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Premise of life cycle synchronization between predator and prey
While reading about the predator satiation hypothesis of the periodical cicadas' 13/17 year life cycles, I started wondering about its premise. By the way, I understand the math behind the prime number life cycle. 13 and 17, being prime numbers are only divisible by themselves and 1, and thus have as few divisors as possible. But my question is about the premise of why a predator would even want to synchronize its life cycle with a divisor of the prey's life cycle in the first place.
If the predator has a set life cycle, but its individuals are evenly distributed in regards to their development within that life cycle at any given time (for example there could be roughly even amounts of mature and immature predators at any given time), then what difference does the life cycle make? Here I am assuming that eating cicadas is most beneficial to a specific developmental stage of the predators, which is the only reason I can think of why there would be an advantage to this synchronization. By the way, is this even a correct assumption in regards to this hypothesis?
To be clear, my main question is why life cycle synchronizations between predator and prey matter when/if predators aren't all undergoing the same stages of their life cycles simultaneously.
edit: To be even more clear, I am asking what the benefits are to the predator to synchronize its life cycle with the prey (the cicadas, in my example).
My reference: Wikipedia says the following: *It was hypothesized that the emergence period of large prime numbers (13 and 17 years) was a predator avoidance strategy adopted to eliminate the possibility of potential predators receiving periodic population boosts by synchronizing their own generations to divisors of the cicada emergence period.
Goles, E.; Schulz, O.; Markus, M. (2001). "Prime number selection of cycles in a predator-prey model". Complexity 6 (4): 33–38. doi:10.1002/cplx.1040.
I have interpreted "synchronizing their own generations to divisors..." to mean synchronizing the length of the life cycle. I am happy to hear of another interpretation.

Thanks for your edits. I've updated my answer. I hope it proves a bit more satisfactory than my first attempt.

New Answer, based on first comment by user2686410 and subsequent edits to the question.

I have interpreted "synchronizing their own generations to divisors..." to mean synchronizing the length of the life cycle. I am happy to hear of another interpretation.

First, the overall goal of Goles et al. (2001) does not seem to test hypotheses related to the evolution of life cycles in the cicadas per se. It seems their overall goal instead may have been to explore the generation of prime numbers from numerical theory, using biologically-based models. For example, from the abstract they state,

The model marks an encounter of two seemingly unrelated disciplines: biology and number theory. A restriction to the latter, provides an evolutionary generator of arbitrarily large prime numbers.

and at the end of the discussion they write,

Although there are traditional methods for prime number detection (see e.g., Ref. 23) that are faster than the methods presented here, it is remarkable that the generation of prime numbers can be performed using a biological model.

To more directly address your question and if I understand their models, Goles et al. (2001) do seem to allow the the life cycles of both predators and prey to co-evolve yet this is not always clear.

We compare now a prey mutating to a cycle Y' with the resident prey (cycle length Y ) at constant X. Analogously, we compare mutant cycles X' with resident cycles X at constant Y (Goles et al. 2001, pg. 34; emphasis added).

Here, they seem to be saying that the life cycle of one (predator or prey) can change while other other remains constant (prey or predator). The life cycles don't coevolve.  Subsequent formulas and statements imply an interactive effect between the predator and prey life cycles. (Honestly, their writing is somewhat opague to me and they do not define all of their mathematical terms, making it difficult to follow the logic of their models.)
Regardless, the results of their initial models, shown in the figure below, shows the prey converging on a 17 year life cycle while the predators converge on a 4 year cycle. Somewhat more complex models tended to converge on 13 and 17 year cycles, although other primes like 11, 19 and 23, had similar probabilities of evolving.

Goles et al. (2001) admit at the outset of their paper that there is no evidence for predators with periodical cycles that align with the life cycles of cicadas. This would be consistent with general ecological observations. Most predators consume multiple prey items. Highly specialized predators would be more vulnerable to extinction if their prey source went extinct.
Another numerical model, developed by Tanaka et al. (2009) explicitly to explore life cycle evolution of cicadas, does not include predator life cycles at all. Their results still converge on 13 and 17 year life cycles although they restricted the possible range of life cycles to between 10 and 20 years. Thus, it does not appear to be necessary for predators to evolve a life cycle that coincides with prey life cycles for the predator satiation hypothesis to work. Of course, this is consistent with the real world observations that cicadas do not appear to have predators with concommitant life cycles.
Original answer, lightly edited
In the case of the cicadas, they are the prey, not the predators. They are not synchronizing their life cycles with the predators (if I am interpreting your entire question correctly). The argument is that cicadas have evolved synchronized life cycles to maximize survivorship.  By having a large number of individuals emerge within a very short period of time, the very high density means most individuals will live long enough to reproduce because the predators (birds, small rodents, etc.) will be satiated (see Williams and Simon 1995 for a review and pointers to early literature). Some predators of cicadas will be always present so the cicadas are not synchronizing to any specific predator.
Goles et al. (2001) used numerical models to argue that such life cycles will tend to converge on prime numbers. (As discussed in the update above)
Tanaka et al. (2009) recently argued, again using numerical models, that the prime number-based life cycles of cicadas evolved as a result of the Allee effect. The Allee effect basically states that there is a positive association between the fitness of individuals in the population and the population size or density. Below a certain size, a population is unable to sustain itself and is vulnerable to extinction. Tanaka et al. argue that the Allee effect results in prime-based life cycles under varying environmental parameters. They further argue that maintenance of alternate life cycles minimize hybridization between groups with different life cycle timings.
What seems to really remain to understand the evolution of cicada life cycles is to unravel the genetic mechanisms involved with timing.
Literature Cited
Goles, E. et al. 2001. Prime number selection of cycles in a predator-prey model. Complexity 6: 33-38.
Tanaka, Y. et al. 2009. Allee effect in the selection for prime-number cycles in periodical cicadas. Proceedings of the National Academy of Sciences USA 106: 8975-8979.
Williams, K.S. and C. Simon. 1995. The ecology, behavior, and evolution of periodical cicadas. Annual Reviews of Entomology 40: 269-295.

I am not sure where you read that I said cicadas were predators. I was referring to the life cycle of the predators of the cicadas, and its synchronization with the life cycle of the cicadas. At one point I even mentioned "eating cicadas." Thanks for your links, though. It looks like the models needed to explain this aren't as simple as I thought they might be.

@user2686410 - Sorry, I completely overlooked that phrase in your question. I interpreted sentences like "If the predator has a set life cycle..." in light of the cicada life cycle, which is why I thought you were thinking of cicadas as the predator. Later this evening, I'll try to edit my answer to better suit your question.

@user2686410 - would you please provide a citation you found that suggests the predators are synchronizing to their prey, especially for interpreting the predator satiation hypothesis. I'm interpreting your question in light of that hypothesis. However, no predator has synchronized it's life cycle to the cicadas (that I am aware of).

OK - I have added a reference to my question.

@user2686410 You're welcome. I hope you found it useful.

Mike Taylor's answer is well-researched and inspired the following thought experiment that might help you.
Imagine a predator of the cicada which takes several years to reach maturity(say, five). The population of this predator is distributed evenly across all the different stages of its life cycle, at least at first.
One year there is a cicada eruption and all the members of this predator species are incredibly well-fed for a month or two. If the effects of this prey glut aren't perfectly evenly spread across all ages of the predator species, there will be a fitness advantage to one age group or another. Maybe the young ones grow faster, or the old ones spend more time looking for mates instead of eating. It doesn't matter which(it can even be both) as long as it's not even across all members of the predator species.
Now examine the next generation, five years down the line. The effects of the prey glut are felt here too (more parents-> more children, bigger parents->stronger children, etc etc). If the cicada cycle is five years, or even ten, every predator generation(or every other generation) that coincides with the cicada eruption gets a fitness/population bump. After many iterations, the age group of predators that matures or spawns or whatever in time to get the maximal benefit from the cicada eruption dominates. Instead of evenly distributed age ranges, you get a big group of predator species that are synced up to benefit optimally from the cicada eruptions, which is bad news for the cicadas.
The thing that regulates the predator life cycle length is the time to sexual maturity, or the generation time. If this is a factor of the cicada hibernation time, cycles develop and the cicadas are in trouble. If the cicadas use a large prime number, the number of cicada generations between matching predator generations is very large. (a five year predator cycle and 17 year cicada cycle only overlap once every 85 years.) For every predator generation that benefits optimally from the cycle, 17 of them have to live without the benefit.
Generally speaking taking a long time to reach sexual maturity is bad news for a predator species(all other things being equal), so no species to my knowledge has evolved to sync up its generations with the cicadas.

Thank you! Very helpful and reasonable sounding explanation.


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What flying insect is this?

Found in Russia. Approx. 7 cm.

possible duplicate of What is this insect?

Out of curiosity, have you observed many more of them this year than normal? I live in the south of France and this year we have had a huge invasion of these things.

@terdon, more than normal, yes. I don't remember that I've ever seen this thing flew into my flat. But this time I've seen even three during one week.

I have ~10 in my kitchen every night this past month. Weird, someone in the duplicate thread suggested it might be because of the particularly long winter this year.

This is Crane fly, of the Tipulidae family. They don't bite humans, adults feed on nectar. Larvae prefer moist environments such as wet soil or decomposing vegetable matter and can consume roots and vegetation, damaging plants. Among others, bats and some Coleoptera are its predators.
Further informations can be found in the Wikipedia article linked above.

As a complement to Mattia Rovetta's answer, notice that this insect has only 2 wings, while insects typically have four.
Like flies and mosquitoes, these are Diptera: the hind wings have evolved into a stucture called "Haltere", and one of these small halteres can be seen on your upper photo.
The wikipedia page about halters is illustrated by a Crane Fly photo (as of June 2013), which is quite similar to your insect, but might be of a different species, if I judge by the fact that yours has a dark spot on the wing.

It is indeed a crane fly and there are >15000 species worldwide. Also see answers to this question: What is this insect?.

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Why is a slow worm not considered a snake?
Slow worms are considered lizards as opposed to snakes, both are reptiles. Now I get that there are traits that distinguish them (eye lids, ears ...). But snake species themselves vary already quite a lot.
The Wikipedia article on snakes states:

Based on comparative anatomy, there is consensus that snakes descended from lizards.

But how comes slow worms are considered lizards despite the loss of their limbs during evolution, whereas the same evidently has happened to snakes?
What's the defining factor here? The time frame when it happened, that it happened independently (like the evolution of, say, an eye)?
Note: I couldn't find any detailed descriptions about the alleged evolution of slow worms, whereas for snakes it is easy to find material.

the defining factor is that the species definition comes from where they species has come from, not only its body plan.  In fact the slow worm has features in its body plan that more resemble lizards than snakes.  The species name is as much a reflection of the history of that animal as it is a description of what may look like.

The number of vertebrae (more than 70, or something like that) is another synapomorphy in snakes (Serpentes). But they are all lizards, in the cladistic sense.

You are correct that the reason is similar to that of convergent evolution of the eye.
Both snakes and legless lizards are lizards (Squamata) that have lost their legs. However they have done so entirely separately much as octopus and human eyes have evolved entirely separately. An easier analogy is between whales and sea cows. Both are legless mammals but as they have evolved separately the must be given separate names.
Unfortunately it seems that the exact position of the snakes in the tree is unknown which makes this explanation less clear.
http://tolweb.org/Squamata/14933
However, the legless lizards (subfamily Anguinae) are within the family Anguidae, most of which have legs. This family is within the Anguimorpha, which includes even more species with legs. Just one small tip of the tree, with around 20 species is legless. On the other side of the tree, separated by many millions of years is the snakes (Serpentes).
A related question is why are snakes given their own name while legless lizards are just considered lizards without legs. This is partially due to the fact that there are so few species of legless lizard while there are thousands of species of snake. It is also probably due to cultural history. As snakes are dangerous to humans and prevalent in most inhabited areas of the world words for snakes are much older than the study of taxonomy. A western example is the snake in the garden of Eden. It is also important in Hinduism
and many other cultures/religions.

thanks a lot for your answer. I am reading through all the links still, but I think it answers what I was asking.

I'd dispute the premise that octopus and human eyes evolved separately! Too many of the molecular mechanisms involved in development are shared in all animals known to have photosensitive organs.

I'd agree that the visual system of cephalopods and vertebrates likely evolved in one common ancestor. However, this was a rudimentary "eye". The modern lens-type eyes of both groups almost certainly evolved independently from this common ancestral organ.

Slow worms share many characteristics with other lizards, such as the presence of eyelids, which no snake has. Leglessness in slow worms evolved separately than in snakes, as can be seen by the fact that other lizards in the same family, Anguidae (and therefore, more closely related to them than snakes) possess legs (see Gerrohonotus and Abronia).
Things are complicated a bit because work by Fry et al. (2006) shows that the Anguimorpha (slow worms), along with Varanids (monitor lizards), Iguanids (iguanas), Helodermatids (gila monsters and beaded lizards) and snakes form an evolutionarily related clade, since all of these possess some or all of the components of snake venom.
However, for anatomical and phylogenetic reasons, it is clear that the slow worm is more closely related to other lizards than it is to snakes.

The argument in the first paragraph is circular because you justify something based on an artificial categorization. Animals have often been re-categorized later into another family etc. Also some snakes do have remnants of legs (pythons), so what now?

Yes, pythons and some boas have remnants of legs. All this proves is that the common ancestor of anguimorphs and snakes was likely to have had legs. So what? The argument is not circular at all. I'm using established phylogenetic relationships to make an  argument about evolutionary relationships between taxa.

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What made this black cluster on a leaf?
I found this black slug-shaped thing on a leaf by my pond in western Sweden. It's about 15 mm long, positioned on a vertical leaf (I bent it to take the picture).

And I don't even know where to start looking. I was thinking it might be an egg cluster, but can't find anything useful without knowing at least what kind of organism made it.

@Canheguess I can't see any parts that I recognize as a larva (head, legs) and it's been completely still for at least 24 hours. Possibly a pupa I guess?

If you see them hatching can you take a photo of that too? I've wanted to see one of these for a long time but never found one.

Nice picture and good question!

After a lot of scrolling through image searches I stumbled upon the answer: this is the egg mass of some sort of horse-fly (Tabanidae). Almost identical egg mass here: http://bugguide.net/node/view/21171

I'm assuming I won't get a more specific answer than this.

Thanks for giving an answer yourself. I was really curious. :)

@AlexDeLarge Yes, me too! (Obviously enough to keep searching, compensating my lacking biology skills with patience.)

I am impressed! +1

Try to hatch them! Another nice picture is found here, which includes recently laid and mature eggs: http://www.pbase.com/image/132217026

@fileunderwater Good idea! But I'm not sure I want to handle a bunch of horse-fly larvae, I would really prefer it if I could watch it happen out where I found it. It's just 50 m from my front door so I could go check it out quite often. Today is the third day that I've seen it in this black "mature" state, so it should happen within a couple of days (6 days seems to be a normal time until hatching) This page http://animaldiversity.org/accounts/Tabanus_similis/ says that they all hatch at once, so it's probably easy to miss!

@picapica You can put the leaf section in a jar (with very small holes for air). When little horseflies hatch out, you can choose their fate :P

picapica , if these are horsefly eggs (which I'm pretty sure looking at BugGuide), do you have many in your area? And do they bite you? I've been bitten by deerflies and they hurt! But never horseflies as they're slow and noisy. Easier to avoid

@Jude Yes, we have quite a few of them around. Mostly to slow to be a problem, but sometimes they manage to bite. The bite is a little bit painful, and then the swelling and itching is worse (but the reaction is very different from person to person).

Thank you! Any deer flies? I'd assume so if horseflies are around.

@Jude Those too! In Swedish (at least in my usual vocabulary) we don't have separate words for the different kinds of Tabanidae, so I can't really tell if some are worse than others.


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How do you determine the length of an annelid?
I'm currently studying a horse-leech, and would like to know if it is fully grown or not. When I read about different annelid species a maximum length is often given, so I wonder if there is some standard way of measuring these elastic animals?
For example, my leech varies from 2 to 10 cm, but often seems to prefer to stretch out to about 6 cm when not moving.
(Possibly I should modify this question to be just about leeches, but I also wonder about earthworms, and probably other soft and difficult worms as well...)

Leeches:
According to Taube (1966)$^1$:

The adults of American leeches range from about 1/4 inch to 12 inches in contracted length.

Because leeches can bloat to more than 10x their "normal" size after a meal (and can undergo up to a 300% change in length), it seems that measuring a leech at anything but their contracted state would lead to wildly too variable of measurements. Therefore, it seems likely that only contracted size would prove to be truly useful.

However, see Klemm (1982)$^2$ (or Klemm,1995 $^3$) for comments about preferred preservation for identification purposes:

[Leeches] have a soft, highly contractile body. Therefore, if leeches are dropped alive into preservatives such as 70% alcohol (ethanol)...they contract strongly and sometimes such features as the eyes, general body shape, and the genital pores become distorted and difficult for the non-specialist and occasionally even for the expert to discern. When leeches are properly anesthetized prior to fixation, there is usually less muscular contraction. the body shape remains more uniform, and there is less variability of the anatomical structures. ... The preserved leech should be straight, moderately extended and undistorted.

However, Klemm does not use body length as an identification feature in his key, and therefore his directions seem to be more concerned with preserving other anatomical features (not to ensure accurate length measurements). He does provide "average size" for species in his key but notes that "contraction during processing" can lead to variation in measured length.

Other Annelids:
Interestingly, naturewatch.ca provides the followign instructions for measuring earth worms:

1.Allow the worm to freely extend itself as if it was crawling.
2.Measure the maximum distance the earthworm covers when completely stretched out.

Similarly, a Ph.D. dissertation by Cynthia M. Hale (2004)$^4$ measured earthworms by preserving them and then

measur[ing] on the longest axis of the straightened individual.

Takeaway:
It seems as though ranges of body length are almost always provided for each species. Although this is not uncommon for any taxa, many sources (including those cited) mention that variability in preservation methods/ body orientation  can lead to variation in lengths recorded (as can age, vitality, gut content, moisture content, etc.). Klemm, in particular, suggests using numerous museum specimens to make conclusions about species because of these variability issues.
As a result of these discrepancies/inconsistencies, I would guess that you're best off citing a methodology source (e.g., Taube 1966) and explicitly indicating your measurement methods.

Lit Sources:
[1] Taube, Clarence M. 1966. Leeches. Institute for Fisheries Research Report No. 1713. http://quod.lib.umich.edu/f/fishery/AAG2862.1713.001?rgn=main;view=toc.
[2] Klemm, Donald J. 1982. Leeches (Annelida: Hirudinea) of North America. EPA-600/3-82-025. Cincinnati, OH.
[3] Klemm, Donald J. 1995. Identification guide to the freshwater leeches (Annelida: Hirudinea) of Florida and other southern states. Florida Department of Environmental Protection. Tallahassee, FL. http://publicfiles.dep.state.fl.us/dear/labs/biology/biokeys/leeches.pdf
[4] Hale, Cynthia M. 2004 Ecological consequences of exotic invaders: interactions involving European earthworms and native plant communities in hardwood forests. PhD dissertation. University of Minnesota.

Wow, after so long with absolutely no activity I had almost given up on this one! Thank you for the thorough answer (and for correcting my sloppy spelling).


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What are the buoyancy control mechanisms of Chambered nautilus?
I'm currently working on an underwater robot and was hoping to use the principle used by the nautilus for buoyancy control. So how do the Chambered nautilus control its buoyancy?

They achieve buoyancy in a similar way to submarines: by drawing water in (via hyponomes) to sink, and expelling it to rise. The expulsion is also how they achieve propulsion.

Voting to reopen, since there are no comments explaining why it is unclear. It is lacking in background research but, to me, it is pretty clear what the Q is asking for.

The various species of nautilus use a combination of active transport of salts and passive diffusion of water for buoyancy (Denton and Gilpin-Brown 1966, Ward 1979, Greenwald et al. 1980). The chambers are filled with seawater. Salts from the seawater in the chambers is removed by a structure called the siphuncular epithelium. This process makes the chambered water hypotonic, meaning it has lower solute concentration relative to the animal. The hypotonic water then diffuses from the chambers into the blood, creating air pockets in the chambers. Greenwald and Ward (2010) have a recent summary of what is known about nautilus buoyancy, if you want to know more.
The diffusion of water in  is not a rapid process. The maximum ascent and descent rate of Nautilus from depths appears to be about 3.0 m m$^1$ (Dunstan et al. 2011).  This does not seem like an efficient process or rate of depth change for an underwater robot.
Literature Cited
Denton, E.J. and J.B. Gilpin-Brown. 1966. On the buoyancy of the peraly nautilus. Journal of the Marine Biological Association of the United Kingdown 3: 726-759.
Dunstan, A.J., et al. 2011. Vertical distribution and migration patterns of Nautilus pompilius. PLoS ONE 6: e16311. doi:10.1371/journal.pone.0016311
Greenwald, L., et al. 1980. Cameral liquid transport and buoyancy control in the chambered nautilus (Nautilus macromphalus). Nature 286 55-56.
Greenwald, L. and P.D. Ward. 2010. Buoyancy in NAutilus. Topics in Geobiology 6: 547-560.
Ward, P.D. 1979. Cameral liquid in Nautilus and ammontites. Paleobiology 5: 40-49.

How does the diffusion hypotonic water  from the chambers into the blood, creating air pockets in the chambers?? Wouldn't that lead to vacuum creation ??

I do not know but I would guess that it might be similar to the swim bladder in fishes. The gases are extracted from the blood stream and diffuse into the chamber. In fishes this happens by countercurrent exchange.

As the siphuncle pumps cameral liquid out of a chamber, the pressure of the chamber falls and nitrogen, oxygen, and some carbon dioxide diffuse into the chamber.  Sea water gas pressures are in equilibrium with atmospheric gases (oxygen and nitrogen) and are in equilibrium with nautilus blood.  Hence as cameral liquid is pumped out of the chamber, gases enter from the blood.  But it would make no difference to the buoyant state of the animal if gases entered or if there were a vacuum.  The emptying mechanism relies on sodium pumps transporting salt out of the cameral liquid.  There is no way to duplicate this biological mechanism in a mechanical system.


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What prevents predator overpopulation?
I've often heard that a population, human or otherwise, will continue to grow as long as there is food available (assuming nothing else is killing them off).  It makes sense: if you have food you can live, and if nothing is hunting you you'll survive to reproduce.
I recently designed a piece of software to simulate an ecosystem, with groups of creatures of different species eating and hunting and reproducing alongside each other.  It was very simplified (each animal had simple attack/defense/speed/stealth values, etc), but something became rapidly apparent: in every simulation the predators overwhelmed the prey, reproducing until their numbers could not be sustained by the herbivores, and leading to an inevitable die-off of both groups.  I could delay the die-off by adjusting different values and initial population counts, but it would always happen eventually.  The predators would eat and breed and eat and breed until the entire system collapsed.
At first I thought it was just the product of my over-simplified system, but it got me thinking: what prevents predators from overpopulating in real life?
It seems like the natural tendency would be for (for example) the sharks to continue breeding and eating until all the fish are gone, or the wolves to eat all the deer, etc.  Obviously some predators have predators of their own, but that's just putting off the question: if the hyenas don't overpopulate because the lions eat them, then what's keeping the lions from overpopulating?  I can't come up with anything that would prevent the apex predators from growing too numerous, then fighting each other over a dwindling prey population, then dying off entirely when there was no more food to find.
Do predator populations self-regulate to prevent putting undo stress on their prey populations?  Or is there some other mechanism to keep the predator hierarchy from becoming top-heavy?

As a supplement to Remis answer, here's a link to the Nature Knowledge Project page on population dynamics: http://www.nature.com/scitable/knowledge/library/dynamics-of-predation-13229468

In history, there are also mass extinctions very well outlined by this video: http://www.youtube.com/watch?v=FlUes_NPa6M. They "reset" the world and allow everything to start over again.

aka - they tend to starve to death when there are too many

Starvation, diseases and bigger predators.

Can you be more specific regarding your model?  Did the prey reproduce with its offspring possessing the same abilities as the parent(s)?  You said you could "delay."  What marked the time?

It sounds like you made it to easy for your predators to kill prey, Predators tend to fail to catch prey a large percentage of the time, and a small percentage of the time they get injured themselves. The more predators there are the more common failure and injury becomes. Predators that attack healthy prey in the middle of a herd have a decent chance of being killed by the prey.

@Nerrolken Be more specific regarding your model?  Did the prey reproduce with its offspring possessing the same abilities as the parent(s)? You said you could "delay." What marked the time?

relevant, @remi.b ?
https://www.sciencemag.org/news/2015/02/do-big-carnivores-practice-birth-control

A fun fact, the human is ultimate predator, and it is overpopulating.

No, I don't think auto-regulation explain much in the population sizes of predators. Group selection may explain such auto-regulation but I don't think it is of any considerable importance for this discussion.
The short answer is, as @shigeta said

[predators] tend to starve to death as they are too many!

To have a better understanding of what @shigeta said, you'll be interested in understanding various model of prey-predator or of consumer-resource interactions. For example the famous Lotka-Volterra equations describe the population dynamics of two co-existing species where one is the prey and the other is a predator. Let's first define some variables…

$x$ : Number of preys
$y$ : number of predators
$t$ : time
$\alpha$, $\beta$, $\xi$ and $\gamma$ are parameters describing how one species influence the population size of the other one.

The Lotka-Voltera equations are:
$$\frac{dx}{dt} = x(\alpha - \beta y)$$
$$\frac{dy}{dt} = -y(\gamma - \xi x)$$
You can show that for some parameters the matrix for these equations have a complex eigenvalue meaning that the long term behavior of this system is cyclic (periodic behavior). If you simulate such systems you'll see that the population sizes of the two species fluctuate like this:

where the blue line represents the predators and the red line represents the preys.
Representing the same data in phase space, meaning with the population size of the two species on axes $x$ and $y$ you get:

where the arrows shows the direction toward which the system moves. If the population size of the predators ($y$) reaches 0 (extinction), then $\frac{dx}{dt} = x(\alpha - \beta y)\space$ becomes $\frac{dx}{dt} = x\alpha \space$ (which general solution is $x_t = e^{\alpha t}x_0$) and therefore the populations of preys will grow exponentially. If the population size of preys ($x$) reaches 0 (extinction), then $\frac{dy}{dt} = -y(\gamma - \xi x)\space$ becomes $\frac{dy}{dt} = -y\gamma \space$, and therefore the population of predators will decrease exponentially.
Following this model, your question is actually: Why are the parameters $\alpha$, $\beta$, $\xi$ and $\gamma$ not "set" in a way that predators cause the extinction of preys (and therefore their own extinction)? One might equivalently ask the opposite question? Why don't preys evolve in order to escape predators so that the population of predators crushes?
As showed, you don't need a complex model to allow the co-existence of predators and preys. You could describe your model a bit more accurately in another post and ask why in your model the preys always get extinct. But there are tons of possibilities to render your model more realistic such as adding spatial heterogeneities (places to hide for example as suggested by @AudriusMeškauskas). One can also consider other trophic levels, stochastic effects, varying selection pressure through time (and other types of balancing selection), age, sex or health-specific mortality rate due to predation (e.g. predators may target preferentially young ones or diseased ones), several competing species, etc..

I would also like to talk about other things that might be of interest in your model (two of them need you to allow evolutionary processes in your model):
1) lineage selection: predators that eat too much end up disappearing because they caused their preys to get extinct. This hypothesis has nothing to do with some kind of auto-regulation for the good of species. Of course you'd need several species of predators and preys in your model. This kind of hypothesis are usually considered as very unlikely to have any explanatory power.
2) Life-dinner principle. While the wolf runs for its dinner, the rabbit runs for its life. Therefore, there is higher selection pressure on the rabbits which yield the rabbits to run in average slightly faster than wolves. This evolutionary process protects the rabbits from extinction.
3) You may consider..

more than one species of preys or predators
environmental heterogeneity
partial overlapping of distribution ranges between predators and preys
When one species is absent, the model behave just like an exponential model. You might want to make a model of logistic growth for each species by including $K_x$ and $K_y$ the carrying capacity for each species.
Adding a predator (or parasite) to the predator species of interest
... and you might get very different results.

This is a great answer, another key factor (perhaps even more important than some mentioned) is - "handling time". Your simulation likely allows a predator to eat a prey infinitely quickly when there are lots of prey around. But even if prey are hitting the predator in the face, it still takes time to eat, and while you are eating one you aren't eating another. Look up Rosenzweig-MacArthur predator-prey model - this modification of Lotka-Voltera which includes handling time prevents your die off problem!

@cell0 please don't edit correct american english spellings to british english variants. Either are correct, but one shouldn't be edited to the other.

Remi.b's answer is an excellent one, and this should be taken as a supplement to it:
It's possible your simulation is correct
The Lotka-Volterra equations are what is known as a deterministic model, and it describes the behavior of predator-prey systems (in a somewhat simplified fashion) in large populations. Small populations are subject to what is known as stochastic extinction - as the predator and prey curves approach their minimums, they may predict populations less than 1, which in reality are either 0 or 1, and when they're 0...well, someone's gone extinct.
Odds are your simulation is on a small population, and if its a simulation, rather than calculus, you should be seeing those stochastic effects (to be sure - if your simulation keeps track of integer animals, rather than continuous animals, and random chance is involved, this is going to be something you have to worry about).
In a similar model I've been working with, that's a pretty simple adaptation of a L-V model that should, deterministically, result in a stable system like in Remi.b's picture, the predators go extinct 20% of the time, and the prey 80% of the time.

What does a continuous animal look like?

@JAB Usually proportions of a population

One of the possible adjustments of these mathematical models is to introduce a "place to hide", making some (small) percent of the prey population not accessible (or much more difficult to access) for predators. After the number of predators decreases from starvation, prey individuals are relatively safer outside the "place to hide" and can grow over this limit before the number of predators increases again.

An excellent notion!

You need to add Bell curves to your simulation. The most important curve to simulate is the nutritional quality of the prey though there are plenty more thing to curve like speed and virility for prey and predators both. Nature uses lots of Bell curves so they must be good for something, such as softening the harsh effects of pure exponential growth. I suspect that the more Bell curves you implement the more stable your populations will become.
If the food value of your prey is all equal then there's no reason for your predators to not eat every last one. That's what I do with a plate full of foodstuffs, all equally delicious and with enough surplus that all the bad food can be thrown in the trash. Problems arise when you are forced to eat the trash because there's nothing else to eat.
Let's eat our prey from all 3 sides of the curve. If we eat from the weakest and easiest to catch on the left this makes the prey population stronger and more resistant to the predator. If we eat from the most common on the top the prey rebound more rapidly. If we eat from the most desirable on the right the rapid quality (but not the virility) reduction of the prey population has serious negative health consequences for the predators. Notice how each direction we eat has the necessary corrective action against the predator as a response. Due to the wild randomness of genetics the weak population can always rebound in quality when the predatory pressure eases. Looks like Nature didn't screw that one up either.
An easy example is seen in the human vs plant food supply. Population should rise with no detriment as we produce more and more food, and it would if the quality could stay the same. The population does rise but because the nutritional quality keeps dropping, the detriment is rapidly increasing on numerous health and population charts.
When plants are forced to make do with what little they have, you are forced to make do with what little they provide.

This boils down to one main reason: competition.
Animals, in general, don’t like sharing resources with direct competitors, but this violence over food, territory, and in the case of intraspecific relations, breeding rights seems to be more extreme the higher up you go on the food chain.
An excellent example of this regards cougars. A dominant tom cat in Montana, for instance, rules over a domain that can easily exceed a hundred square miles. This territory is several times larger than what he’d require just to feed himself, so why is it so large? It’s quite simple: breeding rights. Within the borders of his, hundred or so square miles of territory are lands also used by two or three females and the cubs he’s fathered with them. Other tom cougars enter at their own risk, as he’d be more than happy to run them out or kill them. The same fate befalls any of his sons who reach maturity, so they either disperse to lands unknown or die trying. Dispersing males naturally die frequently in most species as a result.
Females also defend their territories, but since it’s not advantageous for them to have multiple potential breeding partners, their lands aren’t near as large (maybe forty square miles or smaller), just big enough to keep them and their offspring safe and well fed with all the deer, elk, coyotes, and/or bighorns they need, in addition to smaller prey. Female offspring who disperse have an easier time finding territories than their brothers and are less likely to disperse widely because of this fact.
To answer your question, predators self regulate their populations, often violently. In a stable ecosystem, there’s enough of them to keep their prey in check, but due to factors of real estate, breeding rights, and interactions with other predatory species, they simply don’t overpopulate.

I think self-regulating is a confusing term in this case. The individuals absolutely do not self-regulate, it is only at the species level that it occurs.

What you are missing is that not all prey are equally easy to catch. The old, sick animals living in exposed places are much easier to catch than animals that are young, healthy and living in well-protected places. As the predator catches the easy meat, it becomes progressively harder and harder for the predator to get a meal.

If I missed seeing this in one of the other answers, I apologize, but I don't believe anyone has mentioned a very relevant fact about some predators that directly affects their populations at any given time. The fact is that wolves and probably other predators living in a pack-style grouping, allow only the alpha male and female to mate. This obviously severely limits the number of offspring born each year as well as leaving the pack vulnerable to catastrophe when something happens to either or both alphas. This mode of self-regulation is independent of food availability so works in years of abundance as well as famine.

Welcome and +1 for this answer. However, we do ask for any answers to be accompanied by the appropriate references to allow other users to background read on your material.

@Deborah Stephenson , it is not "obvious" that restricting mating to the alpha male and female limits the number of offspring born because the limiting factor in offspring production is commonly the food available to support those offspring.  As long as the group's other members can still hunt, the same food that was available for all offspring would be available for the offspring of the alpha individuals.

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


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To understand synthesis of e-NOS and n-NOS with respect to Ca and calmodulin
I found this sentence in my notes interesting

E-NOS and n-NOS are Ca-calmodulin dependent ferments.
  They are synthesized in small concentration as a response to physiological signals which increases the level of Ca2+ in cell.

Does it mean that e-NOS and n-NOS are synthesized by mediation of Ca and calmodulin?
I remember how RNS can be derived from nitric oxide and superoxide.
Are e-NOS and n-NOS expressed on macrophages after induction by cytokines and microbial products, notably interferon-gamma and lipopolysaccharide?

What is the reference for your notes? Can you cite a valid reference?

Sorry, I cannot. This is a classroom discussion, mostly based on current textbooks in Physiology and Pathophysiology. Good bet would be in Robbins.

Does it mean that e-NOS and n-NOS are synthesized by mediation of Ca
  and calmodulin?

Calmodulin is activated by binding to calcium and NOS is activated by binding to Ca2+-calmodulin. The binding changes the structural conformation which renders the enzyme active. See this.

Are e-NOS and n-NOS expressed on macrophages after induction [...]

Macrophages generally express iNOS upon induction by cytokines. The activity of iNOS is shown to be different in humans compared to mice; humans have low activity [ref]. However mouse macrophages have been shown to express eNOS constitutively and eNOS-knockout mice show reduced NFkB production and iNOS induction.


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Total amount of CO₂ / Oxygen in Bloodstream in Humans
How much carbon dioxide and oxygen from/for respiration are in the bloodstream at any one time? (mass per litre of blood or similar)
And would there be much more aside from the blood in tissue, e.g. muscle, brain, etc.
So far the figures I have are as follows (please double check for me, I dont have a clue)
O₂ molecules per red blood cell: 1 billion. Red blood cells per micro litre of blood in males: 4.7 to 6.1 million. Molecules per mole: 6 x 10^23. Therefore moles of O2 per litre of blood: approx 0.01 (correct?) This seems quite low, since an inhalation is typically 0.5L and about a quarter of the oxygen is absorbed (oxygen by volume, 5% of the air) (1 thousandth of a mole of oxygen absorbed per inhalation?)
Thanks

This is little bit uncommon to use physical units for blood oxygen. Normally one just cares for the oxygen bound to haemoglobin, and doesn't consider the diluted oxygen. And trying to use your numbers I come to 0.8232 mole, that seems to be incorrect too...

Your calculation for O2 is along the right direction, but missing a factor I think.
Each red blood cell holds millions of molecules of hemoglobin, each hemoglobin molecule, when saturated (at the lung), holds four O2 molecules.  So this is off by a factor of millions at least.  Wikipedia estimates that hemoglobin makes up about 35% of the total weight of blood.  We can use this figure and an average of 4.5 l of blood for a human being ( numbers vary, but it will be within 30%).
4.5l blood * 1.060 g/ml density of blood * 1000 ml/l water * 35% = 1667 g hemoglobin
4 molecules O2/molecule hemoglobin * 1667 g hemoglobin / (64000 g/mol molecular weight of hemoglobin)  = 0.104 moles O2
so I get:
0.104 moles O2 * 30 g/mol for O2 = 3.12 g O2 in the blood at a time.
In the muscle and tissues it gradually depletes so that all four molecules will usually end up somewhere in your tissue.  So this is all assuming that counting all the hemoglobin bound O2 will approximate the count of O2 in the body.
We know this is a crude estimate as myoglobin in mammal muscle will store O2 for use later, and the average hemoglobin is not in the lungs and will have given up some of its O2.  It also doesn't count the O2 which diffuses into the blood and is carried by the water.  This is about 0.035 g / l, which is why we need hemoglobin - total blood saturation would carry about 1.15 g of O2.  Hemoglobin multiplies the oxygen carrying capacity of blood by 100 fold.
CO2 is much more soluble in water (blood/tissue) than O2 is- about 1g/l.  There is I think only 2 CO2 binding sites for hemoglobin, which means it carries out only half the CO2 oxygen that it carries  in.  Hemoglobin is is only considered to account for 10% of the total CO2 carrying capacity of humans.  So calculating CO2 respiration by hemoglobin is not a good way to estimate blood CO2.

To get the answers you're looking for, you need a couple of figures to start with:
(1) The amount of O2 dissolved in blood plasma: about 0.3 ml O2 per 100 ml plasma;
(2) The amount of O2 bound to hemoglobin in blood: about 20 ml O2 per 100 ml blood. - Ref: https://www.ncbi.nlm.nih.gov/books/NBK54103/ (which also sources the figures used elsewhere here)
Blood makes up about 7% w/v of the human body, so a 70 Kg (154 lb) person will have about 4.9 litres of blood. 5 litres of blood would hold around 1 litre of O2 bound to the hemoglobin. However, around half of the blood will be venous, not arterial, and that only has about 75% O2 saturation, so the actual amount in arterial plus venous blood will be about 1/8 less than that calculation. Obviously, the figure will vary significantly with body weight.
At normal pressure, the arterial hemoglobin is effectively saturated with O2. However, if the ambient pressure increases, then the amount of O2 dissolved in the plasma will increase proportionately (Henry's Law). Similarly, breathing a gas with a greater O2 fraction will increase the amount of dissolved O2 in a linear fashion. Nevertheless, O2's low solubility means that the dissolved O2 is only about 1/60 of that bound to hemoglobin, so unless that is severely compromised (e.g. CO poisoning), increasing the pressure or fraction of O2 has little effect on the supply to the body.
As for the O2 stored in the body, each myoglobin molecule only binds 1 molecule of O2, compared with 4 molecules of O2 per molecule of hemoglobin, so it will contribute a much smaller amount to the total. Of course, that will vary again with body weight but also with the amount of muscle and other type of tissue making up the body.


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Which types of blood vessels can regenerate in humans/mammals?
Which types of blood vessels can regenerate in humans/mammals?
From what I understand, arteries and arterioles can be created later in life, while this is not necessarily the case with veins. However I don't understand why damaged blood vessels in an eye recover, while this is not the case for other body parts. Also, I don't understand how angiogenic agents work.
The types of blood vessels I've been thinking about include:

Arteries
Arterioles
Capillaries
Venules
Veins

Also, does the capability vary in different organs (e.g. blood vessels in a hand vs blood vessels in an eye)?

Is this by chance a homework question? If so, please read our homework policy. Essentially, we ask you to try and answer as much of the question yourself as you can, and put down your thinking on the parts you're not sure about.

@MattDMo - no, this is not a homework question. I did some research, and it seems that arteries and arterioles can be created later in life, while this is not necessarily the case with veins. However I don't understand why damaged blood vessels in an eye recover, while this is not the case for other body parts. I don't understand how angiogenic agents work. I mean I could spend a month researching the topic and reading every scientific article, but what is the point of this community?


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Interpretation of graph from evolutionary biology
I am studying evolutionary biology, and been presented with this graph:

I am having some difficulties understand its meaning. For a start, why is time measured as a fraction of the population size? Also, what does it mean by allele frequency? Does it mean the frequency of a single allele? But if the first caption it referred to 'frequencies'... Any help? :)

I think measuring time in terms of generations means that time is measured in generation time, time it takes an organism to reproduce. In bacteria, this can be 30 minutes, or in humans it's about 20 years. So I would interpret that graph to mean that within 2 generations, allele frequency probability becomes equal. It's been too long since genetics for me to tell you anything more right now.

This graph shows the probability distribution of allele frequency i.e. it displays the density probability of an allele to be at a given frequency. The time is measured relatively to the generation time and expressed in in relation to the population size $N$. t=2N means that 2N generations occurred and of course it doesn't correspond to the same real time if we talk about rats or lions. It would be good to include the text that accompany the figure so that we could understand at what state was the population at $t=0$.

@max0005 Does the answer help you understand the graph?

I assume that the figure comes from a section on genetic drift (since this seems likely), and it shows how the allele frequency will change over time under drift in a diploid population. So in short, each line represents the distribution of allele frequencies in different hypothetical populations, that all started with the allele frequencey p=0.5.
As for your specific questions, as the comment from @remi.b says, t is expressed as generation time since this is the relevant time scale for evolutionary changes. The reason why it is a function of population size, N, is that genetic drift acts more stongly in small populations, since it is essentially a sampling effect. You can see it as a repeated application of binomial sampling. So in small populations different populations will quicky drift away from the starting point of p=0.5, while this takes a longer time in larger populations. The effect of population size is clearly shown in this article from Nature education, where you can see the distribution of allele frequencies after one generation in populations of different sizes.
The change in allele frequencies over time under drift has been modelled by a diffussion approximation (see Kimura, 1955 for the original results). His results show that heterozygozity decreases at the rate of $1/(2N)$ per generation, and after 2N generations the distribution of allele frequencies is essentially flat (if you started at p=0.5). The degree of heterozygocity at time t is given by:
$$H_t = H_0*e^{-(\frac{1}{2N})t}$$
However, your graph does not show populations where fixation has occured (only heterozygous populations), and this proportion will increase over time in the absence of new mutations. So what is missing are bars at 0 and 1, and these will become higher as time goes by (more populations will have become fixed for one of the alleles). It should also be mentioned that these results deal with the effective population size, so $N$ is really equal to $N_e$.
As for the confusion of frequency/frequencies; the graph shows the frequency of one allele in different populations (so the allele frequency on the x-axis), but each line shows the distribution of allele frequencies in different populations. This is probably why you found this confusing.
However, your question is a bit unclear since you haven't described from where you got the graph and exactly what it is supposed to represent.


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What kind of fly is this?
I found this dude hanging out in my sink, but he didn't fly away when I put a dish in the sink. Turned out it was dead. The front part looks exactly like a housefly. But, I've never seen the back end (abdomen) look like this. Any ideas?

This is probably a fly killed by the fungi Entomophthora muscae (or closely related) or maybe a Cordyceps fungus. These kinds of fungi mainly attacks insects, and you sometimes see attacks as white, swollen abdomens in flies.

(Picture of common infection, from bugguide.net)
These fungi are also known to change the behaviour of infected individuals, so that they e.g. climb up tall plants to die (sometimes called "zombie-insects"), to allow for better dispersal and transmission of the fungal spores. Lots of information about the behavioural modifications of hosts by fungi can be found in Roy et al. (2006), but they can involve both climbing to exposed locations and special mechanisms for host attachement at death:

In many cases the final interactions, or endgames, between a host and pathogen involve complex behavioral modifications such as the infected insect seeking an elevated position where wind currents can effectively disseminate conidia. Elevation seeking by insects at late stages of infection is a common phenomenon that was recognized by early insect pathologists who noted that diseased lepidopteran larvae, such as Lymantria monacha (the nun moth), infected with baculoviruses migrated to the tops of trees where they died (94). This host-altered behavior was named “Wipfelkrankheit” or “Wipfelsucht” (meaning tree top disease in German) for viral diseases (41) and “summit disease” for fungal diseases (24, 57, 106).

and

Some fungi do not produce rhizoids, but the host is held in situ by host structures alone, namely the legs or mouthparts (mandibles or stylets). The pose of the dead insect is generally characteristic of the pathogen species involved. For instance, E. grylli-infected grasshoppers (Figure 3a) and E. scatophagae–infected yellow dung flies (Figure 3b) seek elevated positions on grasses or other vegetation and cling tightly (death grip) with their legs (96). Tipulids infected with fungal species from the genera Eryniopsis and Entomophaga also attach to grasses with their long legs, often overhanging water (Figures 5b,c).

If you do google image searches on "Entomophthora fly abdomen" or "fly Cordyceps" you can see some examples of infections. I don't know about the fly species, but Musca domestica is probably likely.
For some more examples and information on Entomophthora muscae and related fungi see:

Roy et al. 2006. Bizzare Interactions and Endgames: Entomopathogenic Fungi and Their Arthropod Hosts. Annual Review of Entomology 51(1) (pdf)
Biological Control: Entomophthora muscae, webpage from Cornell Uni.
Harmon. 2012. Fungus that controls zombie-ants has own fungal stalker. Nature
Mind-controlling fungus turns insects into zombies (blog post)

Cordyceps-like fungi (there are several genera from two families) have very prominent fruiting bodies, I think this alternative can be ruled out.

authors: Ντίνος Τσακαλάκης


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Nature Scientific Reports vs. BMC Genomics
I do not know if this question to suitable here or not. I posted it as I think biologists can help me in this question. If not suitable here, then I am sorry for that.
I have written paper which I spent about 3 years working on it and it has nice findings and original sequenced data (deposited in NCBI). I submitted the paper to "Genome Biology" and I got editorial rejection but they offered to transfer the paper to "BMC Genomics". However, my supervisor refused this and suggested that we submit to "Nature Scientific Report". I tried to convince him to go to BMC Genomics because it is more focused journal and it is better for my CV, however, he said the second one is better because it has better impact factor and it is Nature! (Impact factor: 5 for Scientific Reports vs 4.04 for BMC Genomics).
What do you think as I am really confused which one to select?

This might also be a good question to pose on http://academia.stackexchange.com/

Not that journal metrics is the answer, but just for the record, BMC Genomics is ranked slighty higher based on the SCImago Journal Rank (SJR rank). In short, the SJR rank is a weighted impact factor, that takes journal prestige of citations into account. Might be useful when you discuss with your supervisor.

Thanks very much @Luigi and fileunderwater for the vey useful comments. Looking forward for more comments from other experts.

Personally, I would go for PLOS ONE, just because I am a big proponent of open-access publishing. I'm not sure about the BMC family, but Nature is notorious for its closed-access policies. I think that if your work was funded in any way by public grants (such as from the NIH in the US), your research should be open for all citizens to read if they want. I'm sure this argument has gone on long tangents on Academia.SE, but that's my view of things :) At any rate, do some research on different impact factors, and their relative advantages and disadvantages, then have a chat with your PI.

@MattDMo ALL BioMed Central journals are open access, as is Nat Sci Reports.

Indeed @blmoore. Even more, the nice chart by fileunderwater shows that Nat Sci Reports is moving fast in terms of citation

@blmoore thanks for the clarification. I've been working on non-publishable proprietary projects for a number of years in industry, so I haven't kept up to the minute on which journals are open-access.

Definitely try academics se - I'd also suggest nsr because it sounds like getting to bmc genomic is a safe card  now

I've voted to close this question because it is clearly opinion based. Whilst @Chris gave a good answer, there are many things I would disagree with on a subjective level.

This is too long for a comment, so I post it here. And these are my personal views, someone else might handle this different. I would submit the paper to BMC Genomics for some reasons:

The editor offered to transfer the paper, so you get past the
editorial review. This is not guaranteed for Nature Scientific Report
(NSR). You still have to get through the peer review, but this is not
different between both journals.
Honestly: Forget about the difference in the Impact Factor. Both are
medium range impact factor journals closely located together. My most
cited paper is published in such a medium impact journal, today you
find papers by a Medline search, so this doesn't matter anymore
(besides prestige). Additionally a lot of citations will raise the
journals impact factor in the future. I would understand this
argument when you would have to choose between Nature and BMC
Genomics, there is quite a difference.
If your work fits better into BMC Genomics the chance for acceptance
is higher, so I would go there. This is of course always a point of
consideration. The same is true for your CV.

If you have the chance to do the decision for yourself without angering your supervisor too much, I would go for it. Even better would be to convince him.

I disagree somewhat with the others comments. Scientific reports has a broader audience, higher impact factor and is associated with the Nature family of journals.
The BMC family of journal family does not have the same reputation and certainly plosONE does not, and has a reputation among some as publishing almost anything. For anyone outside your specific field they will consider publication in SR a better publication. This does not mean that SR is better journal in a scientific sense but if you are looking for prestige SR is better journal for sure.

I certainly disagree with this outdated view of bibliometrics. Impact factor is a highly contentious issue that may be directing science off-track and many people want an end to JIF. I agree association with Nature is still a big deal, and for a careerist that is the one to go for over BMC, furthmore showing commitment to open access science (which there are also problems with, but that's another story) is as important for young researchers. I certainly wouldn't disregard plosONE so flippantly. plosONE has a lot of dross, and a lot of outstanding publications.


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Paralogous genes in genome-wide association studies?
Has anybody tested if paralogous genes are over-represented among the genes identified by genome-wide association studies (GWAS)?
For example, if a GWAS study finds 200 genes associated to the disease/trait, and a number X of those can be classified as belonging to Y different gene families, is there a test to see if X and Y are bigger than expected, given the total number of genes and gene paralogies in a genome? Here I am talking long established copies within a species, not CNVs in different individuals of the same species.
I am thinking there is an interesting question behind this: if a gene has duplicated during the evolution of a genome, and the different gene copies have taken specialized, yet related, roles, an unbiased analysis like GWAS should be able to find cases where different paralogous copies associate to different subdiseases/subtraits within the same global disease/trait.

Hello. Could you help by clarifying your question? Do you want to know whether paralogous genes/regions are over-represented in GWAS hits? It is an interesting hypothesis - have you any ideas/references why this may be the case? It's always best to give as full and clear a question as possible. Thanks

That is an interesting question (thanks for the expansion). If the paralogous genes were still functionally related there is likely to be redundancy between them, so a SNP in one of the copies may not manifest at all. A SNP that affects a sub-trait specific to one of the copies would need to have a massive effect (or the study would require a phenomonal sample size) to find it (unless it was a targeted study only on paralogous genes known to be disease related?). I don't know fo any studies, but will be interested in others answers!

Is a Fisher's exact test (a chi-squared test with more relaxed assumptions) something you've considered?

I actually don't understand what the hypothesis is. First, there are tons of confounding factors to control for -- for instance, regulatory gene families may be more likely to expand than structural gene families, so you'd need to account for that (and a lot more). Your final question regarding subfunctionalization seems to have nothing to do with the original question of over-representation.

Aren't paralogs supposed to have divergent function? I would expect them to be under-represented.

You could test it also by counting paralogs in the hits only, then pick eg. 200 random genes (depending on how many hits your GWAS caught) and count in those.

I think it depends on just how related the paralogs are.  If they diverged a long time ago, then we can assume the SNPs that show up in your hypothetical GWAS are indeed independently associated with the disease.  However, it's not strictly possible for the same SNP to occur in another gene, it's sort of by definition a different SNP.  As GWAS methods generate correlations, not causations, if those same-but-different SNPs are associated with the disease, that's the end of the story.  Deeper inspection is required to learn more.

This is one paper where they separated out-paralogs from orthologs and did conservation of protein-protein interaction studies across species.The methods which they used could be helpful in doing similar studies.http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3447968/

There is no literature report saying such a thing. However, I did a cursory check for GWAS study on neuroblastoma.

Selected SNPs with p-value>0.05
Converted p-values to a score —  -log10(p-value)
Mapped the SNPs to genes while calculating cumulative score for a gene

I just sorted the genes based on their names, assuming that many paralogs have similar names. I know it is not the right way to go about it. However, I found many similar named groups in the list.
Now the next step is find actual paralogs and to score the cumulative score for a paralog-group. This is a little task:

Get sequences of the genes
Run a BLAST search to find paralogs
Assign genes to groups and find scores

I can share the file with genes and scores. I would, however, continue only if someone is actually interested in pursuing this — this could be a research paper.
PS: If you want the file just comment your email id. Some IT admin idiot has blocked rapidshare/4shared etc


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What is the difference between regular blood, a woman's and a virgin's menstrual blood?
There are many stories that blood contains the life-force energy and specifically menstrual (period) blood has always been a feature of many rituals and some ancient Sumerian tablets mentioned that menstrual blood was the 'gold of the gods'.
So it is true that the menstrual blood is highly oxygenated, the purest of all blood and it carries the decoded DNA?
Or what differences are known to modern science between regular blood, a woman's period blood and virgin's period blood?

The "purest of all blood" is fresh out of the bone marrow, i.e. in your circulatory system.
Menstrual blood is a combination of blood, some mucous, and dead endometrial tissue.

The endometrium consists of a single layer of columnar epithelium resting on the stroma, a layer of connective tissue that varies in thickness according to hormonal influences. Simple tubular uterine glands reach from the endometrial surface through to the base of the stroma, which also carries a rich blood supply of spiral arteries... Proliferation is induced by estrogen (follicular phase of menstrual cycle), and later changes in this layer are engendered by progesterone from the corpus luteum (luteal phase). It is adapted to provide an optimum environment for the implantation and growth of the embryo. In the absence of progesterone, the arteries supplying blood to the functional layer constrict, so that cells in that layer become ischaemic and die, leading to menstruation.

So, menstrual "blood" is a combination of sloughed off stromal and glandular tissue, broken down vascular cells and blood, and, no, it is not highly oxygenated (it's kind of darker than normal blood. It doesn't carry any "decoded DNA". It's basically a waste product at this point, dead, dying and no longer functional tissue.
Virgin's flow is just as dead as non-virgin's flow. Cultures obtained at hysterectomy indicate that the endometrial cavity is normally sterile. The major difference between a virgin and a non-virgin is that the possibility of infection of endometrial tissue exists in non-virgins.
Of course myths will arise around menstrual flow. After all, when it was alive, it was the medium for implantation of a blastocyst. But they are just myths.
Endometrium Histology
Infections as a Cause of Infertility


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How will rising carbon dioxide levels in the troposphere affect photosynthetic producers?
Much discussion has been had about the affects of climate change on plantlife, but how will rising carbon dioxide concentrations affect the photosynthetic process itself? Since CO₂ is a reagent in photosynthesis, would we expect higher CO₂ to mean an increased rate of photosynthesis in a real-world context? Has there been any research on this?
I am thinking more of large-scale field tests rather than lab plants.

Its a good starter, although adding co2 to a plant in a box may not be particularly illuminating. Horticulturalists have added co2 to tomatoes in greenhouses for a long time. I was thinking of something more sophisticated. I will edit my question.

There are several key ways in which rising atmospheric CO₂ concentrations will affect photosynthesis, and these are related to the different types of photosynthesis. In order to properly answer your question, I'll provide some background about photosynthesis itself.
Photosynthesis evolved in a high-CO₂ atmosphere, before the oxygen-enrichment of the atmosphere (which actually happened as a result of photosynthesis). Most plant species operate C3 photosynthesis. In these plants, carbon dioxide diffuses into the cell where it is fixed by Ribulose-1,5-bisphosphate carboxylase oxygenase (RuBisCO) into a 3-carbon molecule (hence C3), which is then polymerised to make sugars. A crucial fact about RuBisCO is that it has both carboxylase (carbon-fixing) activity and oxygenase (oxygen-fixing) activity. This means that oxygen and carbon dioxide compete for the active site on the enzyme complex, leading to RuBisCO being quite inefficient and slow at fixing carbon in higher oxygen concentrations. That didn't matter in the high-CO₂ atmosphere of the early Earth, but in todays atmosphere O₂ concentrations are high enough that they severely limit the productivity of C3 plants.
However, plants haven't just been growing slowly all that time - several mechanisms for increasing photosynthetic efficiency have evolved. The most influential systems involve concentrating carbon dioxide in a particular area, excluding oxygen, and concentrating RuBisCO in that same area. This avoids the oxygen competition for the active site and allows RuBisCO to operate more efficiently. The key adaptation here is C4 photosynthesis - the system which is present in most grasses and many of the most productive plants on Earth (e.g. maize, sugarcane, Miscanthus). It has evolved at least 62 times independently. It works by having RuBisCO concentrated within 'bundle sheath' cells which are surrounded by a layer of suberin wax. This layer prevents CO₂ escaping and O₂ from getting in. CO₂ from the atmosphere is then fixed in different cells - 'mesophyll cells' - by another enzyme - Phosphoenolpyruvate carboxylase (PEPC), resulting in a four-carbon molecule (hence C4). This 4-carbon acid, (malate or oxaloacetate depending on the system) is then shuttled into the bundle sheath cells. There, the CO₂ is released again by a variety of enzymes depending on the system, creating a high CO₂ concentration in the cell where RuBisCO can then work efficiently.
In general, C4 plants are much (about 50%) more efficient than their C3 counterparts, and they are particularly well adapted to high temperatures and moist environments. So, to answer your first question: as atmospheric CO2 levels continue to rise, C3 plants will gradually be able to photosynthesise more efficiently. Interestingly though, C4 plants are predicted to also benefit from increased atmospheric CO₂. If global temperatures rise as predicted, both C3 and C4 plants will be able to operate more efficiently than they currently do, up to a maximum temperature beyond which enzymes will begin to denature faster and efficiency will drop. One consideration is that the difference in efficiency between C3 and C4 systems will decrease, which may significantly alter the makeup of plant communities around the world.
This is a vast oversimplification, but it is accurate for the predicted overall effects. Localised effects (i.e. productivity changes in a particular region or for a particular crop) will depend on habitat, physiology, etc.
Some key papers to launch you into the literature:

Leakey, A.D.B., Bernacchi, C.J., Dohleman, F.G., Ort, D.R. & Long, S.P. (2004) Will photosynthesis of maize (Zea mays) in the US Corn Belt increase in future [CO2] rich atmospheres? An analysis of diurnal courses of CO2 uptake under free‐air concentration enrichment (FACE). Global Change Biology. [Online] 10 (6), 951–962. Available from: doi:10.1111/j.1529-8817.2003.00767.x [Accessed: 31 January 2012].
Morgan, J.A., LeCain, D.R., Pendall, E., Blumenthal, D.M., Kimball, B.A., Carrillo, Y., Williams, D.G., Heisler-White, J., Dijkstra, F.A. & West, M. (2011) C4 grasses prosper as carbon dioxide eliminates desiccation in warmed semi-arid grassland. Nature. [Online] 476 (7359), 202–205. Available from: doi:10.1038/nature10274 [Accessed: 31 January 2012].

Thanks for your answer @Richard Smith. Very interesting. I was also wondering whether many plants are nutrient limited or not - i.e., even though CO2 increases, their growth may be deteremined by the availability of N, P, K etc...?

@Poshpaws Good question. It's quite a fundamental one, and important, so it deserves to be posted as a separate question - I'll ask and answer it and post the link back here.

In temperate and cold climate C3 plants do better than C4, becouse they do not have to invest in additional enzymes when photorespiration effect is neglible. So temperature increase would promote C4 plants.

@MartaCz-C yes that's true, good point.

Could you also accout for cell breath in your answer? That is how oxygen deficit affects plants? Also I wonder why researches into plant survival in Martian-type atmosphere show that photosynthesis is more efficient at low pressure CO2-only atmosphere rather than at normal pressure.

@Anixx that is a separate, but related question. If you ask it as a new question I will answer to the best of my ability.

I wanted to add a little more to the excellent answer above, especially since the OP asks about research into this question in a "real-world context".
There is a substantial body of evidence on exactly this question that comes from experiments at "Free Air CO2 Enrichment" (FACE) sites. FACE is an experimental method/technology in which standing ecosystems undergo CO2 enrichment without (much) disturbance to the ecosystem. It has been known that higher CO2 increases plant growth since the 1960s or so, but the motivation for FACE was to understand what the long-term and ecosystem scale effects of rising CO2 in the atmosphere would be. Many different ecosystem types (forests, crops, shrublands, etc) have been studied with this technique to date, some for fairly long periods of time. I think that  many of these sites are now being shut down.
Some key findings:

Net primary production (Plant C assimilation - Respiration) generally increased for plant species, but increases in productivity varied a lot between ecosystem types.
This increase in productivity diminished over time, an effect that was largely mediated by changes in plant N availability.
Different plant functional types show different responses. For example, herbaceous species saw less enhancement of assimilation (due to a decrease in leaf N) compared to woody plants at some sites.
At the ecosystem level, primary production is often limited by factors other than available CO2 - nitrogen or water for example.

There are a couple of excellent reviews available:

Nowak, R. S., Ellsworth, D. S. and Smith, S. D. (2004), Functional responses of plants to elevated atmospheric CO2– do photosynthetic and productivity data from FACE experiments support early predictions?. New Phytologist, 162: 253–280. doi: 10.1111/j.1469-8137.2004.01033.x pdf
Norby, R. J. and Zak, D. R. (2011), Ecological Lessons from Free-Air CO2 Enrichment (FACE) Experiments. Annual Review of Ecology, Evolution, and Systematics, 42: 181-203. doi: 10.1146/annurev-ecolsys-102209-144647 link.

This article discusses the importance of nitrogen in limiting forest productivity under high CO2:

Norby, R.J., Warren, J. M., Iversen, C. M., Medlyn, B. E., and McMurtrie, R. E. (2010), CO2 enhancement of forest productivity constrained by limited nitrogen availability. PNAS, 107 (45) 19368-19373. doi:10.1073/pnas.1006463107 link

+1 the network of FACE sites answers this exact question comprehensively. Still, providing referenced in std format rather than links would make the answer more useful.


text:
Is there a hypothesis that attempts to explain patterns of species richness along all three energy-related environmental gradients?
My question is related to one of the oldest question in ecology: "What determines global patterns of species richness?". However, I want to focus on one particular part of this question, which has been bothering me for a long time.
Background information
One of the most widely recognized ecological patters on Earth, which is found at most scales and in most biological taxa, is the latitudinal diversity gradient (LDG) -- there are more species in the tropics than in the temperate regions, and the further away you move from the tropics, the fewer species you encounter. Furthermore, such pattern exists not only along the latitudinal gradient, but species richness also covaries with altitude in terrestrial environments and depth in marine environments, showing the same diversity gradient!
It seems to be fair to suggest that energy should somehow underline all these diversity gradients and create some sort of universal mechanism that would ultimately affect all species richness patterns on Earth. Unfortunately, there is no consensus on questions as grand as this one, but I'm looking for hypothesis that would specifically attempt to explain all three gradients together.
Question
Is there a hypothesis that attempts to explain patterns of species richness along all three energy-related environmental gradients together: latitude, altitude and depth? If there is, what it's weakness? If there's no such hypothesis, do we have reasons to believe that such a broad link across the three gradients can exist?
Please note how I'm trying to emphasize that I don't want you to list all the hypotheses that describe LDG only, but rather the three gradients together.

Neat question! I imagine any responsible theory would have to take into account the associated gradients of total area (that is, there are few square meters of space to inhabit as you go higher in elevation and as you go up in latitude). I haven't thought about depth, but I guess it might be a skewed hump– there is some area at low depths, much more at mid-depths, and then declining area at lower and lower depths.

Are you only concerned with richness, or with biomass too?

What did you mean "energy related gradient"? Can you give more words about that? Are you talking about temperature? If so, can your question be reduced to "How does temperature influence species diversity"?

@Remi.b, not exactly temperature, however the guy who first discovered LDG (von Humboldt) related it to mean annual temperature. Energy is different from temperature, not only from a purely physical point of view, but also biologically available energy explains why there is not many species in deserts, where temperature can be very high.

Well, I think for a start, except for thermal vents, energy comes from the sun.  So more sun = more energy captured by plants, which can support more non-plant life.  At higher altitudes, the limiting factor is the thin air, which limits plant life, which limits everything else.

@Oreotrephes, good point, I corrected species diversity to species richness in the title and the question. I.e., richness only.

@Oreotrephes, I don't think area can explain the three gradients. Some issues: it relies on area-species positive correlation in the first place, there are places beyond tropics with very high species richness that cannot be explained by area, the deep ocean provides huge volume for life, yet there's not much life there. Clearly, energy must have something to do with it.

@swbarnes2, right, but how does it create more species :-)

@Herman I think the first issue of the question has to do with the concept of energy that you use. You said biologically available energy. So you mean solar radiation + geothermy + warm winds(?) + input of sugar (through a river for example)? You are not talking about photosynthesis over respiration ratio?

Could we replace you question by: "If I take two huge boxes and add many different species from all lineage to make a somehow functioning basic ecosystem. In one box I set the temperature at 11°C and in the other box the temperature is set to 19°C. In which box will I have the greatest species richness if I wait 10,000 years?"

@Remi.b I meant energy + water availability in my desert example. Ok, it's getting a bit confusing. Let's go back to where it all started: "[C]an your question be reduced to 'How does temperature influence species diversity'"? No, I don't think so, because: 1) not species diversity but rather patterns of species richness (gradients) 2) temperature could be one hypothesis, but I believe that there is such a hypothesis and it's flawed. However, I cannot tell you right now with high confidence how exactly it is flawed, I wouldn't ask if I knew everything. I still haven't read the answers though.

@Herman - I agree with you that area alone can't explain the gradients we see; I just think it needs to be included in the null model.

This is a big question and a very active field of research. I'm not deeply into this litterature, but you should look into the the different scaling relationships (often power laws) that have been described on metabolism vs body size, species-area relationships and species richness vs biomass. Also consider that energy-use by species in a community is considered a zero-sum game both in the neutral model (Hubbell, 2001) and in Red Queen models of evolution. You will probably not find a definite answer to your question though, but there are some interesting intersections of ideas out there. As others have suggested you also need to consider and take into account differential historical extinction rates, and how this will influence current patterns (Mittelbach et al. 2007).
Points of entry could be:

Gaston. 2000. Global patterns in biodiversity (essential reading!)
Chave. 2013. The problem of pattern and scale in ecology: what have we
learned in 20 years?
Venevsky & Veneskaia. 2003. Large-scale energetic and landscape factors of vegetation diversity
Mittelbach et al. 2007. Evolution and the latitudinal diversity gradient: speciation, extinction and biogeography
Marquet et al. 2005. Scaling and power-laws in ecological systems

A couple of caveats/ideas though; first of all, it has been argued that the latitudinal gradient of species richness is likely to be due to many different mechanisms in different taxa (see Gaston, 2000). Here you are looking for a hypothesis to explain not only this single pattern, but all three of them, which makes a single explanation even less likely. Second, many non-exclusive explanations have been put forward for the latitudinal gradient. Even if we don't know which ones of these that are the true mechanisms, some are clearly incompatible with being explanations for all the three patterns you mention, while others might be applicable to all of them. For instance, environmental stability in the tropics is one suggested mechanism for the latitudinal gradient, but this doesn't make much sense for a gradient along ocean depth (deep sea has arguably been a more stable environment both over shorter and longer time-frames). It might be relevant for an altitude gradient though. Going through different hypothesised explanations for the latitudinal gradient in this way (from what I know, the best studied of these gradients) could give you a list of ideas that are most interesting to target (maybe somebody has already done this though).
I hope this helps.

Thanks, it does. I have a simple question that you should be able to answer without any research (maybe add it to your post?), and which I tried to include in my original question too: "What's wrong with just saying that all these gradients correlate with the amount of solar energy available for primary producers?" I can't seem to answer it myself. Is the difference in solar radiation really significant for plants in tropics and temperate regions? Is there really less available solar energy at higher altitudes? Does it fail to explain some biodiversity hot-spots outside tropics? Cheers.

I tried to squeeze everything in one comment, but what the heck. I actually remember doing a presentation for an ecology seminar at uni on this very Mittelbach paper :-) I absolutely agree that there might be no actual answer to this question (but that's why I agreed to accept even flawed hypothesis that attempt to explain the three gradients). I also agree that the best way to answer it is to read everything you cited... but to be honest, I was looking for a shortcut specifically on the  three gradients together :-D Just saying, I'm still grateful for your answer.

Well, for one, the amount of solar energy doesn't explain differences in species richness between hemispheres, and I doubt that it can explain gradients over altitude.

Nice question!
For the concern of plant diversity over altitudinal gradient it has been shown in several studies in the alps and in Andes that the greatest abundance and diversity is not found in high altitude neither in low altitude but in middle altitude. Some argue that the abundance and diversity depends on temperature and human impact that is what explain this pattern. There is a theoretical model that cut the mountains into three patches along the altitudinal gradient and assume that plants - when they reproduce - either send seeds in the same patch or in a nearby patch. Because, the patch in the middle can receive gene flow from both "sides" while the "extremities" can receive gene flow only from one "side", the diversity is greater in the middle patch.
In aquatic communities, there is very few physical barrier to gene flow and therefore, speciation often occur through sympatry (I think!). Depth has an important role in isolating population (allowing allopatric speciation) because of the sensory drive evolution. Some fishes (to talk only about fishes) have opsins (proteins involved in vision) that are adapted to deep water while other fishes have opsins adapted to shallow water. This divergence, allows to push fishes to chose a preferential habitat and prevent gene flow.
High temperatures lead to high mutation rate and high mutation rate leads to high speciation rate (I think).
Because of past glaciation, it has been found that species in southern hemisphere are younger in average than those in northern hemisphere. Therefore, past ecology has to be taken in account when talking about present diversity. Land mass of different size might also impact species diversity differently.
I don't think a theory that explain species diversity along these three gradients might be easily found. I would tend to think these three gradients are important because they are correlated with parameters that influence species diversity in several ways. Those correlated variables are temperature, humidity, light, time of daylight, land mass, connectivity (rivers that increase gene from mountain to valley or surrounding land mass for example), human impact, …
What did you mean "energy related gradient"? Are you talking about temperature? If so, can your question be reduced to "How does temperature influence species diversity"?
Sorry for the missing references!

This wiki article lists pretty well (better than what I did in my above answer!) different hypothesis for explaining latitudinal gradient in species diversity. Some of these hypotheses can be used to describe effect of depth or altitude.

Cheers, @Remi.b. As to your paragraph 1, if it's temperature, than the foot of the mountain should have the highest biodiversity, no? Next issue, due to the gravity, shouldn't the seeds move much more easily down the gradient (which, again, would contribute to the biodiversity of the lowest region). Finally, even if the middle patch receives more gene flow, it should reduce species richness, because gene flow acts against speciation, no?

Yes, even though both you and fileunderwater wrote great answers, I must admit that I did know about the Wiki article you cited, and I read some literature on LDG too... but I thought I should ask about the three gradients combined, not just LDG, partly because I have no idea where to look for an answer to this phrasing, partly because I'm curious, and partly because I didn't want to make you write me a book with all these theories listed :-) Thanks anyway. I still hope someone else might chew this up for me so I have only to swallow, but if not, I'm happy to dig deeper into this myself too.

Now let's get back to our temperature/energy thing, maybe I do need to paraphrase the question a little. I was mainly referring to the amount of solar radiation available for photosynthesis. You can't really call it temperature, can you? Does it answer your question or not really? But with this definition, I'm not too sure whether the amount of solar energy decreases with increasing altitude... If it doesn't, than maybe "energy" doesn't correlate with all three gradients either. Also see my question under the fileunderwater's post, maybe we should answer it first.

I've studied diversity of euglossine bees along altitudinal gradients in amazonian mountains. The references I've read showed no consensus regarding altitude. For some groups, diversity were higher at low altitudes; for other groups, it was in the middle. I've found the biggest diversity in the middle altitudes (the mountains were around Equator line). One hypothesis was about randomness: throw a lot of species inside any gradient, and most of them will overlap in the center by chance alone. Other hypothesis said about chance of recolonization. You can have extinctions anywhere, but close to Equator (low latitude) and close to sea level (low altitude) you can have species recolonizing faster, because there is more land around. After all, I don't think one simple rule will explain each and every case. And I have never thought about that below sea level. Aren't marine vulcanoes a rich environment?

Well, I guess they are biologically rich environments, but they would be an exception to the general rule where the deeper you go, the less sunlight penetrates the water, the less plankton to eat there are, the colder it gets, and even the pressure is higher (which is not related to energy). So I guess overall there is such a gradient.

What about the plants that your bees ate, did they exhibit the same trend? I also don't get your randomness explanation: if it is a uniform distribution, by chance alone the bees should be distributed, well, uniformly, no?

In the sea, temperature isn't linearly related with profundity. Look the second image here: http://marinebio.org/oceans/temperature.asp

I see the plants changed with altitude, but didn't measure their richness or diversity. Imagine a gradient from 100 to 3000 meters. Some bees will have a height span of 200m, others of 2000m. Imagine this is random, too. When you put them all together, most will overlap in the center, not in the borders. Look: http://www.sciencedirect.com/science/article/pii/S016953479901767X


text:
Does the process of making a sourdough starter involve Darwinian selection?
In essence - to make a sourdough starter:

Put flour and water in a jar, and leave it in a warm place overnight
Divide the remaining mixture in half, throw out half, add half as much flour and water again.
Repeat for 7 days.

I don't see why you couldn't just add all the ingredients required at the start, open it once a day to let more yeast drop in and give it a stir, and keep in a warm place every day.
The vague idea comes to me that throwing out half the mixture every day has a Darwinian element, but it doesn't involve any 'selection', you're simply casting out half, regardless of adaptability.
My question is: Does the process of making a sourdough starter involve Darwinian selection?
EDIT: There is no 'choice' involved in throwing out half the sourdough. It is entirely arbitrary - and both halves look equally the same.

How does the half you cast out compare to the half you retain?

Dividing it would be closer to genetic drift since nothing the bacteria do has any impact on which half you throw out. Note you don't actually have to throw out any of it is just that the process produces a lot of bulk which is usually too impractical to use unless you own a bakery.

Yes, continually diluting the mix like this encourages the organisms (bacteria, yeasts, fungi) to have more constant conditions (maximum nutrients, fewer waste products) and be in log phase growth. The mix selects for particular faster-growing organisms. if you did not dilute, the nutrient levels would change (lower) and waste products accumulate much faster. Then the conditions would be more different day-to-day.
Practically, the dilution adds more nutrients while still allowing the pH to fall. Without the dilution, particular bacteria tend to take over and lactic-acid producers dont get a chance.
refs
https://en.wikipedia.org/wiki/Bacterial_growth
https://en.wikipedia.org/wiki/Sourdough

How is that "Darwinian selection"?

I abbreviated the term to selection

so step 1 is Darwinian but dividing the culture is not.

There absolutly is selection involved. First, you create a selective environment to culture a subset of environmental organisms (yeasts). Then, by infusing fresh media (flour/water) into the cultures each day, you are essentially passaging a live culture or organisms. It's not rational selection, like that practiced by plant breeders, since you aren't hand picking the lineages you want to passage, but it does allow for natural selection to occur in this environment which would otherwise be stunted in a simple batch culture if you didn't add new flour/water mix each day. This passaging allows for more reproductive growth to occur, increasing the probability of adaptive mutations and creating the conditions for such mutation expands via competative exclusion with other clonal lineages. With more generations, organisms in the starter should become more and more specialized to the unique selective pressures in that environment over time. In theory, as they become more adapted to this environment, it will be less and less likely that any new wild strains or spoilage agents will take up residence in the starter. Richard Lenski has been conducting a series of long term E. coli evolution experiments describing how cultured organisms evolve over many (many) generations. Since people are known to keep sourdough cultures alive for years, decades, or even centuries, it seems like an analagous experimental system.

That is not Darwinian selection, because you are not selecting anything. As you mention yourself, it doesn't matter which half you discard and which half you keep. In fact, you can keep the entire thing. Discarding just makes it more practical.
If all conditions are fine, yeast will grow exponentially, meaning your amount of yeast will double every 2 hours or so. By discarding half of your mix, you simply reduce the volume you are working with. Otherwise you would have to add double the ingredients every time. For example, let's assume by adding fresh ingredients you double your volume. Starting with 250ml you would have 500ml the next day, 1l the day after, 2..4..8.. 16 liters and soon you have a bucket full of yeast.
Handling that volume to avoid overgrowth and insufficient nutrient/oxygen supply is way harder than a small volume. In the lab we grow yeast preferentially on shakers, mixing the solution to ensure all cells get the right amount of nutrients. Otherwise the yeast would die once the nutrients are depleted. So, how do you do that in your yeast bucket? ;) Just stirring it once won't do the job. The yeast would settle and die.
You could keep the halfs in separate smaller containers, but how much space do you have to store these? Here is a video where this issue is explained and what you can do with the discarded half: https://youtu.be/Ye4A2judXck
In the end, what would you do with all that starter? Once you have your sourdough starter ready, you can take half and use it for baking and keep growing the other half. How much bread do you want to bake? Do you need a bucket full of sourdough starter?
Sure, some of the yeast will die and the cells best adapted to the growing conditions will remain. This is a selection process, but it's independent from discarding half of it.

Natural selection does not require that a person is rationally selecting something, only that selection is occuring. Taking any group of environmental organisms and placing them in a new environment will absolutly involve selection. Not just initial colonization selection, but also adaptive selection over increasing reproductive generations. It's the same reason lab strains of bacteria or yeast often lack certain phenotypic traits of their environmental ancestors, while environmental organisms sometimes grow poorly in laboratory conditions at first.

The question was if discarding half of the starter involves a "Darwinian element". As I mention in the last paragraph, there is of course always adaptation/selection happening, but that's completely independent of the fact that you are discarding parts of it or not..

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