text:
What do Illumina HiSeq/MiSeq paired end reads look like?
My understanding is that paired end reads from the Illumina HiSeq/MiSeq platforms looks something like this:
R1:
    AAAAAACCCCCC
R2:
    GGGGGGTTTTTT

Where the reads found in R2 are the reverse complement of those found in R1. This does not appear to be the case however, for my sequencing data. If it helps I have a read pair from one of my MiSeq runs below.
R1:
@M01814:86:000000000-A6MU9:1:1101:15397:1339 1:N:0:2
TACTCGCACCTATCCGGCACAGCAACACCATCTGGGGCTGAATCGCAATAGCATCTCTCACTTCCTCCATATCAGATTGCTCAAGGCAAGCACTACGCTGCAGTGCCCTCCACTCCCAATTCCCTGATGCTGGTCGTAACTTGCCACACCA
+
>>AA?BBBBBFFGGG2EEEGFBGHHHGA2FGHBGHF2EE?GHGHHFFEEHDGHEFGF5FEEFBGHGBCB5FHHH5F553@434FF31G11??233B1/1/?333B?3FB?/B24B2/2B2?44?3?23333B223<>@0CB22@2@F0/?/

R2:
@M01814:86:000000000-A6MU9:1:1101:15397:1339 2:N:0:2
TAAGGGGCCTAGAACAGGCACCATACATTCAATTGGCTGTGGCAAGTAACAACCAGCATCAGGGAATGTGGAGTGGAGGGCACTGCAGCGAATTGCTTGCCTTGAACAATCTTATATGGGGGAAGTAGACGAACCAATGTGGAGTCAGCCC
+
>AA>>>ADDAFFGGGGG4FGGGFHFHFHHHFHHHB3B32EFBGGE25FGHHHHACEGG533BAGFFF355331BG1@1>EF1E23F333/>//134B43?F34B3334B334444?443B?/<C/23333////<0/<11111/?01?G0?

For reference, this is the reverse complement of R2:
GGGCTGACTCCACATTGGTTCGTCTACTTCCCCCATATAAGATTGTTCAAGGCAAGCAATTCGCTGCAGTGCCCTCCACTCCACATTCCCTGATGCTGGTTGTTACTTGCCACAGCCAATTGAATGTATGGTGCCTGTTCTAGGCCCCTTA

This is the alignment (with BLAST; alignment shown only for the HSP):

                                                           60                                                                                148
                                                           |                                                                                |
TACTCGCACCTATCCGGCACAGCAACACCATCTGGGGCTGAATCGCAATAGCATCTCTCACTTCCTCCATATCAGATTGCTCAAGGCAAGCACTACGCTGCAGTGCCCTCCACTCCCAATTCCCTGATGCTGGTCGTAACTTGCCACACCA
                                                           |||||| |||||| |||||| |||||||||||| | |||||||||||||||||||||  |||||||||||||||| || ||||||||||
                                  GGGCTGACTCCACATTGGTTCGTCTACTTCCCCCATATAAGATTGTTCAAGGCAAGCAATTCGCTGCAGTGCCCTCCACTCCACATTCCCTGATGCTGGTTGTTACTTGCCACAGCCAATTGAATGTATGGTGCCTGTTCTAGGCCCCTTA
                                                           |                                                                                |
                                                           126                                                                                38

What was the size of the library and what is the read length?

MiSeq chemistry is 150 cycles and fragment size is exactly 150bp.

Are you sure the fragment size is exactly 150bp? Usually you have a distribution of fragment size.

How many such reads are there; did you remove the adapter sequences?

I am sure of the fragment size and the adapter sequences are removed, but thanks for blasting this, that is more of an overlap that I have been able to force. Maybe I just need to allow for many more mismatches than previously thought.

Where the reads found in R2 are the reverse complement of those found
  in R1.

This statement seems incorrect.
Paired-end reads comes from opposite ends of a fragment (you could learn the reason it happens from Illumina's video). If insert size is 150bp, read length usually is ~60bp as quality score after 60th bp is unacceptably low. In this case, R1 length is ~60bp, and it is 5'3', R2 length is ~60bp, and it is 3'5'. When a number of reads are enough to cover the gap, they form a contig.
Here's an illustration from Illumina's website:

There is a little wobble in the lengths of your fragments, that's why the reads don't exactly overlap.  Is there a reason that you are spending the time and money to do the second read when the first read gives you almost the exact same sequence information?

There is no wobble in these fragment lengths (this is not just fragmented DNA). And yes paired end reads are likely to be necessary.


text:
Is there any artificial species (in particular, an artificial species of animal)?
Dogs were artificially selected from wolves, but a dog and a wolf can produce fertile offspring, and thus are of the same species. I had heard that the aurochs and cattle were different species, but I could not find this information anywhere. I had heard also that some artificially selected flies are considered to be a new species.
Is there any human-made species (especially a species of animal) which is not able to produce fertile offspring witch any other species, in particular with the one from which it evolved?
EDIT: (A similar question in different words.) Is there any human-made animal lineage which was conceived by artificial selection and which is broadly accepted as not being a race or subspecies, but a species on its own.

You might consider the horse, there aren't any wild horses that don't trace their lineage back to the domestic horse rather than a shared ancestor & though they can be bred with some of their closer relatives (notably donkeys & zebras) the offspring are almost invariably infertile, so they may fit your criteria?

Artificial selection leading to new species - Domestication
As you talk about dogs in your intro, let's consider them.
You will fail to breed a great dane and chihuahua for obvious mechanical reasons. You will also fail to breed a chihuahua with a wolf. So, yes artificial selection have lead to reproductive isolation.
Artificial selection leading to new species - lab experiment
Artificial selection have also lead to reproductive isolation in non-domesticated species. See for example the post Have we ever observed two drosophila lineages that evolved reproductive isolation in labs?
Concept of species
As a side note... Above, I consider the so-called 'biological species concept'. For a discussion on the definition of species, please have a look at this post.

There is not clear delineation for speciation, but think more along the line of a spectrum. When I compare the bacteria S. Pyogenes (flesh eating bacteria) and S.Dysgalactiae (commensal pathogen) they are very similar in a lot of their genes but they have also acquired qualities that helps us distinguish these as different species. Still, when found together, they readily undergo bacterial conjugation and exchange genes.
So to comment for the first part of question, the ability to produce fertile offspring does not imply that species are identical...rather compatible.

The OP clearly refers to the so-called 'biological species concept', so it is, IMO, possible to answer the question without getting lost in a semantic argument on the definition of the term 'species'. For such discussion have a look at this post.

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text:
Which type of plants/mosses are these?
During the rainy season in India I see these miniature plants forming a light green mat over the green algae on my house's roof.

The interesting thing is they become very green and mushy after it rains. The rest of the year in dry winters and summers they go off green (kinda brown) and survive till the next rainy season.
I suspect them to be mosses/liverworts. What do you think?
Adding some more pics-

The small wood piece in the above photo is around 3 cm in length. (For comparing the size)
Temperature when these pics were taken was around 35°C and it was quite humid.

Hey guys! I did a bit of research and I think I've found it! - I think it is one of the species of Funaria

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text:
Why do house geckos take so long to react?

This is the Common house gecko found abundantly where I live.
I've been observing this for quite long and I used to ignore it after thinking on it for a short while. Today I decided to write this here on Biology SE.
So in my lawn there's this large wall on which there are usually around 3-4 geckos foraging for their favorite insects in night. Everytime I walk towards them some of them instantly go into their hiding spots (within 1-2 seconds of my arrival) with lightening speed. But most of them initially look cool and not actually bothered by my presence. Not only that -I can even wave at them; go closer towards them and nothing happens. But suddenly after all of my actions they also run towards their hidings as they were daydreaming. (Though not instantly)
Just curious-
Is there any real lag between their signal reception and processing?
Are there some other animals which show such behavioural responses?
(Maybe they are just kidding with me :P)

This is entirely behavioral and is quite widespread.
If they ran away everything something large passed by they would waste a lot of energy, many animals wait first to see if you are just moving through, and thus can be ignored, OR if you are going to hang around and thus are a potential threat (and in the case of camouflaged organisms have a much higher chance of spotting them).
It is seen in many animals gazelle are known for it for instance.  This paper on the behavior in other lizards should help with understanding the evolutionary pressures behind it.


text:
Why do adult insects have 6 legs?
Apparently, there is an advantage to having 6 legs in the insect world. What is that advantage, if anything? Why would such an advantage exist for insects, but not for other, larger land animals?
What do those middle legs do that the front and hind legs cannot, if anything? Are they really essential, or do they just generate more muscle power?

It seems like this question presupposes perfect adaptation. Many features of modern life-forms aren't necessarily 'better' than other possible features, but are the way they are as a result of historical chance and the constraints imposed by development. Would you be satisfied with the answer "the last common ancestor of all insects had six legs, and that worked well enough that it has been kept by most of its descendant lineages"?

Insects are not the ancestors of higher organisms. And BTW octopus is one organism which will be a counter-example.

@WYSIWYG hmm great point. Nevertheless, there is an apparent advantage to having 6 legs as an insect that does not seem to exist for us larger land creatures. I want to know what that is. What are those middle legs used for?

@bshane No I'm not satisfied with that answer, but I edited the 1st paragraph to make it clear there is an apparent advantage. At the very least, I want to know what the middle legs of insects do...and if it's something that 4-legged critters cannot.

This is a little semantically tricky, because not all insects use all of their 'legs' as 'legs', in the sense of 'a thing to walk with'. Consider the raptorial forelegs of mantises - the animal uses them to catch prey, not to walk. They are called 'legs' because of homology, not function. So if your question is 'why do insects have six things that they walk on?' then the answer is that often, they don't. In that case, there is no apparent advantage to explain. If your question is 'why six "legs"?', then the answer is 'by definition, from common descent'.

As it stands I agree with @fileunderwater -- this is a question about evolutionary advantages. However, if you were to make this question about the various functions that insects put their "legs" to then it is no longer a "duplicate" of that question. Even if this question is closed as a duplicate, you can edit it and it can be reopened :)

The question is actually very related to Why don't mammals have more than 4 limbs?

@bshane I disagree that this pre-supposes perfect adaptation. Rather I think we should focus on highly-preservedness. Very few members of Insecta have lost a set of legs. Why would such a body plan be highly preserved, when it has such obvious costs? It must offer broad-ranging adaptiveness. What would that be, exactly?

Short answer
Six legs allow for locomotion, while maintaining a supportive tripod at all times.
Background
There are several million species of insects, all on 6 legs. This implies that any change in this number is promptly selected against. It is generally agreed that insects were derived from many-legged ancestors, e.g. centipedes.
One explanation is the tripod gait that results from having six appendages. This hypothesis, formulated more than 6 decades ago (Lanham, 1951), reasons that a reduction of the number of legs during evolution did not go further than 6, because locomotion of a small animal encased in a rigid exoskeleton is not effective with less than 3 pairs of legs. Insects generally walk by lifting the two outer legs on one side and the middle on the other side, sweeping them forward and placing them down together. Hence, insects support their rigid structures with a tripod at all times. Tripods are among the most stable configurations, and they never wobble (why on earth do tables have 4 legs?). Figure 1 shows an illustration of insect locomotion (Lanham, 1951).

Fig. 1. Insects' locomotion resembles a double tripod. Insects have a cyclic gait which consists of two phases, the stance phase and the swing phase. The stance phase is the power stroke, it pushes the body forwards in the direction of travel while the leg remains on the ground. Three legs are used is this phase by forming a tripod with the front leg and the hind leg on one side of the body and the middle leg on the other side. This formation is why this gait is known as the tripod gait. Source: Insect robotics.
Larger animals can afford to have less legs, because their vestibular systems have more time to maintain balance and adjust gait during locomotion. Because insects are so small, their strides are so quick that the nervous system may not be fast enough to deal with gait control. Instead, insects rely on the tripod gait to prevent any imbalance, rather than adjusting it. In addition, the exoskeleton effectively restricts small bodily movements to control balance. Larger animals such as mammals make small adjustments in their gait constantly to maintain balance. An insect has less opportunities to do so, because of their rigid exoskeleton (Lanham, 1951).
Reference
- Lanham, Science (1951); 113(2946): 663

Great answer! I'm going to go saw a leg off of all of my tables now, that sweet sweet tripod stability!

This answer is interesting and informative but also has many problems. First, "This implies that any change in this number is promptly selected against..." is completely unreferenced and could just as well (probably?) be due to developmental constrains. Overall, developmental constrains is completely overlooked in both the question and the answer, and is me the main reason why this question should be closed as duplicate. [cnd...]

[...cnd] I can also think of several alternative explanations for why 6 legs is useful for insects, which are not mentioned in this answer. To me, this answer is an interesting hypothesis, but it currently reads as an evolutionary just-so story. "*[R]eduction of the number of legs during evolution did not go further than 6, because locomotion...'" is another really strong statement that is not supported at all.

@fileunderwater all the info is obtained from the Science paper, and the figure legend is from the linked robotics web page. There is nothing that I made up and nothing is unsupported. If anything is lacking from my answer, feel free to write a better one. No need to close a question, and especially not due to it being a duplicate of an abstract, general philosophical community question. If you don't like the answer, -1 will do, throw these questions open to allow others to share their views!

So you are saying that the two quotes I highlighted are supported by the Science paper (ignoring for a moment that the paper is from 1951, when quite a lot has happened in evolutionary biology since that time)? Is so, that should be made more clear (direct quote?). And about the reference - is this what you are referring to? If so, it is a book published in 1950 from Cambridge Univ. Press, and not a science paper (it might have been reviewed in Science though).

@fileunderwater - Thanks for the downvote, but I asked for it didn't I :) Somehow I linked the wrong page to the reference - nice catch. I inserted the correct one (Science paper) and placed some direct references in-text. It's not open source, got it through uni library. Thanks. I'm not an evolutionary biologist, just very interested in it. Downvote away, shoot at interesting questions, close the best ones, whatever - I'll stand my ground 8)

And about writing a "better answer": 1) the problem here is that the Q is speculative and extremely broad, which is why it should be closed. It is nearly impossible to write a short consise answer that actually tries to "answer" the question. This is exactly why short, punchy, plausible-sounding, just-so stories (that are not clearly presented as a hypothesis) are problematic. They can be extremely misleading, and might be taken as "truth". 2) I have other things to do, but that doesn't make this answer "better".

Let us continue this discussion in chat.

This article says that cockroaches use the tripod movement at low velocities (upto 1m/s)  but adopt bipedal/quadripedal movement at higher velocities.

@WYSIWYG - There are probably many examples of adaptations in appendage use. Familiar examples being the praying mantis that uses the front two appendages for hunting purposes and the dung beetle walking on fours while rolling a ball with the front two. I have never suggested my answer is all-inclusive, nor that it is the answer to the question. It is an answer. No more, no less.

@AliceD I didn't deny. Was just adding a point :)

Apparently, there is an advantage to having 6 legs in the insect world. What is that advantage, if anything? Why would such an advantage exist for insects, but not for other, larger land animals?

"Legs" is a tricky term, with insects. Colloquially, in the terrestrial world, they are things that an organism walks on. But the scientific definition of 'legs', for insects, relies on homology: many insects have six 'legs' because they all descend from a common ancestor, which had six legs. The anatomical structures derived from those legs, regardless of whether they are functionally used as paddles, or as claws, or as feeding appendages or elaborate mate-signalling devices, all get called 'legs'. Referring to all of these as 'legs' makes as much sense, from a functional perspective, as referring to our arms as 'legs'. We only do it to keep the homology clear when talking about evolutionary relationships between species.
The diversity of uses to which insects put their legs makes it clear that there is no single universal advantage of having six - it is just that completely losing (or gaining) appendages is a difficult evolutionary process, so it seldom happens over evolutionary time. Regardless, some groups of insects (members of the Coccidae and Diaspididae, for instance) have lost their legs completely - an apparent adaptation to their obligate parasitic lifestyle.

What do those middle legs do that the front and hind legs cannot, if anything? Are they really essential, or do they just generate more muscle power? If it's an advantage either way, why don't bigger life forms like mammals have 6 limbs?

In the insect groups which use six legs for locomotion, AliceD's answer provides an excellent description of how all six legs are used. However, there really is nothing special which can be achieved with six legs, which could not be achieved with some other number of legs: mantises handle their locomotion perfectly fine on just four of their six legs, and arachnids (not insects, I know - but with many of the same design challenges such as a rigid exoskeleton) manage equally fine on eight.


text:
What is a partial regulator?

Source: MY textbook-NCERT 12th Biology-Ch: Organisms and Population
(Pg 7 of pdf/Pg 223 of the book)
Is this graph for Partial regulators correct? Isn't it that animals tend to be regulators first and then when they can't maintain homeostasis anymore, they tend to conform aka adapt themselves to the surrounding for better survival?
So shouldn't the graph for Partial Regulators first be a straight-line parallel to the axis (signifying constant internal environment aka Homeostasis) upto certain External surroundings level and then be the inclined straight line when it behaves as conformer ?
I would like to know where I am wrong in my logic or Is it that The graph is wrong in my book ?

Why initial should be regulation? Upto a certain level? When the text says: Some species have evolved
the ability to regulate, but only over a limited range of environmental
conditions, beyond which they simply conform. Could it not be like confirming at both sides of limited range, ie conforming at low and high conditions.

I haven't really encountered this term before and it seems there are not many original sources of this term; I cannot find any scientific article that uses this term. So this term is apparently not a standard one. Also, as pointed out by @JM97, most organism can achieve homeostasis only in a limited range and it doesn't have to be limited at one specific end of the spectrum.

I think, the graph you indicated, might saying the following matter:
Let's take an example. " Some snails and fish  go into aestivation  to avoid summer-related problems-heat and dessication."  Now, when summer comes after the season Spring, the temperature gradually rises. The fishes can generally  withstand upto a threshold limit of temperature, and conforms upto this threshold limit. When their   comfortable weather breaks due to rising temperature, then they enter Aestivation and the graph now starts paralleling the X-axis.
Look, the graph doesn't parallel to the " Conformers' line" from the origin, but deviates with a little angle from that line : that implies the organism was trying to regulate against the external environment at first.
Undoubtedly, it's my own opinion, may carry some shortcomings generally.

Welcome to Biology.SE! Answers on this site are expected to be based on facts (not opinion or speculation) and consequently are much more likely to receive a favorable response if they include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion, and therefore is inappropriate for this site. ——— Please take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site and then [edit] or delete your answer accordingly. Thanks!

well your point of view is really different and original, though I am a little skeptical about it, it really relates to the paraphrase written in the same book on the next page relating to Partial regulator

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text:
How did the tendency to perform death rituals evolve?
Both elephants and humans perform rituals when deaths occur.
However, I do not see any evolutionary benefit of this. The rituals take time, which apparently could be better spent hunting, foraging, traveling, mating, or grazing.
I am interested to know if these behaviours have any significance and whether they confer any kind of survival advantage.
A cursory google revealed nothing about this.

Good read: http://www.bbc.com/future/story/20120919-respect-the-dead

I'm voting to close this question as off-topic because it is more the realm of anthropology. No, there is no Anthropology.SE and yes there is "evolution" in the question, but those two statements are not a reason to believe that all anthropologists are hiding at Biology.SE and that every question about evolution is on-topic here.

@AliceD It's not just about anthropology, because elephants have death rituals as well. Would it be best if I only ask how elephant death rituals originated?

@Kyth'Py1k I would suggest that you modify your question such that it is about animal behaviour. Please try adding details and if possible some more examples/references to support the point.

@WYSIWYG In what way is it not about animal behavior? The question is about death rituals, which is an animal behavior. Also, what point are you talking about? I am not trying to make a point in the question; I'm just asking a question.

@Kyth'Py1k I meant that you add more emphasis on the animal behaviour part and defocus from the human aspect so that it is not interpreted as a question about anthropology. Gosh! I am trying to help you here; this question can be edited a little bit so that it can be on-topic. Why are you getting defensive?

@WYSIWYG My apologies; I did not intend to come across as defensive. I was just trying to better understand what was wrong with the question so I could improve it. What exactly made me seem like I was being defensive. Anyways, do you think asking only about elephant death rituals would be a good idea?

This question is not different enough from the original question. If anything the original question is more on topic because it builds a strong case of showing that habitual social ceremony exists without anthropomorphism, whereas in this question it appears that you're trying to ask why it would benefit elephants to have human-like death rituals.


text:
Why don't mitochondria have plasmids?
According to the endosymbiotic theory, mitochondria are descended from specialised bacteria (probably purple nonsulfur bacteria) that somehow survived endocytosis by another species of prokaryote or some other cell type, and became incorporated into the cytoplasm [ref].
And plasmids naturally exist in bacterial cells, and they also occur in some eukaryotes [ref].
I was however taught that mitochondria have no plasmid and only have circular DNA. If the endosymbiotic theory is true, then how come mitochondria have no plasmid?

The mitochondrial genome is highly reduced; many mitochondrial genes have been transferred to the nuclear genome (see endosymbiotic gene transfer) and therefore the mitochondria are fully dependent on the nucleus to function.
Bacteria need not necessarily have a plasmid. Usually, all the important genes are present in the chromosomal DNA. Since the mitochondria have lost most of their genes and retain only a few genes that are highly essential for their function, the likelihood of retention of any plasmid DNA is very low. However, there are some reports of plasmid-like DNA in mitochondria (mostly in plants).

Handa (2008): in Brassica
Robison et al., (2005): in carrots
Collins et al., (1981): in Neurospora (a fungus)

Likewise, chloroplasts also harbour plasmid-like DNA (google-scholar hits).


text:
How did Portuguese man-of-war evolve?
In particular, how did the close cooperation of its many component species evolve?
My hypothesis is that it began with a few, probably no more than two zooids cooperating in symbiosis, and overtime, either entirely new species of zooid adapted to first parasitize and then cooperate with the existing company, or that some of the existing zooids mutated to acquire different functions. As the new zooids join the cooperation, the other re-adapt to form the "species" we see today.
Is that a somewhat accurate description of the evolutionary history of this colonial organism?
Addendum:
Would the relative simplicity of the polyps forming the colony be a crucial prerequisite in their cooperation and specialization?

Isn't it the case that various types of zooid are actually all the same species?

Googling 'Origin of Polymorphism in Cnidaria/ Siphonophora' should help you.

@AlanBoyd If so, are polymorphic individuals differentiated by epigenetic mechanisms? Also, would the difference between individuals of various functions be "discretely" differentiated (like the difference between queen ant and worker ant) or "continuously" differentiated (like the difference between leaf-cutter ants of various sizes)?


text:
Can two arms-racing species be stabilized?
I am trying to build an evolution simulator in which there is group A and group B, each group has 9 members each generation. Each generation, each member of group A will enter a competition (in the form of combat) with a random member of group B, and fitness will be calculated based on how quickly and with how little losses will one member's army destroy the other. The best few members of each group then becomes the parents of the next generation.
(Note that an "individual" of each group is in fact a genetically determine neural network that controls a swarm of robots, think of it as a swarm of ants sharing the same DNA and thus can be effective consider one individual)
Will this end up with both group A and B having phenotype/strategy that do not change very much over many generations, or will it result in strategies that gradually changes throughout generation, with each successful, significant change out-smarting the opponent's old strategy until the opponent develop a counter strategy?

"Each generation, each member of group A will enter a competition (in the form of combat) with a random member of group B, and fitness will be calculated based on how quickly and with how little losses will one member's army destroy the other."  It is not clear what you mean here.  You mentioned 9 individuals per group; then what comprises each individual's army?

Question updated, to explain in short, an army is made of a swarm of identical robots controlled by said individual.

Consider adjusting your scenario: you are locking time-to-reproduce and you are only considering violence as a winning strategy. Small furry mammals are the best fit for their environments generally by being precocious breeders with massive litters. If you add these two axes, you may avoid the arms race. Consider also that eventually you will have more than two groups, but this will complicate the processing.

To rephrase Cort Ammon. It depends on how you setup the system.
Imagine each combat strategy as a point on a landscape. Good strategies are on higher ground, poorer strategies are on lower ground.
A and B each have their own combat strategy and thus start at different points on this landscape. Mutations allow a species (say A) to explore the strategies around its starting point. Selection will cause the curtail that exploration.
If A find itself on a slop of a hill, selection (ie your combat and mating system) will cause the A population to drift upwards on this slop. However if A find itself on the peak of a small hill, it has no where else to go.
So how the scenario will play out will depend on the initial start conditions of population A and B. The mutation rate/genetic variability of the population (ie how many strategies population can explore around its initial strategy).
Additional factors is the genetic system that you have. If individuals of your species can only have one strategy (haploid), the species will be bound to its local hill. However if an individual can have more than one combat strategy at a time, (ie a diploid or gene duplication in RL), then the individual can have a combat strategy that work (local peak) and have a second strategy that is free to evolve... free to explore the landscape... going down valleys of bad strategies... and may eventually find the foot of a mountain... which a peak fitness higher than even the local peak it started.

Unfortunately, the answer to this varies greatly based on your individual implementations of the simulation.
Let's assume As are dominant at a given iteration.  We can enumerate the genomes of B which can defeat A.  With that, we can see how "close" B is to one of those genomes.  If B is far enough from those "winning" genomes, it can be difficult for B to eventually overcome A.
Note I say difficult, rather than impossible.  Eventually due to random chance B will eventually find the counter to what A is doing if we assume B gets to do this in a vacuum.
Remember that, while your individuals are "competing," its actually the populations that evolve.  If your rules permit enough introspection of how B's operating, A may groom B into weakness.  A may intentionally let a few of B's least fit individuals win a fight, for the expressed purpose of abusing your rules for the next-generation to make sure B remains unfit.  Any B's which start looking interesting will get obliterated as fast as possible.
We actually do this with pest control.  One known method of pest control is to leave one small corner of a field unprotected and spray the rest.  Any insects which develop a resistance are likely to mate with the many insects that grew up on the sprayed corner, increasing the likelihood of those resistant genes getting diluted or even lost.  This increases how long a farmer can use a given pesticide before having to increase its usage or switch to a new pesticide.
On the other hand, there are games where arms-racing species never stabilize.  If you build a system based on the Chinese 5 Elements, the system is designed to encourage two entities to spin eternally on the cycle, never fully stabilizing unless you reach an overacting state (which is considered highly undesirable for both parties).
So it really depends what your particular rules do.  Your rules could permit stability, or they could not.


text:
How much do urban pigeons move around cities?
Do they tend to live their lives in one area of the city or do they move around? For example, do pigeons born on London's Trafalgar Square live their whole lives centered around Trafalgar Square or can they move and become Marble Arch based pigeons?
What is the typical range of a city pigeon? Have Trafalgar Square pigeons ever made the trip to Buckingham palace just down the road from them, or do they hang out in the square all the time?
How different are these behaviors from their wild behaviors and how effected by humans actions in the city are they? For example, do pigeons learn that a particular city square will become busy with tourists in the summer and travel there at these times of the year seeking food?

Good question! You might want to restrict it to one species only though (such as pigeon for exmaple). There are interesting studies about crows for example and how they learned to predict consequences of human behaviours.

This will differ widely between different species, so you need to specify exactly what species you are asking for (e.g. pigeons).

Thanks for the feedback! I'll change the question to be just about pigeons.

I'm only aware of two studies that have looked at Rock Pigeon home range size. Note that this isolated research and may not be representative of Rock Pigeons everywhere nor of other pigeon species.
Rose and Nagel (2006) tracked 80 feral pigeons using GPS receivers and found 32% remained within 0.3 km of their roost location. Only 7.5% traveled over 2km from their roost location. Individuals of this species typically have 1-2 primary feeding locations within their home range which ranged from 3 - 151 ha in size (Rose et al. 2006).
Rose, E., D. Haag-Wackernagel, and P. Nagel. 2006. Practical use of GPS-localization of Feral Pigeons Columba livia in the urban environment. Ibis 148(2):231-239.
Rose, E. and P. Nagel. 2006. Spatio-temporal use of the urban habitat by Feral Pigeons (Columba livia) Behavioral Ecology and Sociobiology 60(2):242-254.


text:
I saw these patterns on a hill. Which insect makes such a pattern?

Description of the location

It is in India
The place is 300-400 m above sea level.
There is no water body nearby.

Which insect makes these patterns?

Welcome to Biology.SE. Can you please add the broader scale location (continent, country/region)?

@Remi.b Continent:Asia,Country:India

Specifically where in India? And which hill?

It could be an antlion. Antlions are a group of about 2000 species that can be found all around the world (including India). Antlions mainly live in the kind of dry areas you describe and that we see in your picture. I don't think one could be more accurate and tell the genus without a picture of the individual but I might be wrong.
Here is an adult antlion:

and here is a larva antlion

The small pits you see are made by larvae. The larvae make these small trap pits to capture ants (and some other small insects). The larvae is buried in the soil at the center of the pit and simply waits for prey to fall into the pit. Below is a picture of such a pit:

Parents had similar sand pits in their garden. It always occurred in groups, always in dry sand areas. It was similar to the one you have posted but different from the OP's images - at the center of the pit there's no "hole" or "well" that exist on every single hole in OP's pictures. At one time when I noticed that holes in the garden, I first thought about antlions, too, but after carefully digging a few pits out I have not found any residents. Maybe in our garden the insects have aleady moved out and the "well" has collapsed.. I don't know. Just an observation. I still think it's antlion.

Wow.  I had no idea that adult antlions turn into dragonflies!

It's not a dragonfly. Dragonflies can't fold their wings, while an antlion can fold its wings in a manner similar to a damselfly or a caddisfly.

authors: Bob Jarvis - Слава Україні


text:
Can a small polypeptide fold over itself and have a tertiary structure?
What I want to know is if polypeptides (those which are not considered as proteins) can also "exhibit" a tertiary structure.

Welcome to BiologySE! I don't think I'm following your question... can you be more specific? Polypeptides are proteins... what polypeptides "are not considered as proteins"?

@VanceLAlbaugh I think my problem comes from that direction. I understand that proteins are a specific case of polypeptides. Is this wrong?

a chain of amino acids connected through peptide bonds is a polypeptide - that chain is primary structure of a protein... there are some semantic differences... there is a nice overview of the basics of protein structure on wikipedia - basically what is covered in a basic biochemistry text...https://en.wikipedia.org/wiki/Protein_structure#Tertiary_structure

Your instinct is valid, there are other molecules which can be defined as having tertiary structure.
The most common example is RNA, which can fold into a vast array of conformations. These can be part of ribonucleoprotein complexes like telomerases, spliceosomes, or ribosomes or they can function on their own like tRNAs and many ribozymes such as RNase P. An example of a common tertiary structural motif in RNA is the pseudoknot; a haripin loop in which some of the bases in the loop have base paired to another portion of the RNA molecule.

It is also possible for DNA to possess tertiary structure, though the term is used less often when referring to DNA. Usually DNA tertiary structure describes topological structures formed by supercoiling, protein scaffolding, etc. However, DNA can also form cruciform motifs similar to RNA hairpin loops (though it is less common). If multiple cruciform motifs and other structures were to interact in three dimensions, this could be another form of DNA tertiary structure.

You may also be interested in DNA origami, in which 3D building blocks made from DNA are assembled in desired ways by using sequence complementarity (generally).
I think that polysaccharides and oligosaccharides are also sometimes referred to as having tertiary structures, but I don't know as much about those. I encourage you to look into pectin, amylopectin, branched oligosaccharides, etc in the context of tertiary structures.

All this information is very useful. Thank you.


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Relationship between DNA strands and mRNA
Does the sense strand or antisense strand of DNA code for the polypeptide product? I'm confused because I know the antisense strand is the template for mRNA but it has anti codons so I do not know how this would be the coding strand. Ok so what I was confused about is when you are getting the code for the amino acid you can look at the mRNA strand which is the same as the sense strand except uracil replaces thymine, this is why I thought the sense strand could have coded for the amio acid instead of the anti sense strand.(the question I was looking asked if its the antisense or sense strand)

I've tried to clean up your question and its title but, as you say, you are confused, and so is your question. I'll try to answer it.

Antisense/non-coding DNA strand as a template for RNA polymerase => mRNA (being identical to the sense/coding DNA except for T -> U). If the sense/coding DNA strand were the template for RNA polymerase you would get mRNA that is identical to the antisense/non-coding DNA (again, except for T -> U). You would not want that ...

How about: "If the sense/coding DNA strand were the template for RNA polymerase you would get mRNA..." that might be "restriction"-RNA that is able to block corresponding "positive" RNA, as "negative" RNA does exist in human. Actually, positive/negative for sense/anti-sense or coding/template only seem "good terms" if you are into viruses.

I would add this as a comment to your question but do not have enough reputation. A simple look at Wikipedia (which is a very good source for general questions like these) would have provided you with an answer. I just did this to see how long it would take if I did not know the answer. It was about 20-30 seconds.
Protein synthesis: Transcription

In transcription an mRNA chain is generated, with one strand of the DNA double helix in the genome as a template. This strand is called the template strand.

Template strand

Only one of the two DNA strands serve as a template for transcription. The antisense strand of DNA is read by RNA polymerase from the 3' end to the 5' end during transcription (3' → 5').

If I understand your confusion correctly, you also do not understand how the seemingly "non-coding" strand can be the "coding" one which seems to be a paradox. If this describes your confusion adequately you have to think of the semi-conservative replication of DNA. The "non-coding"/antisense strand is transcribed by the RNA polymerase into its complementary RNA sequence. As this sequence is complementary to the "non-coding" DNA strand, the mRNA sequence is identical (with U replacing T) to the "coding"/sense DNA strand.

I don't think your Wiikipedia links are the most useful ones for two reasons. First, the questioner asks about the terms 'sense' and 'antisense', for which there is a specific Wiikipedia page, whereas the ones you reference refer to something called the 'template' strand, which is not the term in the question. Second the diagram of transcription on those pages is quite dreadful: over-complicated with unnecessary and confusing three-dimensionality (which of course bears no relation to reality). Simple diagrams are both more honest and intelligible.

I do not agree. @Maria already said that in her (and that is also the way I see it) view antisense and template are corresponding. I am not a big fan of the sense vs. antisense DNA strand concept and find coding vs. non-coding way more intuitive (good that you mentioned that, though). However, she uses the term 'template' in the question, so I find it more natural to use that term to help her with her confusion (the way I understood it). To your second point: I think she grasped the process of transcription - therefore I did not really care for the diagrams. Point taken, though.

— The poster has modified her question now and I have modified my answer. However I would say that I think ‘template’ is a particularly dangerous term to use in this context. In brief this is because 1. the fact that linguistically templates produce a copy, whereas at best one is producing a reverse complement; 2. DNA strands are actually templates for their complementary strands, rather than mRNA or protein. I will add a longer argument about this to my answer when I have a little time.

Referring to your argument of the bacterial genome I would say that template is the best term to use as both sense/antisense and coding/non-roding, as you say in your answer, are relative terms. The template can be both of those strands depending on the gene. You are right, however, that one needs to make clear that the copy is a reverse complement and not identical. To your second point: I would say that DNA strands are templates for both DNA and RNA. Looking forward to your argument.

"DNA strands are templates for ... DNA" only when DNA is copied to DNA for cell division (DNA polymerase)? - If you rated down the difference between DNA and RNA which  is some "OH"  only you might think of m-RNA and its  coding DNA as "copies", whereas the difference between the two DNA strands in their complementarity would look outrageous.

You ask initially about the “sense” and “antisense” strands of DNA. These terms are explained in the Wikipedia reference entitled ‘Sense strand’. This states what you appear to be already aware of, that:

“The sense strand is the strand of DNA that has the same sequence as the mRNA, which takes the antisense strand as its template during transcription…”

Transcription produces a reverse complement of the DNA strand transcribed, just as the antisense strand of DNA is a reverse complement of the sense strand of the DNA. Thus:
5' ...ATGTTT...TAA... 3' : DNA sense strand

3' ...TACAAA...ATT... 5' : DNA anti-sense strand (template for transcription)

5' ...AUGUUU...UAA... 3' : mRNA (translated)

N     MetPhe...End    C : Protein

Qualifying the use of ‘Sense strand’
There is a danger in using ‘sense strand’ of thinking or implying that it refers to the whole of the DNA — after all, the description of a circular bacterial DNA is that it has two strands. However the genes in a bacterial DNA do not have the same directionality, so one can (and should) only talk about the sense strand of the DNA specifying a particular gene.
Disfavoured alternatives to ‘Sense strand’ 1: Coding strand
In your original question you switched from talking about the sense and antisense strands to talking about coding and non-coding DNA strands, although you later removed this. I would argue against this usage. It is the mRNA that does the coding and is actually translated into protein. The DNA can only be regarded as sense or not in terms of conceptual translation. In practice it either serves as the template for transcription or its complement does. There is also the problem that if you call the opposite strand ‘non-coding’, there is a possible confusion with the use of that term for the untranslated regions of the (coding) mRNA.
Disfavoured alternatives to ‘Sense strand’ 2: Template strand
I dislike the use of ‘Template strand’ because the original and primary use of ‘template’ in relation to DNA is replication (not information content). Further, when used in relation to protein-codoning potential it is not immediately apparent to me (and, I would argue to anyone approaching the topic for the first time) which strand of DNA would be regarded as ‘template’.
In English the term template generally means a pattern, mould or former used as a guide to create objects of a similar shape. Its adoption to the molecular biology of nucleic acids involved a subtle change of meaning, as the article produced from the DNA template (the product strand — DNA initially) was not the same shape as the mould, but a complement to it. However, the complementarity rules of the bases meant that the information in the original was preserved (in a manner somewhat analagous to that of a printing plate), and the metaphor caught on as it conveyed a clear meaning. It should be emphasized that this meaning was in relation to DNA replication and transcription. Thus, generations of biochemistry students read in texts like Berg et al. that:

DNA Polymerases Require a Template and a Primer

(whereas RNA polymerase only required a template). Furthermore they could read (e.g. in Wikipedia) that:

DNA is made up of a double helix of two strands, and each strand of
  the original DNA molecule serves as a template for the production of
  the complementary strand…

So if you start talking about the template strand of DNA you are in trouble already.
But what would that mean in relation to transcription of mRNA? Here it is the anti-sense strand of the DNA specifying the gene that is physically serving as template for the mRNA. However to many it would seem counter-intuitive to call this the template strand, so that those who use the term cannot in fact agree how to do so. To quote S. Malloy:

“…one school argues that the strand copied into mRNA should be
  considered the template strand, but the other school argues that the
  opposite strand which reflects the sequence in the mRNA should be
  considered the template because the corresponding codons are copied
  into protein.”

It clearly makes more sense to use ‘sense’ and ‘anti-sense’.

I've updated my answer in the light of the updated question.

I've now completed my arguments on terminology. A bit OTT, but you don't have to read them to read my answer.

To favour "sense" seems to correspond to Crick's dogma seen as a concept of "genetic code". By code is meant the triplets, thus the protein that may be "sense of life", the end, what  information flows to. Linguistically "coding" has got less connotation to the activity, to what templates do.

Maybe some valid (related) question: Refering to "one can (...) only talk about the sense strand of the DNA specifying a particular gene", does "Okasaki" show that Polymerase always reads from '3 to '5, hence "sense" is '5 to '3, thus talkin of a particular gene  defines the direction: of that particular codon sequence. There is only gene, chromosome is none. And, "gene" has direction 5-3! The term Sense might connotate "direction", codon might connotate the protein. And: promoter/primer rules?!


text:
Why does it hurt the next day after doing significant exercise?
I think this is a fairly common observation that if one does some significant amount of exercise, he/she may feel alright for the rest of the day, but it  generally hurts bad the next day. Why is this the case?
I would expect that if the muscles have undergone significant strain (say I started pushups/plank today), then it should cause pain while doing the strenuous activity, or during rest of the day, but it happens often that we don't feel the pain while doing the activity or even on that day, but surely and sorely feel it the next day.
Another example - say after a long time, you played a long game of basketball/baseball/cricket. You generally don't feel any pain during the game/that day, but there is a good chance it will hurt bad the next day.
I am trying to understand both - why does the pain not happen on that day, and why it does, the next day (or the day after that).

I like your question. I've experienced, though, that sometimes this pain is the second day after, instead of next day. Might depend on the nature of the exercise.

@DonBranson interesting point. I have added that in my question now

It should be noted that one warning sign of actual muscle damage, regardless of the mechanism, is "myoglobinuria", the presence of a rust-colored sediment in the urine.  If you experience this (other than perhaps on rare occasions when you know you've "overdone" it) then you should have a neurologist (yep, a neurologist) investigate.

@HotLicks, interesting. Why neurologist?

@user1993 - Neurologists are trained in muscle disorders.

It should be noted that in some people (somewhere between 1% and 3% of the population, depending on who's counting) there is another mechanism for delayed muscle pain.  Myoadenylate Deaminase Deficiency (MADD) is a genetic condition whose primary symptom is pain and cramping with an onset about 36 hours after moderately intense exercise.  The pain often persists (due to muscle damage), resulting in a "pulled muscle" sensation which lasts for weeks or months.
The condition is caused by a genetic defect which causes the AMP<=>ATP recycling mechanism in the muscles to "leak" AMP into the bloodstream, weakening the muscles' ability to continue exercise.
Significant relief of symptoms is often achieved by taking D-ribose orally.
And another somewhat rarer genetic disorder which can result in muscle pain is McArdle's Disease.


text:
In microarray normalization, why is the normalization factor this?
I am working on analysis of a huge number of microarray files. I was trying to understand the need for normalization in microarray data and was going through this paper by John Quackenbush(2002). In the paper, the author mentions that

There are a number of reasons why data must be normalized, including
  unequal quantities of starting RNA, differences in labeling or
  detection efficiencies between the fluorescent dyes used, and
  systematic biases in the measured  expression levels

Then he talks about a simple normalization techniques. Assuming that  the total hybridization intensities summed over all elements in the arrays should be the same for each sample, he defines a normalization factor is calculated by
summing the measured intensities in both channels-

where Gi and Ri are the measured intensities for the 'i'th array element (for example, the green and red (or experimental and control) intensities in a two-color microarray assay) and Narray is the total number of elements represented in the microarray.
Then the author says this -

This is the part I don't understand. What is the need to introduce $G_k^{'}$, $R_k^{'}$ and why are they what they are? Most importantly, why is $T_i$ equal to $R_i/G_i$ first and then ($1/N_{total}$)*($R_i/G_i$)?
Any ideas?

$G_k^{'}$ and $R_k^{'}$ are normalized values of $G_k$ and $R_k$.
Take say G as $[1,2,3,4]$ and R as $[100,150,200,400]$ as your values and you want to normalize them. This is scaling one of them onto the other and bringing them on an equal level to compare. So in your case the factor is $85$ units. So a unit of R amounts to $85$ units in G.
So to scale G to R, multiply G by $85$ or you can scale R to the level of G by dividing R by $85$. So the values are either $[85,170,..]$ and $[100,150,200,400]$ or $[1,2,3,4]$ and $[1.17,1.76,..]$ from our example.
I think it should be mentioned as $T^{'} = R_i/(G_i*N_{total})$ as in log ratio from the statement in your question.

does your final line mean that in the text, it should be $T_i$ = $R_i^{'}$/$G_i^{'}$ = $R_i$/$G_i$*$N_{total}$

I mean $T_i = R_i/G_i$ but $T^{'}i = R_i/(G_i*N{total})$


text:
Does posture matter while drinking water?
I have heard a lot of people (where I am from, India) say that one must drink water sitting, not standing. Recently, I also came across a video that said the same thing (link). The reason given is that when you drink water standing, it goes to the colon too quickly, whereas while sitting, the water is better absorbed by the organs. Is this true? Is there a biological basis for why I should drink water sitting?
I tried to find literature on this matter, but apparently there isn't a whole lot. I found this paper where they tried to see the water passage rate in the GI tract of rabbits, mentioning how the water goes from stomach to cecum to proximal large colon, but obviously did not study posture.
Note: I think this question belongs here better than Skeptics.SE as I am looking for a biological explanation

Nothing you drink goes straight to the colon; the small intestine - between the stomach and the colon - is 20 feet of twisted tubing. So this is a colorful myth. If you do a bit of helpful research and add it (no videos please; I don't want to spend that amount of time), I'll be happy to answer what happens to fluids when drunk in any position, even upside down.

@user1993 it would be cardiac sphincter of oesophagus which is affected by drinking water while standing not colon. As it in not a true Valve the force of impact of water which goes straight down the oesophagus while drinking water fast and standing would damage it's activity upto some extent so that regurgitation may happen.

I'd imagine that literally billions of people have drunk water (or other beverages) while standing, but I've yet to hear of any adverse health effects from the practice.  While I'm no anatomist, I'd think anything you drink or eat, sitting, standing, or laying down, would spend some significant time in the stomach before entering even the small intestine.  Indeed, practical experience suggests that the greater part of any liquid consumed gets absorbed into the bloodstream before reaching the colon, and eventually excreted via kidney & bladder.

@user30561 - That's pretty much a less colorful myth.

@anongoodnurse, i tried to research a bit, you can have a look

Related question:http://skeptics.stackexchange.com/questions/27338/is-drinking-while-standing-unhealthy

@Mesentery, great find! but sadly the study mentioned there did not compare sitting and standing :(

The stomach is equipped with the pyloric valve to regulate transpyloric flow to the duodenum.
Both cold and warm drinks stimulate a pattern of motility associated with retardation of transpyloric flow.

The pyloric valve is responsible for acidifying water that you drink, and if the body's guard against amoeba's and dysentery depended on body position, it would be low survival performance, given that sedentary posture is associated with poorer health outcomes, including an increased risk of type 2 diabetes. You will benefit from minimizing time spent sitting each day, and from breaking up periods of time spent being sedentary, as often as possible. It's aperture at rest is 3mm, so it's of minimal difficulty for the stomach to hold water as required for optimal health. It's highly likely that water is kept for enough time to expose it to stomach acids, regardless of body position, and then it's transmitted.
Water doesn't flow straight through the stomach like a straight tube when it's empty.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1382811/pdf/gut00528-0043.pdf

First off: pure, reverse osmosis treated, bottled water HAS NO NUTRIENTS. Secondly, of everything you swallow, nothing goes too fast on it's way to the colon. The small intestine is a network of twisted tubing, around 20 feet long. Nothing is going through there "Too fast".
Sources: https://carta.anthropogeny.org/moca/topics/smalllarge-intestine-length-ratio

could you comment on the difference when a person is sitting vs standing while drinking water?

There is no observable difference. It does not matter whether the drinker is standing or sitting, the small intestine is the same length, and is still folded accordingly.


text:
What is the difference between GFP and rhodopsin?
GFP and Rhodopsin are both fluorescent proteins. What is the main difference between GFP and Rhodopsin in terms of how they work? I know that their excitation and emission wavelengths are different, but in terms of the biological mechanism, how are they different?

Rhodopsins are photo-signal receptors. GFP does not function as a receptor.

@RoniSaiba so do you mean to say that rhodopsins carry out a subsequent biological function upon being exposed to light, whereas GFP does not have this subsequent function?


text:
"Genotype structure"?
What does a geneticist mean when they write "genotype structure", e.g. the sentence "...represents continuous allele frequencies for both tumor and normal samples, while leveraging the expected genotype structure of the normal."
Citation: http://bioinformatics.oxfordjournals.org/content/28/14/1811.long

Please [edit] your post and add a citation to where you read this. Context is very important.

Sorry about that @MattDMo

The line can be found in the Results subsection of the Abstract in the second sentence @MattDMo


text:
Why are sperm cells not attacked by the female immune system?
Whenever a foreign particle enters into someone's body, it is attacked by the white blood cells. I just want how it is that, when sperms enter the female body, they are not attacked by the the woman's immune system?

Studies show semen does mount a considerable immune response in the female mucosa, however:

Seminal plasma redirects the differentiation of human dendritic cells (DCs) toward a regulatory profile. By promoting a tolerogenic profile in DCs, seminal plasma might favor fertility, but might also compromise the capacity of the receptive partner to mount an effective immune response against sexually transmitted pathogens.

Semen promotes the differentiation of tolerogenic dendritic cells.


text:
Which spider is this? Is it dangerous?
So today while clearing the trash out of my room I found this orange spider on an abandoned piece of foam.

 It is carrying a weird ball with it wherever it goes. What is this? And to which genus does this spider belongs?
For a better contrast I placed it on  paper.

EDIT-1
Size: Roughly 1cm in length
Location: Uttar Pradesh, India. Coordinates- https://maps.app.goo.gl/svXoxaH4Z2lK2rFH2
Temperature: 34°C and Humid.
EDIT-2
Adding few more pics

It is clearly a Theridiid (cobweb) spider, but it doesn't look like the Parasteatoda tepidariorum I'm familiar with here in the US.  The egg sac it's holding indicates it's a mature female, and the regular pattern on the abdomen is both distinctive and unlike the variable, blotchy pattern of tepidariorum.  Unfortunately, not being familiar with Eurasian spiders likely to be found in your area, I can't be of much help as to what it might be, beyond limiting it to the Theridiids.
Oh, yes - it's pretty clearly not one of the Widows (Latrodectus spp.), and since those are the only medically significant Theridiids we know, it's not dangerous.

https://en.wikipedia.org/wiki/Parasteatoda_tepidariorum
I have personally come across these little spiders at my place and they look very similar to the Parasteatoda tepidariorum.

Can you add an image, check whether its distribution includes India, add a little background why you think it is this species  etc? We discourage one-liners

@AliceD I am sorry as this was meant to be a comment but was not able to do so because of the reputation policies that encourage to write answers when you are new.


text:
Why does HIV chooses the Macrophage cells to infect first?
Upon entering our body HIV directs the macrophage cells to manufacture more virus particles. It injects the Viral RNA into the Macrophages. With the help of the enzyme reverse transcriptase the Viral RNA converts into viral DNA that embeds into the DNA of macrophage cells. In this process the macrophages remain alive.
Just Curious-
Since Macrophage cells have phagocytic activity, why does HIV chooses them to be their Virus producing factory and not some other cell like RBCs which are apparently much more abundant and have no phagocytic activity at all.
In other words what facilitates the macrophages to be HIV's manufacturing plant?

Your title and final question are not the same question.

I think they are just the two different ways in which this problem can be represented

Short answer
HIV infects macrophages because macrophages display the CD4 cell surface receptor needed for initial HIV attachment, and also display the co-receptors CCR5 and/or CXCR4 that are also needed for virus entry into the cell.
Cells that aren't good hosts for HIV don't have these receptors.
Addressing some confusion
You ask why HIV chooses macrophages as a virus producing factory. Be careful that you don't excessively anthropomorphise viruses - viruses 'choose' which host cell to infect in the same way that you 'choose' to feel pain when you stub your toe. It is a product of evolution, and not the result of a logical thought process by the HIV virus.
Other viruses happen to infect epithelial cells, or liver cells, or plant cells. HIV infects CD4+ cells. There is no 'best' option that viruses will somehow 'choose'. Anything that allows for successful reproduction and transmission is a viable option, and the rest is down to random mutations and evolution.
Red blood cells as virus factories?
Finally, you ask about red blood cells as a better host for viruses. In fact, red blood cells make very poor host cells for viruses, as they lack the cellular machinery required for DNA replication and protein production. It is this cellular machinery that is usually hijacked by viruses in order to replicate. Red blood cells lose their nucleus early in development, and it is only more complex organisms (such as the Plasmodium species that cause malaria) that can effectively hijack a red blood cell. These Plasmodium parasites have their own nucleus for protein production and DNA replication.

Thank you very much! I think I asked kind of a silly question


text:
What is the scientific name of this lovely orange black flying beetle?
Found on Rangoon creeper (Combretum indicum)

@GerardoFurtado Thanks captured with my phone in my terrace garden


text:
What triggers meiosis in gonadal cells?
What specific biochemical processes are involved in inducing meiosis rather than mitosis? Why are gonadal cells the only cells in the human body which do undergo meiosis?

What specific biochemical processes are involved in inducing meiosis rather than mitosis?

It's a difficult question because every step in the development of a germ cell is ultimately necessary for the final differentiation, which includes a meiotic division.  Meiosis requires a lot of specialized components to pair and segregate homologues, to induce and resolve recombination, etc.  What starts it all is still largely unknown.  There are plenty of mutants that halt the process, but these are required along the way, so damaging the pathway ultimately stops it from progressing.  At least one study has been able to initiate the program of meiosis in yeast:
Induction of meiosis in Saccharomyces cerevisiae depends on conversion of the transcriptional represssor Ume6 to a positive regulator by its regulated association with the transcriptional activator Ime1. I Rubin-Bejerano, S Mandel, K Robzyk, and Y Kassir
Basically, they turned on a transcription factor, which activated an entire suite of downstream genes necessary for meiosis.  In essence, they turned on the "meiosis pathway."  Bear in mind this is yeast, so does't have separate germ cells, but the concept is probably the same.

Why are gonadal cells the only cells in the human body which do undergo meiosis?

All other cells are diploid.  Only in germ cells does the organism induce reductional divisions (to make haploid gametes for ultimate fusion in the zygote of the next generation). Creation of haploid somatic cells would uncover recessive lethal mutations and cells would die.  In sperm and eggs, which do not express any genes until after fertilization and karyogamy, this is not a problem.

Ultimately, it seems that follicle-stimulating hormone (FSH), released from the pituitary gland, may be the direct signal for spermatocytes to enter meiosis [1]. It's worth noting, though, that these results come from in vitro studies, where spermatocytes were co-cultured with all cell types of seminiferous tubules in an artificial medium, which makes it a rather crude approximation of in vivo conditions: mimicking the complete spermatogenic cycle in vitro remains to be done [2].
It's a little bit more complicated with oocytes. They start meiosis during prenatal development, are arrested in diplotene stage of the first meiotic division, and then a surge of luteinizing hormone (LH), just before ovulation, makes them resume. But they are arrested again in the last phase, and only after conception do they finish meiosis. The pause occuring in prenatal development is thought to be induced by some kind of an "arrester" secreted by cells in the oocyte environment (specifically, mural granulosa cells) and sustained by high cAMP levels, that are produced in response to both intrinsic and extrinsic stimuli. [3]
Another matter, and quite interesting, is the issue of timing: meiosis starts in a distinct moment of a male mammal develompent, and then goes on continuously, but mammal oogenesis is a series of starts and stops. More on this can be found in [3] and [4].

[1] Tesarik, J., Guido, M., Mendoza, C. & Greco, E. Human spermatogenesis in vitro: respective effects of follicle-stimulating hormone and testosterone on meiosis, spermiogenesis, and Sertoli cell apoptosis. J. Clin. Endocrinol. Metab. 83, 4467–4473 (1998). PMID: 9851795. Free access.
[2] Sousa, M., Cremades, N., Alves, C., Silva, J. & Barros, A. Developmental potential of human spermatogenic cells co-cultured with Sertoli cells. Hum. Reprod. 17, 161–172 (2002). PMID: 11756382. Free access.
[3] Zhang, M. & Xia, G. Hormonal control of mammalian oocyte meiosis at diplotene stage. Cell. Mol. Life Sci. Epub ahead of print. (2011). PMID: 22045555.
[4] Albertini, D.F. & Carabatsos, M.J. Comparative aspects of meiotic cell cycle control in mammals. J. Mol. Med. 76, 795–799 (1998). PMID: 9846949.

Let's start by answering the second part of your question first. I can ask you a similar question like "Why do parietal cells secrete HCl?" or "Why are skeletal muscle cells multinucleated?". The reason why the cells in our body carry out different functions and undergo difference processes, despite having the same DNA, can be due to a multitude of factors. Here are some off the top of my head:

Differential gene expression
Alternative splicing
Regulation of gene expression at the mRNA level (silencing)
Chromosomal inactivation (as seen in XX females)
Cell-cell interactions
Environmental factors that influence all of the above

Now to answer what the specific mechanism in which gonadal cells undergo meiosis:
For one, histone modification (and therefore differential gene expression) has been implicated in the regulation of spermatogenesis. You can read about it in this paper:  Song N, Liu J, An S, Nishino T, Hishikawa Y, Koji T. 2011. Immunohistochemical Analysis of Histone H3 Modifications in Germ Cells during Mouse Spermatogenesis. Acta histochemica et cytochemica 44: 183–90.
At first glance, I didn't find anything on oogenesis; will update if I see anything.

This study really only shows that chromatin modifications are part of meiosis, not that they are causal.  For that matter, this study does't even show they're necessary, just that they happen.

@jp89: The link in your answer got broken, I've replaced it with reference via DOI, which should be more robust. Please, check that it is the same paper you originally referenced (since the link is broken I can't be sure).


text:
What could account for an apparent loss of mass at death?
An interesting tidbit floating around the internet these days is that Dr. Duncan MacDougall apparently weighed people shortly before and after death, and found an average of a 21 gram discrepancy, to which he attributed to be the soul departing. As we all know, this certainly can't be the right explanation.
Putting aside likely extreme bias and instrumental/experimental error, is there any bodily process at death that could potentially explain a small decrease in observed mass?

Snopes.com gives a discussion of possible issues with the original experiment.  Evaporation or bowel or body movements for instance.  I think the biggest complaint about the experiment is that it has not been reproducible and that the original experiment was flawed.  MacDougall only took six measurements and he threw two of them out in his original work.  The Wikipedia link you give cites a paper where sheep were found to gain weight at least for a time after death.  Dogs are found to have no weight change.
MacDougall and his contemporaries were inclined to interpret their results such that animals simply do not have souls, or have different sorts of souls.  But if you look at an average of all experiments cited, it could also be said that the average weight loss up on death averages to zero.  3/4 of an ounce of a human being (or a sheep) over the course of something like a death is not an easy measurement.  You can't give them a drink of water, you worry that they are breathing too much and losing water.  Its not an easy experiment, at least for human beings where you can't control the circumstances of death so well.
In any case this really needs to be measured better.  In 90 years it doesn't seem that there's been a real rush to do it.
I just stumbled across this blog post that talks about an effort to measure a change in blood flow to the brain when in intense mental activity popularized in the late 19th century.  The investigator Mosso claimed he measured a difference, but the result is disputed today.  It could not have been more than a few grams. In any case a description of how difficult this measurement can be.

Sheep souls are buoyant, I guess. This sort of thing is tricky to do, even today. I'd be amazed if his scale was even accurate to 21 grams over a 100 kilo human.

I would too - especially after I had kids and tried to weigh them at their checkups :)

Well, did anybody found a centre in a brain that could be called "soul"? If not, and the soul is considered to be some state of current consciousness (of mind), is that what the body loses?

its likely that no real weight is lost... sorry.  if they were able to show this beyond a doubt it would definitely be strong with the internet!

There will be a quantifiable change in mass in any living object dies and then more with decomposition. The loss of energy from the living organisms changes the kinetic mass of the original subject. When death occurs other the process of decomposition now begins converting the organic materials of the organism into inorganic material and energy which in turn changes the kinetic mass of the subject

It would be much appreciated if you could cite your sources for the various points in your answer.


text:
What kind of arthropod/animal is this?

Can anyone identify this strange creature? I live in a very urban part of Montreal, Canada. It wasn't moving (seemed dead) and although the image is huge, it wasn't as big as it seems (a couple of centimeters).

It's a type of centipede.
Based on the long legs, I would bet on something like that:
http://en.wikipedia.org/wiki/Scutigera_coleoptrata
Or at least a Scutigeromorpha http://en.wikipedia.org/wiki/Scutigeromorpha#Scutigeromorpha

I live in Japan and here they are called "gejigeji". As mentioned, they are a member of the centipede family and are as creepy as hell. I live in a newly-built house, so thankfully there are no cockroaches, but every now and again one of these little blighters will scurry across my floor in my peripheral vision and scare the bejesus out of me.
They are not dangerous (at least not to humans). I have been told they eat the larvae of other insects, like cockroaches so they are not so bad really. Also, and I assume this is just a Japanese myth, but it's said they hunt in pairs.

It is a common house centipede. Apparently they're everywhere but I've never seen one before.


text:
Is there an evolutionary reason for the 5 electron transport complexes in plants and animals?
The electron transport chains of both the light reactions of photosynthesis (in plants) and oxidative phosphorylation (in animals) both contain 5 complexes including ATP synthase, as shown below.

Image Source

Image Source
Is this coincidence, or does this possibly suggest that both chloroplast and mitochondrion precursors derived their energy-obtaining mechanisms via an ancient evolutionarily-related metabolic pathway which diverged?

Your latter assumption is the best we have so far, to my understanding.
Here are a few excerpts from "Early Evolution of Photosynthesis" published in Plant Physiology, October 2010 (emphasis mine):

There is suggestive evidence that photosynthetic organisms were present approximately 3.2 to 3.5 billion years ago...
Overwhelming evidence indicates that eukaryotic photosynthesis originated from endosymbiosis of cyanobacterial-like organisms, which ultimately became chloroplasts (Margulis, 1992). So the evolutionary origin of photosynthesis is to be found in the bacterial domain.

And then there's the abstract from this paper: "Do photosynthetic and respiratory electron-transport chains share redox proteins?"

In purple nonsulfur bacteria and cyanobacteria, there is close interaction between the photosynthetic and respiratory electron-transport chains, which share identical redox proteins.

Purple bacteria and cyanobacteria are some of the oldest known lineages (>3BY, whereas Mitochondria parallel Eukaryotic origins at about 1.4BY - and the endosymbiosis which created Chloroplasts probably came after [plants have both Chloroplasts and Mitochondria, whereas most Eukaryotes just have Mitochondria]), and since the respiratory chain and photosynthetic chain share identical proteins in cyanobacteria and purple bacteria it's not a huge leap to assume that - yup - the 5-protein structure is probably the template used by both Chloroplasts and Mitochondria because of a common source.

The second paper and associated paragraph is EXACTLY what I was looking for. +1, thanks.

Well, according to the endosymbiosis theory both mitochondria and chloroplasts derive from ancestral bacteria that invaded/were phagocytosed (fancy word for eaten) by eukaryotic cells.
So, the electron transport chains of both mitochondria and chloroplasts would indeed share a common bacterial ancestor.


text:
Do male marsupials have a pouch?
Do male marsupials have a pouch, or is it a female organ only (like the womb)?

In most marsupials, only the females have a pouch. However, males of the water opossum and the extinct tasmanian tiger (or thylacine) also have a pouch.  The males of both the thylacine and water opposum used/use their pouch to keep their genitalia from getting entangled in vegetation.

...evolution can even make underwear!

Not all male thylacines had it, but yes, some did.


text:
What restriction enzyme was used in cutting this DNA piece?
So, i was given this cut piece of dna and i was required to choose the restriction enzyme used to cut it. I had to pick either XhoI(CTCGAG) or TaqI(TCGA), where the sequence between parentheses is their palindrome sequence. Which one is it and why? I've picked XhoI since i know that the enzyme cuts in between the palindrome

GAGCT        C
C        TCGAG

DNA after the cut.

In order to keep this on topic, I will try and give a more general answer.
The most widely used restriction enzymes, and the ones typically taught first, all cut within their recognition sequences, however, this is not necessarily so as most Type I and Type III enzymes cut at a distance from their site, sometimes this is a fixed distance, sometimes it is not. It is only Type II enzymes that cut symmetrically within their sites, and even then, not all of them. However, cutting within the site is usually the most useful kind of cut for molecular genetics and thus these are the most common enzymes to encounter in the lab (see here for more).
For a particular enzyme, the best way to find the cut site is simply to google it or search directly on the NEB site (where you will likely find the top Google hit anyway), doing this for XhoI would get you a page containing information like this:

Where the little arrows in the given recognition sequence indicate where each strand will be cut, whereas as for enzymes that cut outside the recognition site you will get something like this (for AlwI) where the $(N)_4$ part tells you that the enzyme cuts four bases away on the 5'-3' strand, and the $(N)_5$ part tells you it cuts one base further away on the opposite strand.

In order to identify which of a number of enzymes cut a certain sequence you need only find the appropriate information for the relevant enzymes so you can compare these cut diagrams for the relevant enzymes.


text:
Is it possible to see the microbes on your hand without using UV light or a microscope?
I know that black light (UV) is often used to see the microbes (colloquially referred to as germs) on people's hands but is there any way by which we can examine the microbes on people's hands without having the surroundings be completely dark (what is required for black light to work) or using a microscope? I am trying to show a roomful of people the microbes on my hand but the surroundings aren't going to be completely dark and there is no way I can use a microscope.

The term germ is generally not used in biology as it is poorly defined. In general, it is defined as a microorganism, which would mean that by definition you can't see them with your bare eyes. I don't think a black light would be of any help though. You can detect specific disease with a black light but I don't think it would help you see individual germs (as they are too small by definition, at least if you want to define a germ as being a microorganism). What make you think a black light would help?

A germ is typically defined as a pathogenic agent. Is there any reason you want to find something that is pathogenic? Or maybe, you just meant that you would like to see a microorganism?

I understand germs isn't the best use of vocabulary. I meant microorganisms/bacteria. The answer about the agar plates works perfectly but now if I kill the microorganisms in a roomful of people, how can I show that the microorganisms are killed in front of them?

@aadityak_968 You should move your comment to the answer. You are commenting on the answer, not the question.

Given your constraints, the only solution available would require some amount of preparation. If you are so inclined, you can purchase sterile, ready-to-use agar plates online, which you can then inoculate with microorganisms from your hands by simply touching the agar surface with your palms, and letting the plates incubate at room temperature. A day or two's time should be sufficient for plenty of microorganisms to grow, allowing you to demonstrate that your hands have "germs" (although some of the microorganisms you'll find on your agar plate may very well be airborne contaminants if you don't take some precautions).


text:
Difference between crossover rate and recombination rate?
I am not a biology student and therefore, need clarification if crossover rate and recombination rate are the same thing. So if the text says 'recombination rate per base pair per generation' or 'cross over rate per locus per generation', is it the same thing? And if not then what is the difference? Also, is 'per base pair' and 'per locus' the same thing?

Let's start with the second question.

Is 'per base pair' and 'per locus' the same thing?

No, not necessarily. A locus (plur. loci) is a location in the genome. It can be of any size. A locus can be a single base pair or it can be 10 base pairs, or a whole gene or anything you want.

'recombination rate per base pair per generation' or 'cross over rate per locus per generation', is it the same thing?

Recombination rate and crossover rate are not exactly the same thing!
Let's define two loci. Here is a drawing of two haplotypes (the maternal one and the paternal one). Let's represent the loci on the maternal haplotype with capitalized letters and the loci on the paternal haplotype with lower case letters
---A---------B---

---a---------b---

Let's Let's say that between these two loci there are on average 0.2 crossover per reproduction. The crossover rate is therefore 0.2.
Let's draw the two haplotypes after crossover(s) in a case with...
... 0 crossover
---A---------B---

---a---------b---

... 1 crossover
---A---------b---

---a---------B---

... 2 crossovers
---A---------B---

---a---------b---

... 3 crossovers
---A---------b---

---a---------B---

... 4 crossovers
---A---------B---

---a---------b---

You might see a pattern here! If the number of crossovers is even (including 0), then the association between the two loci is unchanged. If the number of crossovers is odd (including 1), then the association between the two loci is changed.
The recombination rate is the rate at which the association between the two loci is changed. Let $P(n)$, be the probability that there are $n$ crossovers between our two loci. The recombination rate is therefore $P(1) + P(3) + P(5) + P(7) + P(9) + P(11) + ...$.
To make a long story short, the recombination rate is the rate at which the number of crossovers is odd.

Thank you for such a detailed answer. It makes a lot more sense now.


text:
How do mutations with very little fitness benefit get fixed?
I have one little issue with evolutionary theory that I have not been able to understand.
Suppose genetic mutations happen from generation to generation. Nevertheless, from one generation to the next the mutation will present very small changes (I don't suppose a giraffe's neck would grow 10cm). If this were the case, then the advantages one gains from this mutation would be very small. So shouldn't it be the case that the mutation in the case of the giraffe and every other mutation for that matter present very very little advantage so shouldn't transmission of genes at this stage be random? If this were the case I don't see how natural selection could take place?

In the long run (over hundreds or even millions of generations), small statistical advantages are bound to accumulate.
Even if a mutation gives only a +1% average reproductive advantage, it is still above chance and therefore this mutation is more likely to spread through the population.
(If you can code, I have found it to be an interesting exercise to write scripts that simulate generations of evolution.)
It is also not necessarily true that effects of mutations have to be small. Single mutations can be deadly, they can change colors, create large morphological changes, and so on. It just happens to be the case that most mutations that have large effects are deleterious, and therefore won't generally spread for long throughout the population. But some mutations will be beneficial and therefore have improved odds of being passed on.

Consider genetic drift: if a particular mutation is selectively neutral, it may persist indefinitely in the population, but it is subject to random changes in its frequency due to various non-selective influences.  As a result of the random fluctuations in frequency, the allele may be eliminated from the population or may become fixed in the population despite having no influence on the natural selection of the individuals of the population.
Now consider if rather than being neutral, the mutation is slightly deleterious.  Since its effect is only slight, it can persist in the population for a long time.  Still, like a neutral mutation, it is subject to random fluctuations in frequency and so can be eliminated or fixed in the population.  However since it is slightly deleterious, it is more likely that the fluctuations will eliminate the mutation.
Similarly, if a mutation is slightly selectively beneficial, it will still be subject to random fluctuations and can be eliminated or fixed, but in this case it is more likely to become fixed in the population.
One view of this process is formalized in the "nearly neutral theory of molecular evolution".


text:
What created the first ribosome
If a ribosome is made of protein, yet is used in protein sysnthesis, what created the first ribosome?
What created the ribosomal RNA?

This question has been asked before in several variations and has several detailed answers as I recall. I’m away at the moment with only my phone. Perhaps someone else could look up the actual question to mark it a duplicate.

@David yes, there are similar questions about DNA and DNA polymerase and ATP synthase. I didn't mark this as a dupe of them because it could be argued that ribosomes are different. However, we can mark all subsequent questions on this topic as a dupe of this one or the others

@WYSIWYG I’ll have a look when I get back this weekend. It would be good to have one or two definitive questions (the ribosome may require its own) with a selection of comprehensive answers. I have my own contributions to make, but would rather do so in a coordinated manner. Perhaps the way to handle it would be on meta.

@WYSIWYG — Found the previous question —  almost exact duplicate.

This is one of the "chichen and the egg" quesitons about early origins of life. The answer is: we don't know. There is a RNA world hypothesis which suggests that RNAs were the primary versatile biomolecules before proteins. This idea stems from the fact that there are self-replicating RNAs and ribozymes (RNA-based enzymes). Also, the fact that the catalytic center  (peptidyl transferase) of the ribosome is RNA, is also used in support of the the RNA world. However, this is still an idea and we cannot conclusively say that an RNA-world existed.

As the question is clearly a duplicate you might wish to migrate your answer to the original. I am considering writing a second answer (I already included a devil's advocate one) because I do not feel the current RNA world answer there is adequate.


text:
Selection coefficient of gorillas
I've been reading about selective sweeps. And I found a case study that talks about drosophila and how their selection coefficient is between 0.0001 and 0.005.
I want to know what it'll be like for gorillas? That is what would be the selection coefficient range for them and why? Also, I was told that N*s of gorillas is between 100 and 10000 where N is the current population size and s is the selection coefficient.
Help would be really appreciated. I do not have a biological background therefore, it's taking some time to wrap my head around these things.

I found a case study Whether it seems to matter or not, please always link to your source.

A selection coefficient is not so much specific about a species as much as it is specific to a given mutation. What mutation are you talking about in gorillas?

Do you mean mutation rate? Per site mutation rate is 1.5e-08

No, I did not talk about mutation rate. A specific mutation has a selection coefficient. A species does not. It makes no sense to ask "What is the selection coefficient in gorillas?", it only makes sense to ask "What is the selection coefficient of the p.P252R mutation in gorillas?"

It's not a specific mutation. I want to simulate sweeps in the genome. I have all the parameters I need but I am struggling with the selection coefficient. I've edited the question and have added the parameters so you can see.

There are no correct answer then. If you simulate a selection coefficient of 0.3, then you will likely simulate something that is very rare. If you simulation a selection coefficient of 0.0001, then you won't even really have a selective sweep. Just pick a number in between. But there are no right or wrong.

ok. So what is usually the range for a strong selection? It'll be close to 1?

I would personally consider anything above 0.01 as being strong selection. You will likely never find a new beneficial mutation with a selection much higher than 0.1. On a side note, you might be interested in the Distribution of Fitness Effects of new mutations (DFE; although in general such distributions are only estimated for deleterious mutations as they are much more common).

On another side note, you might be interested in the post Sequence evolution simulation tool


text:
Does anyone know a good pancreatic-cancer metastasis cell line?
Researching about pancreatic cancer. We have mostly "main-tumor" cell lines in our lab, and I´m currently looking for cell lines originating from metastases (liver, lung, etc.).
Does anyone know a well-established pancreatic-cancer-metastasis-cell line?

Did you check this article?

Thanks, but I already know this one. Good paper nonetheless

Perhaps you should mention that and explain what different do you expect.

SUIT-2 cell lines are derived from the liver metastases of Pancreatic Ductal Adenocarcinoma. The subline S2-007 is highly metastatic. The other sublines are S2-013, S2-020 and S2-028 which have decreasing metastatic capabilities.
You can probably refer these articles for more info :
1. https://www.ncbi.nlm.nih.gov/pubmed/3102439
2. https://link.springer.com/article/10.1007/s10585-017-9840-3


text:
Can anyone identify this chrysalis? (Identified)
It's about 5 or 6 cm long. It's on the outside (north facing) wall of my garage about a metre above ground level.
Photo taken in Thailand near Hua Hin (about 12N 100E) in December 2014.

What a great find! :D Fantastic chrysalis. Thanks for sharing.

I've found it - it's a Common Rose Swallowtail (Pachliopta aristolochiae)
A few images on this page.
http://flickrhivemind.net/Tags/aristolochiae,butterfly/Interesting including these two

There is a picture also at http://en.wikipedia.org/wiki/Pachliopta_aristolochiae but this one is upside down compared to mine.

Mystery solved.


text:
what's the vascular cambium?
is the vascular cambium equivalent to interfascular cambium or intrafascular cambium?
isn't the vascular cambium similar to the intrafascular cambium because both occur inside the vascular bundle

Welcome to Biology.SE. 1) You should chose a title that is much more specific. Don't be afraid if your title already states most of what you have to write in your post. 2) You should always limit your posts to only 1 question (I am not qualified to judge whether the fact that the current post contain two questions makes it too broad or not). 3) As the questions sounds like homework questions (although you tell those are not homework questions) you should tell us your thoughts and your attempt to answer the question. Knowing what you know and think make the answers much more helpful for the OP.

okay i will edit my post.


text:
Games with non-uniform interaction rates
Background:
Many models in evolutionary game theory assume uniform interaction rates. For instance, consider the $2\times 2$ game:
\begin{array}{l c c}
    & A & B \\
    A & a & b \\
    B & c & d
\end{array}
The fitness of the strategy $A$ is $xa + yb$, where $x$ and $y$ are the frequencies of the strategies $A$ and $B$, respectively.
Taylor and Nowak "Evolutionary game dynamics with non-uniform interaction rates" (link to the paper) rewrite the fitness function to allow for non-uniform interaction. In particular, the fitness of the strategy $A$ and $B$ become:
\begin{equation}
f_{A} = \frac{ar_{1}x + br_{2}y}{r_{1}x + r_{2}y}; \quad f_{B} = \frac{cr_{2}x + dr_{3}y}{r_{2}x + r_{3}y}
\end{equation}
According to this model, ``[a]nalogous to a chemical reaction, an $A$ player interacts with another $A$ player with reaction rate $r_{1}$, an $A$ player and a $B$ player interact with reaction rate $r_{2}$, and a $B$ player interacts with another $B$ player with reaction rate $r_{3}$." (p.244).
Question: What would be an intuitive interpretation of $f_A$ and $f_B$ (as defined by Taylor and Nowak)?

Further comments: When $r_1 = r_2$ and $r_2 = r_3$, we have the situation with uniform interaction. But I am not sure how to interpret the above fitness function for when $r_1 \neq r_2$ (and $r_2 \neq r_3$). I thought of interpreting $r_1$ and $r_2$ as the conditional probabilities $P(A\mid A)$  and $P(A\mid B)$. However, if I'm right about this, $f_A$ would have to be  $r_1 a + r_2 b$ instead. For this reason, I am under the impression that the $r$s should not be conditional probabilities. But if the $r$s are not conditional probabilities, what are they exactly?

To make sure I understand your interpretation, does it involves that 1) $r_1+r_2=1$, 2) if $r_1=r_2$, then individuals interact randomly without preference, 3) If $r_1>r_2$, then individuals interact preferentially when individuals playing the same strategy and 4) if $r_1<r_2$, then individuals interact preferentially with individuals playing a different strategy? If the above is true I would expect the mean fitness in the population to be $\frac{1}{2 (x+y)(r_1x+r_2y)}$ while the equation suggests that the mean fitness is $r_1x+r_2y$.

@Remi.b 1). Yes, if my interpretation is correct. 2). Yes. 3 and 4) Here is a quote from the paper "If r1 > r2 and r3 > r2, then players prefer to interact with their own kind. If, however, r1 < r2 and r3 < r2, then mixed interactions (between A and B) are more likely."

@Remi.b Note that I added a formula for $f_B$ to make my question more clear.


text:
Replicator equation for mixed strategies?
The the replicator equation is usually defined for pure strategies. More specifically, the replicator eqn for $n$ strategies is given by:
\begin{equation}
  \dot x_{i} = x_{i} \left( \sum_{j=1}^{n} a_{ij}x_{j} - \phi \right)
  \qquad i = 1, \ldots, n
\end{equation}
where $x_i$ is the frequency of the strategy $i$, $A=[a_{ij}]$ is the payoff matrix, and $\phi$ is the average fitness of the population. Basically, what the replicator equation is saying is that the per capita rate of increase of the strategy $i$ (i.e., $\dot x_i/ x_i$) is the difference between the fitness of $i$ (i.e., $\sum_{j=1}^{n} a_{ij}x_{j}$) and the average fitness $\phi$ of the whole population.
Question: Does anyone know of a formulation of the replicator eqn for mixed strategies?

When you allow for mixed strategies, you essentially have an infinite strategy set. There is a branch of evolutionary dynamics concerned with infinite strategy spaces. I know of this paper, for example: http://link.springer.com/article/10.1007/PL00004092


text:
How can I improve efficiency of Ecoli transformation?
I am an intern in biology institute. I have a 17.3kbp plasmid need to transform to Ecoli. But I have tried many time but have no or very few colony on LB plate.
I know large plasmid have less frequency in transformation, How can I improve chance of successful transformation?
Thanks everyone.

Welcome to Biology.SE!  It is expected that you will demonstrate that you have done research on your own before asking questions here — for example you could start with this: https://www.researchgate.net/post/How_can_I_improve_transformation_efficiency_using_a_12kb_recombinant_plasmid_with_a_cloning_strategy_using_DH5a …. –––––––– Thank you for taking the tour — for details on how to ask good questions on this site please see: biology.stackexchange.com/help/how-to-ask. Thanks!

Other than what tyersome has suggested, I want to add that questions that involve troubleshooting of lab experiments should include the detailed protocol used (or provide a link to a protocols article if it is exactly followed).

The plasmid is quite big which might explain why it is difficult to transform bacteria (is it a lentiviral vector?).
If you could give additional details you might have a chance to have improved answers to your question.
Hello, I suggest you follow this protocol:
At step 7 instead of this "Add 250-1,000 μl LB or SOC media (without antibiotic) to the bacteria and grow in 37°C shaking incubator for 45 min. "
Do this " Add 250 μl LB or SOC media (without antibiotic) to the bacteria and grow in 30°C shaking incubator for 2 hours. Do not shake too hard, gentle motion might be fine (500 rpm).
At step 9 instead of this "Incubate plates at 37°C overnight."
Try to incubate at 30°C. I would even suggest to try to grow them at lower (25°C, or 16°C) temperature if you can prepare a second plate.
It will take much longer than overnight to grow the cultures, probably more 48 hours (might be 72 hours at 16°C).
Hope that helps good luck!