starting point for some algorithmic considerations of EGT).

Have you looked into "Fundamental of Molecular Evolution" by Dan Graur & Li.
Another suggestion in line of population genetics and different evo. theories would be -
Evolutionary Genetics: Concepts and Case studies
(Multi-author book. Editor Fox & Wolf)


text:
Identification of this spider?
I find these in forests in Oregon, western half, though they're probably on the eastern half as well. They live under pieces of wood and bark, and have a small web across the ground. Mine will eat crickets, but I think they eat carpenter ants, termites, and maybe pillbugs/sowbugs. It seems about an inch long, red on the thorax and legs, and dark grey and slightly hairy on the abdomen. The closest to this spider I've found is sowbug killers -- they're in my backyard, but they're smaller then this spider and also are a light tan on a hairless abdomen, with lighter colored legs. The fangs also seem different shapes but I'm not sure about that.

Thanks for getting the images up there, I still can't figure out how to do it. Is there a way on mobile?

There is on iPhone at least, I'm not sure on other platforms.  You can always type up the markup manually (though it is a little cumbersome on mobile): ![an image](http://example.com/image)

I thought it was the woodlouse spider too which is why I posted an answer but I am unsure now since you already suggested it. It should belong to the genus Dysdera though

Oregon has over 500 spiders so its hard to identify which one this is

This is very likely a species in the Amaurobiidae superfamily, and I agree appears to be Callobius severus (the hackled-band weaver or the hackledmesh weaver).

 Source: Bugguide.net

 Source: Kyron Basu 2012
Moldenke et al. 1987 provide a key to spiders of the Pacific Northwest. Importantly, they note:

adult genitalia are necessary for identifying species and separating
Callobius from Amaurobius.

For example, here is a picture of Amaurobius ferox (Hackledmesh Weaver)

 © Danny Steaven 2008

I've seen numerous sites conflate this species with C severus and actually I've seen sources that identify them both as the "Hackledmesh Weaver".

So although the OP's specimen strongly resembles Callobius severus, a scope is necessary to truly identify to species. This Penn State page provides good information regarding these similar looking species in the superfamily.

Callobius and Amaurobius species have similar life histories and behaviors. They are most often found in damp locations under bark, leaf litter, and stones, as well as in woodpiles and other protected areas.

Stephen Ellis Lew (2011)  produced an atlas to the genitalic morphology of the Callobius genus, and he proposed a morphological diagnosis that is more consistent with principles of homology than those previously in use. [See the link for his dissertation on the subject].
Callobius severus
Description:

Cephalothorax and legs = reddish to dark brown [Source].
Abdomen = dark to light grey with fine hairs; often with large, bilaterally mirrored paler spots.

Ecology:

Nesting woodland species commonly seen in the Pacific Northwest

McIver et al. (1990) suggests that this species of spider is one of many that is characteristic of young forests.

Is it Dangerous?:

Not according to this Penn state website:

The one verified record of a bite by an immature Callobius species resulted in pain, itching, swelling, redness, and nausea.

Vetter & Antonelli provide evidence for how to differentiate this species from the "more dangerous" hobo spider.

in the side view, the palp of Callobius males has large, conspicuous, pointed projections (Fig. 7).

It look like Callobius severus to me.

I agree with the above that the spider is probably Callobius severus, especially since you found the spider in a forest in Oregon.

The spider in found in parts of the United States and Canada with nests most widespread in the U.S. state of Washington and the states bordering Washington, making them most common in America's Pacific Northwest region.


text:
Studying the fruitfly nervous system
I'm studying Neuroscience and Fruit Flies are a pretty big deal but I don't know as much as I think I should about them.  Are there and comprehensive sources that I could read?
I'd like a review of all the important parts of the nervous system, where they are, what they do, and how they connect.

Drosophila by Ashburner (and others) is a standard drosophila book (found in many drosophila groups). Also check out resources like flybase, flyatlas, Bloomington drosophila stock center - they will often have some info. Not sure about neuroscience specific though

Please narrow this down a little, you could fill libraries with the sources of info on this little fly. What exactly are you after? Text books? Reviews? Original research? On what? Anatomy? Nervous system? Immune system? Sex determination?

I'd like a rundown of all the important ports of the nervous system, where they are, what they do, and how they connect.

Flybase is a generally useful source for Drosophila anatomy/physiology including the nervous system. From there I found this link which has some neuroscience-specific info.


text:
Can more than one antibody bind the same antigen
I'd like to clear something up about antibodies that I'm not sure I've understood in the articles I've read. Looking at concepts such as "affinity maturation", "monovalent antigens" and "polyvalent antigens" it seems as if there are multiple antibodies which can bind to the same antigen. (Although I think I'm right in saying that individual antibodies can only bind to one antigen?) However, when I read sentences like "It has been estimated that humans generate about 10 billion different antibodies, each capable of binding a distinct epitope of an antigen" on the Wikipedia page (for antibody) it does make it sound like it's one antibody per antigen? Is this the case? Or is it one antibody per epitope. Either way, to put this question in a nutshell:
Is it true to say that the same substance could bind with (and, therefore, be recognised by) more than one antibody, or not?
Also, if the answer is no, does that mean that antibodies with different binding affinities are classed as the same antibody or not?

Let's clarify the terms. An antigen is a molecule that can be associated with a particular substance (virus, pollen, dander.) When an immunoglobulin or antibody recognizes an antigen it binds to a specific epitope. An antibody recognizes an epitope using its paratope.
Some antigens have multiple epitopes; this means that different antibodies can simultaneously bind to them (if the epitopes are far-enough apart from each other so that binding to one doesn't preclude binding to the others.)
An example from my work is influenza (flu) hemagglutinin, which is a major viral coat protein. Here's a low-resolution structure showing a "head-binding" antibody fragment (actually three of them), and here's a similar structure showing a "stem-binding" antibody fragment. Our immune repertoire (and physiology) greatly predisposes us towards producing head-binding antibodies over stem-binders. Note that each structure has three antibody fragments bound in the same state. Because the head-binder and stem-binder antibodies are well-separated in space they can both be accommodated in a single complex (as is experimentally confirmed.) In this case, up to six antibodies, using two distinct paratopes, could simultaneously bind to a single antigen.
For matured (high affinity and high specificity) antibodies, each binds a specific epitope. The typical state of affairs is then explained "one antibody per epitope" which is overly simplistic because some epitopes can be recognized by multiple paratopes (which would be found on different antibodies.) So a given epitope can be recognized by no antibodies (a new antigen, or one that is poorly immunogenic) or by multiple ones.

Is it true to say that the same substance could bind with (and, therefore, be recognised by) more than one antibody, or not?"

Yes, that's true.

Is it, then, true that one paratope could bind to more than one epitope?

Yes. The process of affinity maturation starts with low-affinity and low-specificity interactions, with the paratope getting progressively improved with respect to affinity and specificity.

Yes, this idea is called a polyclonal or polyspecific antibody. It is known that antibodies before they are fully matured are polyspecific. That is how we can recognize nearly limitless 'things' with only a limited number of antibodies. This is because each antibody you initially make can take on the job of binding more than one epitope.

Yes -
Its all binding kinetics - even a monoclonal antibody will bind many different antigens. The affinity/avidity will be different depending on the interactions. The target antigen may have the lowest known K_d, but antibodies will still bind to many many other antigens. This is why when doing research using antibodies you often have to "block" your specimen with something like BSA or milk to try and reduce the "non-specific" binding.

Although right in principle, this idea is misleading. Yes it is true that at some equilibrium that you can bind anything, even if the Kd is 20 grams/ mL, but that's not adding to the discussion and really diluting it with semantics of concepts that are not physiologically relevant.


text:
Why did abiogenesis only happen once?
If the "primordial soup" theory of abiogenesis is to be believed, self-reproducing organisms spontaneously arose on Earth at least 3.5 billion years ago, surprisingly soon after the Earth cooled down enough to potentially harbor life.
It may never have happened again, however, since all lifeforms on Earth today are similar on a molecular level (DNA), suggesting a common origin.
This appears to imply at least one of the following:

Immediately after the first spontaneous abiogenesis, environmental conditions on Earth changed dramatically, making a repeat impossible.
The first organisms that arose consumed any subsequent organisms that came into being. This was suggested by Alexander Oparin, but I find it very difficult to believe since it would have to happen everywhere on Earth. Also, most single-celled organisms found today do not consume other organisms, and even where they do that does not usually lead to their complete extinction.
The common origin theory is in fact false, despite the similarities between organisms, and abiogenesis did occur multiple times in the same way.
Abiogenesis happened more than once, but only the descendants of one occurrence survived till today.
Spontaneous abiogenesis never occurred on Earth after all because the conditions never allowed it; instead, a proto-organism arrived on Earth from a planet where the conditions do (Panspermia).
The standard theory of geological history is wrong (i.e. the Earth was in a "fertile" state for much longer before the eventual origin of life than commonly thought, due to some unknown mechanism causing radiometric dating to give wrong results).

None of these seem likely to me, yet even less likely I find the idea that life arose spontaneously almost immediately (within a few hundred million years, possibly even faster) after the Earth's crust solidified, and never again afterwards.
What are the currently held theories on that matter? Can poeple provide references to relevant publications.

Are we sure that all life on Earth shares a common origin/ancestor? Even if all multi-celled life does, there may be single-celled organisms which are not related to any of these related species. Plus, we have not witnessed every location on Earth, like the bottoms of some oceans...

This question shows how any new life would have to compete for resources with existing life:  https://biology.stackexchange.com/questions/59892/is-abiogenesis-possible-today

It is so strange to hear human say "few hundred million years" are "almost immediate". Sure, it is short compared to age of earth but it is also almost incomprehensibly long time compared to anything else. Seventy years is an eon to microorganisms. What is "few hundred million years" to microorganisms?

@trysis yes, we are sure, because all organisms have the same DNA code and chirality.

As @BagIM has correctly noted, quantitative qualifiers in science are meaninful only in comparison to something else: e.g., a million years is a long/huge time compared to human lifetime, but it is of the same order as the existence of humans as species, and it is a very small time period compared to the existence of life or Earth.

It may never have happened again, however, since all lifeforms on Earth today are similar on a molecular level (DNA), suggesting a common origin.

An important distinction to make here is that all extant life on Earth has a common origin.
It's completely possible that abiogenesis occurred many times, but whatever organisms emerged as a result became extinct early on or are not preserved in the fossil record.

Immediately after the first spontaneous abiogenesis, environmental conditions on Earth changed dramatically, making a repeat impossible.

Nope. The red bands and subsequent dating techniques suggest it took a very long time for a change to occur.

The first organisms that arose consumed any subsequent organisms...

Possible, but we have solid data suggesting the first functional organisms were autotrophs. That is, they made their own food from whatever they were exposed to, and the predator/prey relationship had yet to play a major role.

The common origin theory is in fact false, despite the similarities between organisms, and abiogenesis did occur multiple times in the same way.

The Common Origin Theory - as you've defined it - is almost certainly true. DNA is a constant, as is RNA, mitochondria, etc.
That, however, doesn't mean abiogenesis couldn't have happened more than once. As I said above, the Common Origin Theory applies to extant (living) species, not necessarily all organisms that have ever existed. Species go extinct all the time.

Spontaneous abiogenesis never occurred on Earth after all because the conditions never allowed it; instead, a proto-organism arrived on Earth from a planet where the conditions do (Panspermia).

That merely pushes the question of abiogensis back a bit. Why did it evolve on another world and not Earth, then? How did it survive in space? Why was it so well suited to Earth's environment if Earth-like planets are (relatively speaking) rare?

The standard theory of geological history is wrong (i.e. the Earth was in a "fertile" state for much longer before the eventual origin of life than commonly thought, due to some unknown mechanism causing radiometric dating to give wrong results).

Estimations and conclusions have come from more than radiometric dating. We have fossil records, geological records spanning continents, and even ice-core records from the poles that both confirm radiometric dating and establish themselves as independent evidence.

None of these seem likely to me, yet even less likely I find the idea that life arose spontaneously almost immediately (within a few hundred million years, possibly even faster) after the Earth's crust solidified, and never again afterwards.

Why?

What are the currently held theories on that matter? Both random speculations and references to relevant publications are welcome.

This SE is not the place for random speculations. I don't have publications handy, so I may return and edit my answer when I have the impetus.
The most widely held theory is that all extant life, with a few possible exceptions, has evolved from a single organism that existed billions of years ago. That organism may or may not have been the only one to arise. If it was one among many variations of progenitors, we have yet to find the progenitors in the fossil or biological records. Given the extremely long time span between now and the beginnings of life, we don't expect fossil records to exist of all the organisms that existed some 3 B.Y.A. so the best we can do is speculate on what might have existed to account for what we see today.

Great answer, but what "few possible exceptions" are you talking about? I'm genuinely interested.

@ChinmayKanchi - I remember a few years back that some researchers found some (assumed) Archae members that had some surprisingly different inheritable material. Not completely new genetic material, but odd nucleotides IIRC. I haven't heard about it since, so I don't know if it was ever verified.

Right. I seem to remember that vaguely as well. Wasn't it something like a tetrose sugar instead of a pentose?

The narrative that life arose once a few hundred million years after the crust solidified and then never again doesn't add up from a probabilistic perspective. If it took a relatively short time for abiogenesis to happen once, it means it isn't an extremely rare event. But if that is the case, why have we never seen it happen again in billions of years?

@RohitPandey -- A brief of the theory of "why doesn't life arise these days" is that early Earth presented a completely different environment to what exists now. Conditions some 4 BYA were extremely different, and so different chemistry was taking place. Another possibility: New variations of life exist, but the populations are very small or well hidden and we haven't found them.

For the extraterrestrial abiogenesis question, although I agree on the first statement, we shouldn't ignore the fact that our observation methods currently favour detection of big, heavy planets quickly and closely spinning around their star, for several reasons (including access to telescope time), so it's still too soon to catalogue the Earth as a rare planet type.

It may never have happened again, however, since all lifeforms on
  Earth today are similar on a molecular level

Actually, the similarity is at the chemical level where the chirality of all known-life's amino acids are "left-handed" (see http://en.wikipedia.org/wiki/Hypothetical_types_of_biochemistry#Alternative-chirality_biomolecules). Since there is no advantage to having left-handed proteins over right handed, we would expect the chemistry in a spontaneously organism to randomly chose one or the other. So, it's 99% likely that life didn't arise more then 7 times: (1/2)^7 < .01.
Or, all the descendants of the right-handed protein life could have died-off, but this seems unlikely if there is no inherent efficiency difference.

The first organisms that arose consumed any subsequent organisms that
  came into being. This was suggested by Alexander Oparin, but I find it
  very difficult to believe since it would have to happen everywhere on
  Earth

This is where your missing a big point:

It's not necessarily eating them, or even outcompeting them once they arise, it's about cutting the legs out of the environment - eating the primordial soup of any loose complex organic matter. The places where the minimal materials for self replication machinery would have been available (since crystal-based origin of life was rejected in the 60's) would be very rare, and only on very specfic parts of the Earth...
Two of the current theories for this location, were in seafloor thermal vents, or on beaches with radioactive sand. Once life arise once in one of these niches, it will gain a strong foothold in these exact locations, crowding out those places orginal "ideal conditions" that led to the generation of life in the first place.

Ultimately, we'll probably be better able to answer this question by looking out to other planets than by un-earthing any satisfying evidence that could be found intact from 3 billion years ago.

Some people think that abiogenesis did occur more than once, and that the results of those occurrences are still with us. Paul Davies, for instance, is a proponent of what he calls 'the shadow biosphere' (here's a link to a popular article on his views: http://www.theguardian.com/science/2013/apr/14/shadow-biosphere-alien-life-on-earth).
I've seen him talk about it, and while he has pretty much zero evidence for the idea, it's an intriguing thought. His argument is basically that we're not finding the organisms in the shadow biosphere because we're just not looking in the right places or in the right way;  our discovery techniques are all biased towards our particular RNA/DNA-based life.
Note that this doesn't really put common origin in the ground, it would just mean that there's more than one common origin for each 'type' of life.
Also, it isn't necessary for early organisms to consume each other in order for there to have been multiple origins that subsequently went extinct. Our brand of life could simply have out-replicated the competition.

There are essentially two ways this can be interpreted:

Why did only one type of life evolve at the beginning, as opposed to multiple types coexisting?
Why have no other forms of life evolved much later than the one we know about (i.e. when relatively "modern" cells already existed?

I think the answer to 1) is "we don't actually know if it didn't". During the "RNA world" and earlier, it's quite possible that many self-replicating molecular machines evolved totally independently from each other and coexisted much like separate species today. However, once whole cells came along, any "free agent" self-replicating molecules that hadn't joined forces with others to make cells (or didn't evolve to exploit cells, like viruses) were likely left in the dust.
As for the answer to 2), similarly to the last comment above, once the familiar type of life was on a solid footing, it would have probably eaten or starved any competing form of life before it could get off to any kind of start. A crude new self-replicating molecule could never outgrow a highly evolved cell containing multiple already highly evolved self-replicating molecules within it.

The OP mentioned this possibility: "Abiogenesis happened more than once, but only the descendants of one occurrence survived till today."
This seems to be a viable hypothesis. Suppose that around 4 billion years ago life did arise at multiple locations on the Earth. Most theories invoke very small localized environments where very complex organic chemistry would lead to life via an intermediary RNA-World scenario. The origin of life could not have been a global phenomenon, it would take place in some miniscule pore in a rock, perhaps in a hot-spring environment. It's then hard to see why this happening at one location on the Earth would preclude the same sort of thing happening on the other side of the Earth.
So, if we assume that life originated here on Earth, then given that it started so fast after the environmental conditions would allow for it, instead of billions of years later, it follows that it must have started at many different locations on the Earth.
So, the fact that all life that exists today descends from one common ancestor, would then suggest that all the other lifeforms went extinct. But this does not have to have happened soon after the origin of life. As pointed out in Winawar's answer, Paul Davies has suggested that alternative lifeforms could exist even today and have escaped detection because we haven't been looking for them using the right methods. While that's a rather far-out hypothesis, the possibility that multiple lifeforms existed until, say, 2.8 billion years ago is a lot less far-out hypothesis, and certainly shouldn't be dismissed out of hand.
Assuming that Paul Davies is wrong about different types of life still existing today, the question is then why they would eventually have died out. After all, lifeforms compete mostly with their closest related versions, life today is very diverse and the more unrelated living organisms are the less they compete over resources.
The answer could be mass extinctions, particularly those caused by living organisms. Take e.g. the great oxygenation event. Oxygen is a rather basic chemical compound that could reasonably have been toxic to most lifeforms that would all have evolved under hypoxic conditions. So, it's entirely possible that until the great oxygenation event there existed multiple weakly interacting parallel biospheres. One of these biospheres started to produce large amounts of oxygen, destroying all other  biospheres, only narrowly escaping killing itself.

None of these seem likely to me, yet even less likely I find the idea that life arose spontaneously almost immediately (within a few hundred million years, possibly even faster) after the Earth's crust solidified, and never again afterwards.

I think that's exactly what happened and it isn't even surprising.
All the answers here assume a-priori that the rate of abiogenesis is high (since we saw life start early here). However, this isn't consistent with two facts:

We haven't observed abiogenesis again, either here or anywhere else in the universe. Granted, it would be hard to observe it if the resulting life didn't progress to a certain extent, but if one doesn't find fairies one must seriously consider at least the possibility that there are no fairies (or they're exceedingly rare).
We tried to replicate abiogenesis in the lab and to date haven't succeeded. Unlikely we will anytime soon. So, it can't be that easy.

The observations made by the OP can also be explained in the context of a very low rate of abiogenesis by invoking survivorship bias and the anthropic principal. Here, one doesn't have to assume a wildly fluctuating rate of abiogenesis or extreme extinction events (the argument still works even with those assumptions, but doesn't need them).
Note that we really are in a sweet spot where we've evolved intelligence and started thinking about expanding beyond our planet when a relatively short time is left (a few hundred million years; according to [2], all life might be wiped out in a billion years, and conditions for intelligent life will be gone sooner; also see [3]). So, if the whole process had started a few hundred million years later (not such a long time compared to the total span of time the planet has been suitable for life), no one would be around asking such questions.
Essentially, this argument is invoking survivorship bias and the Anthropic principal [1]. The idea is that abiogenesis is indeed very rare, but if it doesn't happen soon enough, intelligent life doesn't get a chance to evolve. We have one sample where intelligent life did evolve (or at least, intelligent enough  to ask such questions) and are making observations on this one sample. So we have to condition on the fact that intelligence did evolve in that sample. When we do that, the probability of life evolving "early" becomes much higher (whereas it would be close to uniform over the time-line of the planet being "fertile" for life without the conditioning and a low rate of abiogenesis). The question merely isn't taking this conditioning into account.
Another thing to note - intelligence took about 4 billion years from abiogenesis to evolve here. In reality, there will be some random distribution for the "time till intelligence". Did we get a typical sample from this "time till intelligence" distribution or did we draw a short straw? Conditioning on the fact that intelligence evolved here before it was wiped out by an expanding Sun tells us its likely we did draw a shorter straw. The typical timeline from Abiogenesis -> Intelligence is likely longer than what we saw here.

This argument addresses the Fermi paradox as well, as a bonus. And it paints an optimistic view of the future since the "great filter" becomes life starting soon enough for intelligence to evolve and would therefore be behind us.
Unless there are multiple filters. Such as self-destruction.

References:
[1] https://en.wikipedia.org/wiki/Anthropic_principle
[2] https://theconversation.com/a-billion-years-from-now-a-lack-of-oxygen-will-wipe-out-life-on-earth-156241
[3] https://image.gsfc.nasa.gov/poetry/venus/q79.html

The poster may welcome speculation, but this list does not. It is specifically a question and answer list about biology. I have edited his question.

In my view, the best we can do with questions we don't know the answer to is speculate (probably why he solicited it in the first place). Indeed, that is a very good (only?) way to find the answer. So banning speculation in all contexts might be unwise, even for a question and answer forum.

I don't see BTW why invoking selection bias is any more speculative than the other arguments here. To me, its the most likely explanation, frankly. It's a very old argument applied to other questions like "why is the universe so fine tuned for life".

@David Every reply to this is speculation, I don't see how this is any different

@0x777C — You may be right. Or not. But as I recall, at the time I edited the question it already had too many answers for there to be a hope of closing it. My aim was not to encourage speculation that was  not based, at least in part, on scientific arguments. But, whereas I have contributed answers to speculative questions on the relative times of origin of RNA, DNA and protein, I had nothing other than the obvious to contribute to this, and was only involved in site hygiene.


text:
ligand binding fluorescent protein
does anyone know of a fluorescent protein that upon binding of a substrate its fluorescence is activated? i've been looking on this and perhaps my keywords are not the right  ones. Thanks in advance

You can try looking for fluorescent sensors. These schemes sense (bind to) certain ions to increase fluorescence. BiFC (bi-fluorescence complementation) is a way to see fluorescence increase upon binding of two protein entities.

what is your substrate ?? Fluorescent proteins can be attached with a tag that specifically binds certain nucleic acid or protein domains..

There are only 3 classes of fluorescent proteins proteins known I think.  Two of them are relevant to your needs maybe.
The first are usually called 'fluorescent proteins'.  These proteins are usually derived from the A victoria jellyfish.  Its entirely passive in its fluorescence, but has been tuned to many levels of quantum yield and color.
There was a new sort of fluorescent protein cloned recently from japanese eels.  It is activated by binding to bilirubin.  Its so new that its not likely to be available, but there you go.
The third class would be the luciferases.  They are luminescent, not fluorescent but in producing light involves binding from a cofactor called luciferase which is oxidized to produce their light.  This is not really fluorescence since the electrical stimulation that causes light production is not from incident light, but since what you are looking for might not exist I wanted to remind you of the luciferases, which bind their redox substrates to activate.  The luciferin molecule actually varies as there are several classes of luciferase.  I think Flavin and NAD are the most common substrates.


text:
Why do some animals and fungi prefer asexual reproduction?
Animals like Sponges and Hydra and fungi like Yeast and Mushroom can reproduce both asexually and sexually. However, they only reproduce sexually if the 'circumstances' are 'bad'. Is there a specific reason for that?

Here is a quite intuitive and straight forward possible explanation:
The key is to rephrase "if the conditions are bad" into "if the focal individual don't fit its environment" or "if the genome of the focal individual is not fit" or "if the focal individual is not fit".
If an individual has a high fitness, it has better to create clones which will be fit as well.
If an individual is not fit, it has better to take the risk to reproduce sexually hoping that some of the offsprings will be fit thanks random recombinations and mutations (there are usually much more mutations during meiosis than during mitosis).

Note:
Sex allocation and evolution of sex is a very broad subject. Your question is linked with discussion on sex allocation. You might be interested by these books:

Eric Charnov
Stuart West
Perrin and Beukeboom

But you might simply have a first look through wikipedia sex allocation, Muller's ratchet or have a look to the diversity of reproduction. You could also have a look to specialized literature, the work of S. Otto for example. Usually introductory books on evolutionary biology contain a chapter on the evolution and diversity of sexual reproduction.

On the long term creating clones will be not advantageous, because the species misses the chance to rearrange and exchange genes. Especially the later can be advantageous for developing further.

Well, yes under the consideration of group (or species) selection, cloning is not advantageous (because of Muller's ratchet for example). But it is not an argument against my answer. I just meant that in orgnaism that can reproduce both sexually and clonally (note: I did not want to make the discussion more complex by talking about various "intermediate" mode of reproduction), sexual reproduction is performed in order to explore the possibility space of genome hoping to fall on a good combination!

It wasn't meant as a counterargument, more to supplement it.


text:
Sporophyte and gametophyte

My textbook says that in both groups of seedless plants (vascular plants, non-vascular plants) the gametophyte is a free-living plant, independent of the sporophyte.
I don't understand this statement and am now wondering if the sporophyte and gametophyte  are stages in a plant's lifecycle, or are they individual parts of the plant, or are the sporophyte and the gametophyte different plants altogether? Secondly, does this differ depending on the organism?

Different plants or different structures that make up the same organism?

The sporophtye is the diploid stage in the life cycle. In comparison, with humans, you and I would be sporophytes.
The Gametophyte is the haploid stage in the life cycle. In comparison, with humans, spermatozoids and ovules are gametophytes.

Independence
Note for what follows: "independent" can be understood in terms of "ability to survive". Being independent according to its ability to survive. One might use the word "independent" for other concerns though! For example: "Independent" in the sense "no nutrient exchange between the two"
Therefore, one could say that in humans, the gametophyte is not independent (in it's ability to survive) of the sporophyte. Similarly, in moss (bryophyta), the gametophyte is not independent of the sporophyte because the gametophyte grows on the sporophyte using its nutrients (one could say that the gametophyte parasitize the sporophyte but that would be a bit misleading!). If the sporophyte is independent of the gametophyte (or vice-versa), it means that there is alternation of generations. In other words, sporophyte and gametophyte live separately (like two different individuals).
Life-cycle
You can find tons of examples of weird life cycles, in particular in plants, fungi and parasites but not only. And you may find many examples for which the type of sexual reproduction or the type of life-cycle are hard to defined with these relatively simple concepts.
Identity
The question of identiy (how separate or genetically different should two individuals be so that we consider them to be two different individuals) is rather a question of philosophy. Such discussions about identity occur when we talk about clones (ramet and genet), about life cycle or about level of organisation/level of selection. The book Major Transition in Evolution (Revisited) provides many of the philosophical discussion on the subject of identity in population genetics.

great answer.. but your book reference link is not recognised by Amazon? Do you have the title of the book instead? Thanks

Oops I missed your comments 2 months ago. I edited the link. Thanks you!


text:
What does dominant generation mean
In my texbook it is written that for non- vascular seedless plants the dominant generation  is the gametophyte as the gametophyte generation is larger and longer lived.
Is the criteria for dominant generation?-( Which generation the plant spends most of its life in?)

According to "Wile, Dr. Jay L. Exploring Creation With Biology. Apologia Educational Ministries, Inc. 1998" and reported here,

In alternation of generations, the dominant generation is the generation that occupies the largest portion of the life cycle

I guess that it has to be understood in terms of "time". I am not quite sure though if it has to be understood in terms of generation time of life span. Intuitively, I would say that generation time would make much more sense. Therefore, I'd say that, the dominant generation is the generation which have the longest mean generation time (=mean time from the birth to reproduction).
As @Shigeta said in the comments: For example, in Homo sapiens, the dominant generation is the diploid phase (sporophyte, you and me) and the non-dominant generation is the haploid phase  (gametophyte, sperm/ovule).

an example is the human animal, which is dominant over the gamete (sperm/egg) generation.

The wikipedia page Alternation of Generations actually has a pretty sophisticated discussion of this issue, and discusses the fact that plants can and do fall at a lot of different places on a gradient of one generation being dominant over another.
I think the root of this complexity is that this is an issue of terminology, and is connected to your concept of "what is an organism", which is a complex issue in and of itself (see this answer).
Despite this, I think that you can still usefully discuss use a number of criteria which argue for a generation being more or less dominant, including generation time, but also:
1) size (as you say in your question)
2) morphological complexity
3) ability to independently undergo "life" processes like photosynthesis and mitosis
4) conspicuousness/salience to humans (as we're the ones making up these categories)

I should also link to @Remi.b's answer to OPs other question, which is very similar: http://biology.stackexchange.com/questions/14186/sporophyte-and-gametophyte