text:
Books for learning how plants function
Can you recommend a good, detailed book on how plants function? A book that explains plant processes on a molecular level from roots up to the fruit.
I am interested in home crops production, such as tomato and peppers, but I expect the principles to be the same for most of the plants. There are lots of "how to garden" books, but this books don't explain things, they just tell what to do.
Background: I have a degree in chemistry so I am confident in my knowledge of chemistry and chemical analysis. But this knowledge is useless unless you mixed it with other science branches, such as biology.

I think you would need a plant-physiology book and a biochemistry book.

I wanted to comment because I don't think my answer will be the best, but I can't because of my low reputation... Anyway, here are two suggestions:

Plant Physiology and Development, by Lincoln Taiz, Eduardo Zeiger & al.
Biochemistry and molecular biology of plants, edited by Bob B. Buchanan, Wilhelm Gruissem and Russell L.Jones

These are the two main books we are using in my university (I'm studying biology) and I think that together they cover a lot of topics. You can probably buy the pdf versions online as well. I hope it helps!


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Why some traits are more desirable in the sexual selection?
For example, why do peacock females choose males with the biggest tail? If there is no advantage in such tail.

Have you done some work looking for an answer?

Wikipedia is often helpful....Have a look at Fisherian runaway and Zaahavi's handicap and eventually just at sexual selection.

Sexual selection is a big topic and while I am not quite an expert in this field, I doubt anyone would be able to really make a good summary of the possible reasons leading to sexual selection. It is even more true that there are big issues of semantic in the field (see the work of Hannah Kokko). Note however that reading the wiki article on Fisherian runaway will already bring you a long way.

Oh You should read about the sexy son hypothesis too

Also you can mark an answer as accepted.

There are two common explanations both are difficult to demonstrate. I personally favor the former but I will not claim it is the only explanation.

selection starts as either a random occurrence or as some initially beneficial trait (a slight increase in tail length may have been beneficial originally)
Then runaway selection takes over. Any increase also causes increased attraction because the evolved behavior of the desire in the females only functions as bigger is more attractive(or whatever=more attractive). This pushes further and further into absurdity becasue there is not behavioral regulation to say enough is enough. So any increase in the males increases attractiveness meaning any individual male with less can't reproduce in the current population of females no matter how beneficial to the individual male survival. Additionally no female will develop a favoring of smaller tail feathers becasue her smaller tailed offspring will not be able to find mates for the same reason. A positive feedback loop like this won't stop until it hits a point where the cost of tailfeather is more than the advantage of increased mating becasue the individual never lives long enough to mate.
By carrying a handicap the organisms shows it can withstand a greater burden and thus must be better.

so the desire of some trait can be transferred by genes ?

of course, most behavior is controlled by genes. The genes that control the structure of the brain control behavior. Even In humans a significant amount of our behavior is controlled by genes.

most behavior is controlled by genes is misleading and sounds like you might misunderstand the concept of heritability. You would at least need a reference for such claim.

I don't think that FIsher Runaway process (your first bullet point) necessarily require an initially beneficial trait under the sexy son hypothesis (but I am not 100% clear with all these concepts in sexual selection)

I said a beneficial trait or a random occurrence.

@remi. I think you are misunderstanding how many organisms exhibit behavior. Behavior is itself a poorly defined term. How much insect behavior do you think is learned?  but you also have the problem with what is considered controlled. language as an example the brain has a critical period for learning syntax, yet what language you speak is clearly learned so it both controlled and not controlled by genes.

My main issue was that "controlled by genes" is misleading. One can tell whether a behaviour is innate or learned or whether phenotypic variance is due to environment variance or genetic variance. When saying "controlled by genes", it makes me feel that you are stating that most of the variance in behaviour is explained by genetic variance (which I think would require a reference).

very few behaviors are one or the other, most complex behaviors are a mix of the two. But I perhaps, "Modulated by genes" would have been better. The massive gray area makes giving an exact number impossible. It is all about arbitrary categorization which makes it largely opinion.

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text:
Why is a mosquito feeding on human blood not a parasite?
I recently read in my Ecology course notes that a mosquito feeding on human blood is not considered as a parasite. However, since it sucks blood from the human body, shouldn't it be regarded as a parasite, just like lice and ticks?

What research have you done before asking it here?

@another'Homosapien' While its understandable that OP should do some research before posting a question, I still feel we should encourage new and interesting questions as our Biology SE needs much more questions (given how vast Life Sciences are!)

@talhairfan I have no problem with the question as well as your point. But we must also not forget the website policy. The same question, with some prior research, would be a nice hit...

How is the mosquito feeding on blood different from the lion that kills its prey?

not killing prey/reducing its fitness to zero (see my comment on the accepted answer)

female mosquito , indeed is considered as a parasite and it comes under the category of temporary parasite.

Its not considered a parasite

@JM97: reference please?

@BenBolker http://learning.uonbi.ac.ke/courses/SZL310/scormPackages/path_2/lecture_5__categories_of_parasites_and_hosts.html

OK, thanks. FWIW "Temporary parasites are often referred to as micropredators" (which links with Lafferty and Kuris).  Obviously there is a variety of terminology circulating, depending on sub-field ...

A mosquito is a biological parasite, it is not a medical parasite.
There are two definitions of parasite. A biological/ecological definition and a medical/physiological interaction definition.

A parasite in biological terms is an organism that benefits from a parasitic relationship; a parasitic relationship being a non-mutual relationship between species, in which one species benefits at the expense of the other. Generally the host is not killed by a small number of parasites. When the host is killed the organism is usually called predator or parasitoid.
A parasite in medical terms is an organism that lives on or in a host and gets food from or at the expense of its host.

The difference is small but important; only the medical definition requires the parasite to live in or on the host for prolonged periods. It is a much narrower definition.
Biologically, a female mosquito is an indirect ectoparasite, it can be facultative or obligate depending on the species. It harms its host to benefit itself, that is all that is needed to be a parasite by the biological/ecological definition. And just like a leech or vampire bat it is hemophagic and leaves the host as soon as it is done feeding. Brood parasites are another great example of a biological parasite that does not live on or in the host. So a cuckoo would be a biological parasite but not a medical parasite. When you consider the function and practice of medical science the more narrow definition makes sense, they are not concerned with parasites that are not going to stick around or not affect the host organism's physiology directly. By the narrower medical definition, none of these organisms are parasites even though by the biological/ecological definition they are.
Consider the wiki or a paper on parasite evolution vs say the CDC to see the difference.

So, to clarify, you are saying that a mosquito is a parasite and consequently that the OPs "Ecology course notes" are incorrect? @AlwaysConfused John's answer would appear to state that a mosquito is a parasite "in biological terms".

Correct, which is not surprising the quality of textbooks vary widely, especially with things that have two or more discipline based definitions like this. Plus one thing you learn about biology as you advance is that there is a lot of gray area since living things dont care about our attempts to categorize them or the imprecise language we have to use to do so. JayCkat points one our very nicely, what constitutes "harm".

@AlwaysConfused Biological definitions of behavior are more like blurry venn diagrams than exclusive boxes.

Short answer
Female* mosquitoes are generally not to be considered ectoparasites because they spend so little time with the host. Instead, they are sometimes classified as micro-predators.
*Male mozzies don't practice hematophagy at all
Background
According to some sources, the term parasite hinges on the time the parasite spends on, or in its host and hence it is a gray area whether a mosquito is considered a parasite or not.
The CDC, a renowned center on disease control & prevention, states the following:

Although the term ectoparasites can broadly include blood-sucking arthropods such as [female] mosquitoes (because they are dependent on a blood meal from a human host for their survival), this term is generally used more narrowly to refer to organisms such as ticks, fleas, lice, and mites that attach or burrow into the skin and remain there for relatively long periods of time (e.g., weeks to months).

In contrast, female mosquitoes need only about 4 minutes to finish their drink.
Wikipedia, being explicitly not my favorite source of information, says on their Mosquito page:

Females of most species are ectoparasites...

But then, when clicking through to the Ectoparasite Wiki page no mention of mozzies are made and the more accepted parasitic arthropods are discussed, namely the ones stated above by the CDC (lice, ticks and fleas).
However, as mentioned in the comments below, with credits to Fileunderwater, other sources like this veterinary work on Ectoparasites also discusses mosquitoes.
Hence it seems to be a gray area whether mozzies are classified as (ecto)parasites. Personally, I would stick to the careful definitions provided by credible sources like the CDC - mozzies are not considered ectoparasites, because they spend just a few minutes siphoning blood before they are off again.
But then, as rightfully probed in the comments, what are they then if not parasites?
One classification I've found for insects practicing hematophagy for short periods at a time is

Micro-predator: a temporary parasite (source: English Encyclopedia);

or

Micro-predator: e.g., the mosquito, that derives elements essential for its existence
  from other species of organisms, larger than itself, without causing
  their destruction (source: Medical Dictionary).

Then what is the relationship between mosquito and the animals it sucks blokd from called? There's gotta be a name for something with that much significance (eg. spreading of diseases).

@hyde,very good question and I looked for it too, but to no avail. Above the term 'grazer" is brought up. I couldn't verify it's use, but it sounds quite apt :-)

in this context (disease transmission) a mosquito is called a vector and the animal sucked from is called a host

@BenBolker afaik, a mozzie is only a vector when talking about the transmission of diseases carried by them such as the malaria parasite. Outside of disease transmission they are not a vector

I agree, it depends which aspect of the relationship you're talking about. In the ecological/evolutionary context "grazer" is indeed the most common term, e.g. see http://bit.ly/2oPhlRa . Lafferty and Kuris use "micropredator", but in my experience that's less common.

I is quite easy to find other examples from "credible sources" where mosquitos are called ectoparasites, outside of Wikipedia; see e.g. "Veterinary Ectoparasites: Biology, Pathology and Control"

@fileunderwater - thanks for that. I might have to rephrase my answer and stress the grayness of the matter. Thanks.

For the record, I find the CDC criteria for determining parasitism (time period used) quite silly, as a way to define ecological interactions.

@fileunderwater - you may be right and thanks for your comments here. I mentioned your source in my answer now. It is definitely a gray area. However, when I think of ectoparasites I think more of lice, fleas and ticks but that may indeed be a personal bias. I think John's answer matches your view better.

The CDC don't seem very consistent to me re: being used as a reliable source for definitions; they still define bedbugs as parasites on their own webpage, even though their own definition shouldn't agree with this. To me, mosquitoes and bedbugs are obvious parallels - they both rely on bloodmeals, but only stay in proximity to their hosts for occational access and do not live on the host(s).

@AlwaysConfused - It's Ozzie slang for mosquito, yes :)

Micro -predator and parasitoid are both areas where parasite and predator overlap.

To be a parasite, an organism needs to fulfill two criteria
1) It needs to have a non-mutual relationship between itself and its host.
The organism derives benefit and the host suffers harm.
2)The organism also needs to live in or on their host for an extended period.
Often, a parasite will also have biological specialization to mediate the relationship between itself and its host.
However in reality, there is a spectrum of relationship. So a parasitism is not always very clear cut. How much "harm" is needed to be harmful enough? How long does a relationship need to be?
In your example the first criterion is fulfilled, but the second is not. The mosquito benefits from the blood meal and the host mammal does not. However, only female mosquitoes feed on blood and only when they are about to lay eggs. A mosquito does not spend most of its life in or around its host.
So by definition a mosquito is not a parasite.
https://en.wikipedia.org/wiki/Parasitism

Your own source does not agree with your definition.

another ref: https://parasiteecology.wordpress.com/2014/02/05/predator-vs-parasite-vs-parasitoid/ Lafferty and Kuris would call mosquitos "micropredators", another commonly used term is "grazer"

The reference to the wiki page is indeed off as it explicitly counter argues your answer..

I also disagree with this answer -1

Additionally, not benefiting from something does not imply harming per se.

Where does Wikipedia disagree? "Unlike predators, parasites typically do not kill their host, are generally much smaller than their host, and will often live in or on their host for an extended period."

@BenBolker “will often” is very distinct from “always do by definition”

A flea would be an ectoparacite because both male and female fleas feed and spends their entire life cycle on its host. As for a mosquito.. only the female has blood meals and only when they are laying eggs. It is a very specific part of its life cycle, and only one sex. A vampire bat in contrast... both genders feeds on bloods and it does so as a normal part of its diet.

@BenBolker Looks like I was beaten to it but I would agree Lafferty and Kuris is the key source here - why don't you write their explanation up as an answer? I would myself but apparently my laptop battery is about to die :(

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Can a phenotype only have one allele?
A phenotype such as hair color
like blonde hair.
I am curious because mutations cause new alleles but does that mean that there always has to be a dominant or reccessive allele?

Related: https://biology.stackexchange.com/questions/111402/what-are-the-relative-frequencies-of-dominance-and-codominance-in-genes-underlyi

This is actually a really good question.

Can a phenotype only have one allele?

Yes. Some diseases arise only from one known allele. Some common phenotypes can be predominantly controlled by a single allele, but are affected by more than one. On an individual level, it is common to see one allele creating the phenotype, such as rare diseases cause by de novo mutations or familial rare disease. On a population level, it is harder but not impossible to find a phenotype that has only one allele for everyone because genes typically contain many alleles.

Mutations cause new alleles but does that mean that there always has to be a dominant or recessive allele?

No, there doesn't. In fact, we've lied to you in school a little bit to make things less complicated. It is easy to teach dominance and recessive alleles and do punnet squares, but the reality is that dominant alleles have little effect on complex traits like height or how much education someone receives. You've stumbled upon the same intuition that led Fisher to develop the currently prevailing additive model in 1918.
All complex traits, i.e., most things that aren't a rare or Mendelian disease, do not have important dominant/recessive alleles. Instead, each allele contributes a little bit regardless of if other alleles are present or not. So not only does there not have to be a dominant or recessive allele, but it is the norm for there not to be.
Dominant alleles arise naturally due to loss of function mutations. They are very important in the discussion of monogenic genetic diseases, and frequently contribute to the phenotypes of rare disease, even though they are rarer than additive alleles.

"dominant alleles are quite rare" I would take issue with this. Simple example: loss of function mutations necessarily leave a dominant allele (LOF is recessive). Granted, they are certainly numerically rarer overall, especially as you say for complex traits or neutral variation. But you will encounter them quite often in doing genetics on things people care about! Related: https://biology.stackexchange.com/questions/111402/what-are-the-relative-frequencies-of-dominance-and-codominance-in-genes-underlyi

Good point; I will edit it with that in mind

Can there be only one allele at a given locus?
An allele is a variant of a gene. If there is only one allele at a given gene, it means that there is no genetic variance at this specific locus (a locus is a position in the genome. It can typically correspond to a gene). It is not rare at all that the whole population is fixed for the same allele at a given locus.
Number of alleles
In courses, it is common to consider only the case of 2 alleles. In reality, there might be any number of strictly positive allele. At a given locus, you might have 1, 2, 3 or 11 alleles for examples. The reason why we typically teach about the 2 allele case is that 1 allele is not of much interest as there is not genetic variance at this specific locus and 3 or more alleles makes everything a little more complicated.
Dominance relationship
In courses, it is also common to consider diploid individuals, 2 alleles and the phenotypes of the three possible genotypes assuming $h_N = 1$ (see here to understand $h_N=1$). In reality, the relationship between two alleles may be vastly more complicated. There is a gradient from complete recessivity to complete dominance (passing through perfect additivity). It is also possible that the heterozygote is more extreme than any of the two homozygotes.
Dominance relationship - Number of alleles
As the number of alleles varies, any pair of alleles have a specific relationship of dominance. While empirical studies suggest that if allele A is dominant over B and B is dominant over C, then A is likely dominant over C, it is not impossible that C could be dominant over A. And again here, I am considering only cases of complete dominance but any scenario is possible.
Dominance relationship - Ploidy
The ploidy also varies from one species to the other (and also from one moment in the life cycle to the other for sexually reproducing organisms). If you have  a polyploid, then the number of possible genotypes is higher than 3 (even for a 2 allele case) and therefore the concepts of recessivity and dominance don't necessarily apply that easily.
Dominance relationship - Epistasis
Finally, there might have interaction between loci making that the relationship of dominance at one locus may depend upon the genetic background (that is the other variants present at other loci). Of course, it may as well depends upon the environment but let's not talk about that for the moment.

@NeelSandell Please, let me know if it answered your question or not.

This may depend on how precisely you wish to define an allele. Cystic fibrosis is a disease effected by mutations in a chloride ion transport channel. Because this is an extensively studied illness, now over 500 different mutated versions of the gene are known. Each of these genotypes gives rise to the disease although there is much variation in the severity of the disease pending the exact mutation.
https://www.ncbi.nlm.nih.gov/pubmed/8949420

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Plant identification — Phuket, Thailand
Found in Phuket, Thailand. White flower, five petals, 5 stamens. Strings of flowers hanging down from red stems. Buds white, tear-drop shape.
RHA, Here are the leaves. The flowers hang from a bush about 6 foot (2 metres Tall)
Bli, thanks, but not honeysuckle. No scent.

Nice pictures of the flowers! Do these flowers hang from a tree? Any idea what the leaves look like?

This vaguely reminds me of Lonicera, but is clearly not the species I know.

This is Clerodendrum schmitii similar to C. wallichii (Bridal Veil). It is commonly called Chains of Glory and is native to Thailand.
It belongs to Verbenaceae family.

Chains of Glory is a shrub to small tree, multi-stemmed, with hanging branches. Each winter it grows long, pendent, dark red racemes, 1.5 ft long, of delicate white flowers. The cascading white fragrant flowers are held in loose hanging clusters, similar to Bridal Veil. The white flowers on long dark red flower stalks look very attractive against the dark green leaves. Chains of Glory is native to Thailand.

(from flowersofindia)

The genus is native  to tropical and warm temperate regions of the world, with most of the species occurring in tropical Africa and southern Asia, but with a few in the tropical Americas and northern Australasia, and a few extending north into the temperate zone in eastern Asia.

(from wikipedia)
Picture reference:
 Chains of Glory $^1$
 Bridal Veil $^2$
$^1$ (Source: tuoitre.vn)
$^2$ (Source: Cebuano wiki)

Excellent find! It would be nice to include a picture or at least a link to a picture; your wikipedia only points to the genus.

@RHA Updated the answer.


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What flower is this?
I received this flower as a gift.

So far, I couldn't identify what flower it is. My family thinks it may be either some sort of Clematis or an Ipomoea purpurea.
The main reason I want to identify this flower is to know if it can live outside most of the year (I live in France).

my first impression was that it was mandevilla. We had this plant in a pot on the porch when I was growing up. The plant stayed outside until winter (temps typically below 0 C for 3 months) at which point we stored it inside. Mostly dies back each winter and we clipped it. Each summer, we put it back outside and it grew nice and big again.

The leaves are most similar to this Mandevilla
It may be a hybrid periwinkle, in France and UK there are blue ones in wild and there are pink ones i.e. in Madagascar. If it's a periwinkle you can tell by the fruit and veins of the leaves. It can be a variant of Vinca minor. It has evergreen type leaves, it may be tropical. It is also similar to the Oleander family. Clematis and Ipomea have new foliage every year.
Also see this.

@comprehensible is right: it's a Mandevilla, most likely the Mandevilla sanderi which is common in cultivation.
You can find further information on wikipedia, and of course on a lot of gardening sites.


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Identification of a caterpillar
My daughter has become one with nature somehow and came across an odd looking caterpillar. The odds of finding one never found before is great,  however I'm unable to find what kind it is. It's head is bright red.
From Eastern North Carolina, USA.

Would anyone be able to point me in the right direction?
Thanks!!!

From eastern North Carolina

This is a tussock moth caterpillar in the Lymantriidae family.
The image is not clear enough for a definitive ID, but it appears you have some species in the genus Orgyia.

Likely, this is a white-marked tussock moth caterpillar (Orgyia leucostigma).

From Auburn University:

The full-grown larva (Photo 2) is around 35 mm long. The head and shield on the segment behind the head are red. There are two long black pencils of hairs on the first segment of the thorax that project forward. A single black hair “pencil” arises from the eighth abdominal segment and projects upward and rearward. The back is mostly black and the sides yellow, cream, or grayish. There is an erect brushlike tuft of white or yellowish hairs on each of the first four abdominal segments, and a conspicuous red dot on segments six and seven.

Range: Entire eastern U.S. and west to Minnesota and Texas. [source].

@Brittany glad i could help :). If you're satisfied with the answer, please "accept it" by clicking the checkmark next to my answer. And don't forget to upvote if you like the answer ;)


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Do any amphibians start their lives on land?
Most amphibians - at least, all the ones I know of - start their lives in the water (at least, after they hatch). They then spend time maturing before venturing onto land, where they can breed. The cycle than begins again.
Are there any cases where the reverse is true, i.e. a young amphibian starts life on land before venturing into the water as an adult?
Wikipedia hints that this may be the case, but fails to provide examples:

Amphibians typically start out as larvae living in water, but some
  species have developed behavioural adaptations to bypass this.

I believe that most amphibians lay their eggs in the water because their food (larvae,fish etc.) lives in water.So their newborn babies will have something to eat.

From wiki:

Most amphibians lay their eggs in water and have aquatic larvae that undergo metamorphosis to become terrestrial adults

This suggests clearly that not all of them do so.
Here are a few interesting cases I could think of:

The common midwife toad carry the eggs on their back. The eggs are not necessarily submerged by water then.
To my knowledge, the Seepage salamander have terrestrial larvae but they don't feed before they reach the adult age.
The lungless salamanders has a larval stage that is within the egg. When the egg hatches, the individual that comes out is already an adult.

Arguably, since this frog spends the entire larval stage inside a pitcher plant on land, it has started its life cycle on land.

A group of zoologists with Conservation International say they found
  the frogs by the side of the road in Borneo, near a national park.
  They were very hard to locate because of their small size, but the
  scientists followed the frog's loud calls (you can listen to some
  here) and discovered them living among pitcher plants. They lay their
  eggs on the inside of the pitchers, and tadpoles grow up swimming in
  the tiny pools of rainwater that collect in the bottom of these
  plants. While most species of pitcher plant are carnivorous, the ones
  preferred by these tiny frogs only eat leaves - in fact, the frogs
  most likely help break down the leaf material and aid in the plant's
  digestion.

The moss froglet is an example of a frog which lays eggs on land and the tadpoles develop over several months in the egg mass amongst moss.

The Moss Froglet is a most unusual frog in that tadpoles develop on land. Breeding occurs from November to February. Four to 16 large eggs are laid in clumps of sphagnum or lichen and the tadpoles develop within the egg. After hatching the tadpoles do not feed, but spend the following 9-10 months of development within a fluid derived from the broken-down egg capsules (a gelatinous mass).

Source: http://www.parks.tas.gov.au/index.aspx?base=5258


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How do C. elegans manage nutrition?
If there is ample amount of food, do C. elegans worms know when to stop eating or do they store extra energy? Could they put this extra energy to use by moving faster or putting more eggs?

The answers are:

Yes, they know when to stop eating. See this paper.
Yes, they store extra energy as fat in the intestine.
This one is a little more complicated. They can use extra energy, but not to move faster. Movement doesn't take much energy, and until they're close to death from starvation, they continue to move quite well. As for eggs, they do indeed slow down the rate of embryo production when nutrition is inadequate. But the total number of eggs is limited by the supply of sperm, so there is an upper limit on how many they can produce, even in unlimited food. Probably the main benefit of stored nutrients is to allow them to survive longer if the food runs out. They are very, very good at dealing with a variable food supply -- much better than you, for instance -- and they do it partly by storing up extra energy. This paper and references therein describe some starvation responses. You can also look up L1 diapause, the dauer larva, and adult reproductive diapause.

Any references available for 2) and 3)?

@Chris Stronks: I added some references. Unfortunately, some of this is just common knowledge among C elegans researchers that's hard to track down in published form.

Great. I understand, it is not my expertise. Looks good.+1


text:
Which of the following lacks DNA?
a) An Enucleated ovum
b) Mature RBC
c) A mature spermatozoan
d) Hair root
According to me, there can be 2 answers, a and b because an ovum whose nucleus has been removed lacks DNA. And also, initially RBC has a nucleus but as it matures it's nucleus disappears. So, mature RBC should also lack DNA. Then which one will be a more appropriate answer ?

If it's a mild trick question, then note that it doesn't say "genomic DNA" but "DNA". Enucleated ova would still have mitochondrial DNA, while mature RBC would not.

This should not be closed - OP has clearly attempted to answer and justified it!

@layork - nice  one - write it up as an answer - +1 from me :-)

@iayork Thank You. I understood it. You can post this as an answer.

It should be closed! It's not a question about biology it's a stupid MCQ. it's no use to anyone else than the questioner to have it here. It's the sort of rubbish that demeans this SE.

Further to my last, I have posted a proposal on the Meta site to automatically disallow MCQs. Those who find this acceptable are asked to argue their case at: http://meta.biology.stackexchange.com/questions/3369/change-homework-policy-to-disallow-multiple-choice-questions-mcqs

One last comment. How could the moderators react constructively to an MCQ under my proposed ban? In this case they could rephrase the question as something like "Are there any cells in the human body that lack DNA? I can think of two..." This would transform a specific a, b, c or d MCQ into a general biological discussion.

its a tricky one but the answer of mitochondrial genes may help us to eliminate the option of enucleated ovum and we can go for rbc

I agree with @David. Although, the asker has attempted to find an answer, questions like this are not useful. They are not straightforward questions about biological facts and are primarily intended to confuse the students (or test their ability to read the question carefully instead of actually testing the knowledge).

There are two answers if the question refers to genomic DNA (neither enucleated ova nor mature RBCs have genomic DNA).  However, since the question doesn't specify genomic DNA, we can exclude enucleated ova, which would still have mitochondria and therefore mitochondrial genomic DNA.  Mature RBCS (at least in most mammals) do not have mitochondria, so the safest answer is probably b) Mature RBC.

First of all, 2) mature human RBCs don't have DNA. With the maturation of human red blood cells, the nucleus disappear. DNA is located in the nucleus so mature human RBCs don't have DNA.
However, your question didn't say "human RBC". Bird RBC have nucleus thus have DNA.
Then, both ovum and sperm cells have nucleus, thus have DNA, no matter which stage they are in.
I would say the possible answer be 4) hair root. The question didn't make it clear whether it's referring to the hair root cells or something else. But I would say that hair root is not made of body cells. No cell, no nucleus, no DNA.

the answer will be mature DNA.
We know that except for nucleus other organelle such as mitochondria also have ability to replicate an as mentioned in the question the enucleated ovum (ovum lacking its nucleus) do have the other cell organelles, whereas for the mature erythrocytes, they lack nucleus as well as other cell organelles such as mitochondria and golgi bodies; and hence RBC can't divide on its.
hope it helps!

You are repeating the point made by an existing answer. If you have a new point to add then please [edit] your answer accordingly.


text:
ExAC Browser: What does a "dubious variant annotation" mean?

I am studying a protein in the ExAC browser. However it is flagged with a "LoF flag". What exactly counts as a "dubious" variant in ExAC.
I couldn't find any further information neither at the variant's page nor in the FAQs.
Link to ExAC browser.
Link to variant site (This is a bad example, because there is a multi-allelic warning, but this is the variant shown in the picture)
Further links to variants with LC LoF flag:
14-45636336-C-T
14-45636346-C-CTA

Link please. I've never heard of it and shouldn't have to search.

This is interesting. Could you also show exactly what the variant page says?

I have asked for the definition of a dubious variant in the ExAC browser, or a source where I can find that definition. I can not imagine a clearer question. Pls don't mark my question as unclear on the sole ground that you don't know ExAC or can not answer the question.

It wasn't the unfamiliarity with the site and software, it was the fact that the original question had a result that didn't have enough information to reproduce the problem. If you could provide a link to your search that reported the dubious annotation (and maybe some additional context) I think initiating a reopen would be successful. Note that @David did not vote to close.

Not sure if this is related but theres been an effort recently to validate some of the predicted functional annotations. Its possible that the flag relates to inconsistencies between predicted function (LoF) and actual function in cell line systems. btw for reproducibility, this is the link to the page (press LoF button above export tables)

LC LoF stands for low quality loss of function. The variant is predicted to be a loss of function but has been filtered by LOFTEE. If you click on the transcripts drop down under annotation next to FANCM you'll see that at least one functional prediction is filtered. The FAQ gives more details in to how the filter criteria for LoF was set. Unfortunately, the question is on hold so I cannot post this as answer.

Briefly speaking you expect more or less uniform coverage for reads. So if you see a systematic difference in quality scores or coverage for minor and major alleles or for forward and reverse strand, it could be an SNV, but most likely it is a technical issue. That's a 'dubious variant'.
A lot of such biases are described in "Genotype and SNP calling from next-generation sequencing data":

Other types of filtering based on deviations from the HWE — generally
  low-quality scores, systematic differences in quality scores for major
  and minor alleles, aberrant LD patterns, extreme read depths, strand
  bias, and so on — can also help to improve the accuracy of genotype
  and SNP calling. The appropriate filters depend on the sequencing
  protocol and the upstream analyses. For example, a site with strand
  bias (where a disproportional number of plus and minus strands are
  observed) could be an indication of a problematic site that is more
  error prone and should be filtered out. However, if the sequencing has
  been performed on captured sequences, such as those used for exome
  capturing, then the bias might not be an indication of a problematic
  site but rather an artefact of the capture array.

Update
I've just received an answer from ExAC:

The "LC LoF” means that the variant was marked as a low confidence
  loss of function variant. If you click on the “Transcripts” dropdown
  on the variant page it will show the reason why the variant is of low
  confidence for that transcript. In this case it was flagged as
  “END_TRUNC”. An explanation of the LoF filters can be found here:
  https://github.com/konradjk/loftee

You are describing a dubious variant CALL. I think a dubious variant ANNOTATION refers to the classification as Loss of Function (LoF).
Maybe there is an inconsistency in ExAC, but I'm not sure. Are you?


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Examples of bifurcations in real-life systems
Does period-doubling bifurcation and Neimark-Sacker bifurcation happen in real-life systems? Are there some examples? I'm particularly interested in biological host-parasitoid and predator-prey models.
As far as I know, Neimark-Sacker bifurcation is interpreted as oscillatory behaviour of system, while period-doubling represents the situation when cycles of period 2, 4 etc. appear. It may lead to chaotic, unpredictable behaviour of system.

I'm going to limit my answer to biology since that's what I know about.
This is a surprisingly hard question to answer, especially in ecological (including epidemiological) and evolutionary systems, because it's very hard to be sure that you know enough about an ecological system to prove that the dynamics you're seeing are chaotic, let alone reliably inferring the existence of bifurcations. In ecology, the most reliable examples I know of are experimental, i.e. Fussman et al. 2000 (Hopf bifurcation — I do know that's not what you're looking for) and Cushing et al. 2001 (period-doubling bifurcations).
Beyond that, I looked for reasonable-seeming papers that at least referenced a particular biological system. This is not a perfectly reliable approach, as lots of modeling papers will use an empirical system as loose "inspiration" for a purely theoretical investigation of some model or set of models.

it has long (since the 1980s) been suggested that infectious disease epidemics can undergoing period-doubling bifurcations due to seasonal forcing or many other mechanisms (Aron and Schwartz 1984) [classically measles, with its very high $R_0$ and seasonal forcing through aggregation of school children, was the poster child for this phenomenon], although strong evidence that this is the dynamical mechanism for a particular disease is hard to pin down. Aguiar et al (2009) gives one example that involves some reasonable biology for dengue.
Guill et al. 2011 (Neimark-Sacker, Pacific salmon) and Kamimoto et al. (period-doubling, red coral) are two papers that are based at least loosely on evidence from real ecological systems, and use models to illustrate the plausibility of certain bifurcations
chaos and bifurcations are a little easier to pin down for within-organism dynamics, because the systems are more controllable/easier to experiment on/the models may be a little more tightly linked to the actual biology (although this may be my ignorance speaking), e.g. Ryashko and Slepukhina (2017) mention Neimark-Sacker bifurcation in the context of stochastic neuronal dynamics; Quail et al 2015 discuss period-doubling in (stochastic) cardiac systems.
two other examples of putative period-doubling bifurcations: cAMP waves/communication in slime models (Dictyostelium) (Goldbeter and Martiel 1987) and katydid chirping (stridulation) (Sismondo 1990).

Aguiar, Maíra, Nico Stollenwerk, and Bob   W. Kooi. “Torus Bifurcations, Isolas and Chaotic Attractors in a Simple Dengue Fever Model with ADE and Temporary Cross Immunity.” International Journal of Computer Mathematics 86, no. 10–11 (November 1, 2009): 1867–77. https://doi.org/10.1080/00207160902783532.
Aron, Joan L., and Ira B. Schwartz. “Seasonality and Period-Doubling Bifurcations in an Epidemic Model.” Journal of Theoretical Biology 110, no. 4 (October 21, 1984): 665–79. https://doi.org/10.1016/S0022-5193(84)80150-2.
Cushing, J. M., Shandelle M. Henson, Robert A. Desharnais, Brian Dennis, R. F. Costantino, and Aaron King. “A Chaotic Attractor in Ecology: Theory and Experimental Data.” Chaos, Solitons & Fractals, Chaos in Ecology, 12, no. 2 (January 2, 2001): 219–34. https://doi.org/10.1016/S0960-0779(00)00109-0.
Fussmann, G., S. P. Ellner, K. W. Shertzer, and Jr N. G. Hairston. “Crossing the Hopf Bifurcation in a Live Predator-Prey System.” Science 290 (2000): 1358–60.
Goldbeter, A., and J. L. Martiel. “Periodic Behaviour and Chaos in the Mechanism of Intercellular Communication Governing Aggregation of Dictyostelium Amoebae.” In Chaos in Biological Systems, edited by H. Degn, A.V. Holden, and L.F. Olsen, 79–89. Springer, 1987.
Guill, Christian, Barbara Drossel, Wolfram Just, and Eddy Carmack. “A Three-Species Model Explaining Cyclic Dominance of Pacific Salmon.” Journal of Theoretical Biology 276, no. 1 (May 7, 2011): 16–21. https://doi.org/10.1016/j.jtbi.2011.01.036.
Kamimoto, Sayomi, Hye Kyung Kim, Evelyn Sander, and Thomas Wanner. “A Computer-Assisted Study of Red Coral Population Dynamics.” arXiv, September 30, 2020. http://arxiv.org/abs/2008.08011.
Quail, Thomas, Alvin Shrier, and Leon Glass. “Predicting the Onset of Period-Doubling Bifurcations in Noisy Cardiac Systems.” Proceedings of the National Academy of Sciences 112, no. 30 (July 28, 2015): 9358–63. https://doi.org/10.1073/pnas.1424320112.
Ryashko, Lev, and Evdokia Slepukhina. “Noise-Induced Torus Bursting in the Stochastic Hindmarsh-Rose Neuron Model.” Physical Review E 96, no. 3 (September 14, 2017): 032212. https://doi.org/10.1103/PhysRevE.96.032212.
Sismondo, Enrico. “Synchronous, Alternating, and Phase-Locked Stridulation by a Tropical Katydid.” Science 249, no. 4964 (July 6, 1990): 55–58. https://doi.org/10.1126/science.249.4964.55.

Thank you very much for the answer and references!

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


text:
Do animals only breathe through one nostril at a time like humans?
Humans breathe through one nostril at a time.
Do non-human animals also do so, or do they breathe through both nostrils at once? Has any actual study been conducted on this topic?

From the explanation given here (which you should definitely have a look at if you haven't yet), there is really no reason to expect that it would be any different in other mammals or at least primate. However, I doubt we will find a study that investigates this question though as it is extremely specific and I would guess of little interest to most people! My best guess that probably all mammals do that! By the way, there is a Ted talk on how dog smell

Humans do breath one nostril at a time...generally. Those who practice Yoga tend to train themselves to control the side of the nose through which they breath.

Suggested edits: correct spelling "breathe" in title; change "animals" to "non-human animals" in title and question (humans are animals too!)

The post linked by @Remi.b says

The nasal cycle is a natural ultradian cycle (see here and here. Not only is it present in humans, the nasal cycle has been observed in rats, rabbits, domestic pigs, cats and dogs (see references in Eccles 1996).

Proceeding to Eccles 1996 (p. 372):

The nasal cycle is not only limited to the human nose, as it has been found in the rat and rabbit [31], the domestic pig [32, 33], the cat
  [34] and the dog [35], and appears to be a universal phenomenon at least in all mammals and possibly other animals.
  ...

Bojsen-Moller F, Fahrenkrug J. Nasal swell bodies and
  cyclic changes in the air passages of the rat and rabbit
  nose. Anat 1971; 110: 25–37.
Eccles R. The domestic pig as an experimental animal
  for studies on the nasal cycle. Acta Otolaryngol (Stockh)
  1978; 85: 431–436.
Campbell WM, Kern EB. The nasal cycle in swine.
  Rhinology 1981; 19: 127–148.
Bamford OS, Eccles R. The central reciprocal control
  of nasal vasomotor oscillations. Pflügers Arch 1982;
  394: 139–143.
Webber RL, Jeffcoat MK, Harman JT, Ruttimann UE.
  Demonstration of the nasal cycle in the beagle dog. J
  Comput Assist Tomogr 1987; 11: 869–871.

A Pubmed search for '"nasal cycle" animal' gets a total of 18 hits, including refs 32 and 35 above, as well as

Spontaneous nasal oscillations in dog. A mucosal expression of the respiration-related activities of cervical sympathetic nerve. Asakura K, Hoki K, Kataura A, Kasaba T, Aoki M. Acta Otolaryngol. 1987 Nov-Dec;104(5-6):533-8.
Proceedings: Studies on the nasal cycle in the immobilized pig. Eccles R, Maynard RL. J Physiol. 1975 May;247(1):1P.

A bit more digging forward & backward through citations finds the article on cats (also by Eccles):

R. Eccles & R. L. Lee (1981) Nasal Vasomotor Oscillations in the Cat
  Associated with the Respiratory Rhythm, Acta Oto-Laryngologica, 92:1-6, 357-361, DOI: 10.3109/00016488109133272

You might find more if you poke around (Google scholar/Pubmed, look at citations backward & forward, try search terms like "'nasal cycle' bird" or "'nasal cycle' reptile"), but at this point I doubt that anyone's bothered to check this in non-mammalian animals ...

Good answer (+1). Citing the post I cite, you proved wrong my assumption that we would not find a reference on the subject.


text:
Fluctuations in disease burden of respiratory viruses (especially influenza/coronaviruses)
Compared to peaks in terms of disease burden (morbidity and mortality, or incidence of severely symptomatic cases and deaths caused by a viral strain within a population), is the relatively light burden of most endemic respiratory viruses due to
(a) a high level of population immunity
(b) the selection of variants that are less virulent
(c) something else?

Comments are not for extended discussion; this conversation has been moved to chat.

Each cam play a role.
a:  Population immunization.  By this I mean evolved resistance.   Measles was not a big deal for Europeans.  But when they brought measles to Hawaii it killed 80% of the population.  Europeans had evolved resistance to measles; a degree of intrinsic immunity.  Populations that co-exist with a pathogen for a long time can evolve a degree of intrinsic immunity.   There are viruses to which humans have little intrinsic immunity, like Ebola.  We have not coexisted with Ebola for long.
b.  Variants that are less severe.  Nepalese peacekeepers brought cholera to Haiti.  Usually with cholera you pour out feces and die, but these soldiers were deemed fit for duty.  They had a less virulent strain and they were carriers.  That strain reverted to massive virulence in Haiti because they had a transmission advantage there.  But in circumstances where sick people are less likely to transmit disease because they are not getting out, less severe variants have an advantage as regards transmission.  As regards respirator viruses, this is probably relevant to the common cold - if it leaves you well enough to go to work, you will transmit it.
C:  Immunization.  Of vaccines US children get, 11 are to respiratory viruses or bacteria.   They can be bad diseases if you catch them but because of mass vaccination they are rare.  If we stopped vaccinating, they would eventually come back.  Except for smallpox, hopefully.

Neither have ebola coexisted long with humans. Population and pathogen usually mutually adapt or one or bothgo extinct.


text:
How common are boy, girl twins?
In the human population, if you meet someone how likely are they to be a twin with someone of opposite sex?
That includes non-twins, not just people who are twins.

Tried Googling but just came up with probability of boy/girl twins vs other twins

The answer will vary a lot by time and location because of changes in the use of fertility treatments, which increase the proportion of twins enormously, and changes in maternal age: from 1980 to 2009 "[twinning] rates [in the US] doubled among non-Hispanic white mothers, rose by about one-half among non-Hispanic black mothers, and by one-third among Hispanic mothers"(US CDC). Globally, "Researchers analysed records from more than 100 countries and found a substantial rise in twin birthrates since the 1980s, with one in 42 people now born a twin, equivalent to 1.6 million children a year. According to the study, the global twin birthrate has risen by one-third, on average, over the past 40 years." (Guardian, Monden et al 2021).
A twinning rate of 15/1000 looks like a reasonable global average.

Taking this information as true: given 15 pairs of twins and 985 single births, (2 × 15/(985 + 2 × 15)) ~ 3% of babies born are twins. Identical (monozygotic) twins are always same-sex, but are at least 10x less common than dizygotic twins, so we can ignore them for a rough estimate. Given a 50/50 sex ratio (I think this is true/close enough for dizygotic twins), 1/2 of twins have an opposite-sex twin, so 1.5% of people are part of an opposite-sex twin pair.
So about 1 out of every 68 people is a member of a male-female twin pair.
Monden, Christiaan, Gilles Pison, and Jeroen Smits. 2021. “Twin Peaks: More Twinning in Humans than Ever Before.” Human Reproduction 36 (6): 1666–73. https://doi.org/10.1093/humrep/deab029.

Of every 30 births, there will be 31 babies if 1 in 30 is a twin gestation. You also ignore the fact that this number reflects fertility treatments and IVF which is more common in higher income brackets of wealthier nations. Many of the more successful fertility treatments were not available, say, 40 years ago, so the age of the individual matters. Taking that into account, it depends on a lot more than one or two numbers. It depends on where the individual is from, their economic background, their age, and more.

I feel like I've accounted for your first sentence (I said that 2/31 babies were twins). I know that this number will vary a lot, but I don't expect that it's really possible to get more than an approximate answer to this question anyway ...

I've updated. (I don't understand where the 1/30 number came from - I looked at the original source, but it seems out of sync with the Monden paper - maybe a twins vs births confusion somewhere along the line)

I didn't see the calculation that you made in either of your sources. "...but I don't expect that it's really possible to get more than an approximate answer to this question anyway..." Neither do I, but you did anyway: "So about 1 out of every 68 people is a member of a male-female twin pair." The better answer is, it depends on too many factors to say with any degree of even speculation.


text:
What causes the activation of "Late acting deleterious genes" in late age but not in young age, whose accumulation causes ageing according to Medawar?
Sir Peter Medawar proposed that aging is the byproduct of "late acting deleterious genes". Evolution is good at weeding out genetic mutations that are harmful at an young age, before the organism has a chance to reproduce, because the organism will not survive to pass on those genes (genes that are weeded out are genes that reduce fitness, confer disability and generally reduce chance of living long enough to reproduce). However, genes that exert their effect at a later age pass through the sieve of natural selection, because natural selection cannot act on them. According to Peter Medawar it's the accumulation of such late acting deleterious genes that causes aging.
I have two questions: What kind of "genes" are we talking about (whose accumulation in late age and its deleterious effects lead to ageing)? Genes with some essential function at young age: such as genes involved in reproduction, survival, functioning of organs etc - or "neutral" selfish genes (i.e genes that are "neutral"or have non-essential functions during the organism's youth, but individually  mildly deleterious  during late age) that kind of "hitched a ride" to the next generation? These kinds of "neutral genes" could arise over evolutionary time simply due to genetic drift?
Second question: What causes these late acting genes to become activated at late age (but not at young age)? Epigenetic landscape in late age, internal biochemistry? Is there any experimental evidence, and examples of such genes? I am guessing they are mildly deleterious on their own but collectively debilitating.

Austad, Steven N., and Jessica M. Hoffman. 2018. “Is Antagonistic Pleiotropy Ubiquitous in Aging Biology?” Evolution, Medicine, and Public Health 2018 (1): 287–94. https://doi.org/10.1093/emph/eoy033.

It's not that genes become 'activated' at late age, but that they aren't relevant until late age, so high performing versions aren't selected for and poor performing versions aren't selected against. As for which genes, we can see some in the answers to another question,
What is the longest-lasting protein in a human body?
The accepted answer is crystallin, in the lens in your eye. These proteins eventually cross-link and degrade, leading to cataracts and blindness, which decreases fitness. Newts can regenerate their lenses, and more stable versions that take longer to degrade could presumably exist, so it's biologically possible to avoid this loss of fitness. However, doing so wouldn't affect the fitness in the first ~50 years of life, so selection can't maintain those mechanisms against genetic drift.
Crystallin is one example of long-lasting proteins, and those are just one example of how genes can have fitness costs that don't reveal themselves until late in life. When 'accumulation' is used in the context of Medawar's hypothesis, it refers to the accumulation in the population over many generations of these late-acting mutations, because natural selection can't remove them the way it can early-acting mutations.

Maybe more precisely, it isn't that the genes aren't relevant until late age, it's that the deleterious effects aren't relevant until late age.

I went back + forth on how to phrase that, and decided to be more focused on the OP's misunderstanding. Also, if we think of, e.g. "a gene to regenerate crystallin", it doesn't exist because it wouldn't be relevant to fitness until late age

That's fair; I agree we do not need to get into all the detailed debates about what exactly a "gene" is for this Q&A.

I thought that it was mutations accumulated throughout life that affected genes. Which genes are responsible for ageing, and whether they are activated or their product is just changed, I have no idea, but I find an answer solely in terms of damage to long-lived proteins very constrained. Could you cite references that this is the modern interpretation of Medawar's hypothesis, and perhaps mention other ideas about ageing.


text:
What is this white/translucent with brown back, larva/worm creature I found, in the UK, on my lettuce?
I'm in United Kingdom, East Anglia. I've just started to grow lettuce in my back garden, taking my first harvest today, I found one of these creatures:

They have a distinctive brown/white mark along the top of their behind. The black dot appears to be its front, as it scouts with that, and moves in that direction most of the time. This is about 10mm long, give or take 50% depending on how stretched out it is.
They appear to have transparent skin, as I think we can see its organs in there. It moves almost peristaltically (similar to a worm), but with direction, not just flapping around, and seems to like the undersides of things.
They're not particularly segmented, though they have those tiny, tiny ridges as you can see. And there are no legs or meaningful features to speak of on its underside. They were also slightly sticky, with a white-ish secretion.
I have since looked and found a few amongst the other lettuce, which all look incredibly similar to this. Usually hiding inside the outer leaves, but not exactly an infestation (yet!). They don't seem to be on any other plants at the moment. There's no evidence that they've eaten any leaves, or anything, currently.
I have done a lot of searching and attempts to identify, but I can't for the life of me find this online. My amateur guess is some sort vermiform fly larva, but it could be anything from a baby caterpillar to a worm, for all I know. Any help in narrowing it down, or especially in finding out if I should be worried for the plants, would be helpful.

I confirm it is most likely Episyrphus balteatus, was searching for the same-looking larva identification (the colors may vary depending on what it feeds on), but was eventually able to grow mine to a mature animal. Photos of both stages attached.

Interesting! I can't deny that these larvae seem to be a near-perfect match - Thanks!

It's a kind of hoverfly larva (don't know which one, maybe Episyrphus balteatus), they eat aphids on cabbages.
Image on wiki commons

Hi Claudia, welcome to Bio.SE & thanks for providing a response to this question. Though I agree that your answer appears to be a valid guess, it really comes across as just that: a guess. What we're looking for in this SE community are answers that are well-supported and descriptive. Please [edit] your answer to provide details (i.e., why your answer is right and what characteristics led you to your conclusion) and either citations or links to reputable support for your answer. Our goal is to educate others, so the more info you give the better.

Editing your post will surely result in more positive response from our community. Please see How do I write a good answer? and suggestions for writing [tag:species-identification] answers. Thanks!

I think this answer is right, so I've added a link to a picture. Feel free to roll back if you disagree.

They indeed really look like "maggots": fly larvae (number 15 in the "section 2" figure: https://entomology.ca.uky.edu/ef017.
These ones look to me like Drosophila larvae, but much larger than the common laboratory fruit fly, so they are probably a different genus.
Maybe they are simple housefly larvae, like in this video: https://www.youtube.com/watch?v=F6TcIybY7Qo

Thanks for the interesting link, but could you explain why it is nr 15 and not nr 16?

@RHA, I'm familiar with the typical shape of a fly larva (number 15). Admittedly, I'm not familiar with the aspect of aphid predator larvae (number 16), which could have very similar features. The description for number 16 mentions "they tend to have green tinged bodies" while for number 15 it mentions "a cream to white body", which better matches the photos given in the question. I would not exclude number 16, though.


text:
Why does supercoiled DNA run faster?
The DNA exists in linear and cirular forms. The latter form has interesting feature called Supercoiling. The more number of writhe makes it more supercoiled because of which it gets more compact. Hence the supercoiled DNA runs faster compared to other forms in a gel electrophoresis experiment.
But why does the circular DNA run slower than linear DNA? Isn't circularity supposed to make it compact?

I thought circular DNA would run slower because it isnt compact? In order to make linear DNA, dont you need to apply some type of chemical to "straighten" it out and get rid of the proteins attached to it, like SDS? So wouldnt the faster one in the gel be the one with less proteins on it, assuming they are both the same length of DNA and so on?

You have different conformations of circular DNA that result in different bands of the same thing: Supercoiled, relaxed and linear. Supercoiled runs very quickly by comparison, and relaxed or linear plasmid run slowly, but you'll find that linear DNA runs faster than the open circular DNA, which is often a result of DNA damage like single-stranded nicks. Remember: Your DNA is moving through a polymer matrix, so the more potential to get "caught" in the pores, the slower net movement.

Doesn't it follow the logic: writhe 2 > writhe 1 > writhe 0. Here '>' means faster. Then writhe 0 means circular dna which has to be slower just compared to writhe 1 dna and linear dna should be the slowest. Isn't it so?

Can you write a title that more closely relates to the question? Reading the title, I thought the question was about snakes.

It's compact so that it can go through faster agarose pores.

To understand this, you have to understand how an agarose gel is able to effect the size separation of DNA in the first place.
The reason agarose gels work to separate DNA based on size is that the electric field produced the electrophoresis machine is imparting force on the DNA. The effect of the increasing charge for DNAs with increasing nucleotides is offset almost exactly by the increasing mass of those larger DNA molecules, so in the absence of the gel, all pieces of DNA would migrate through the apparatus at a constant rate.
The reason they don't is because of the mesh framework of the agarose gel. This is like a dense forest or a large number of sieves with random sized holes. There's small holes (of varying size) and in order for large pieces of DNA to work its way through the gel, it has to weave through these pores. Smaller pieces of DNA can go through smaller pores, so they take a faster, more direct path, while larger pieces have to make detours, and even when they find a pore they can fit through have to spend a bunch of time flopping around before they can stuff themselves through the pore.
So it's not strictly speaking "size" or "compactness" by which the agarose gel separates molecules, but instead it's the ability of the piece of DNA to navigate through the mesh of agarose molecules. While relaxed, circular  DNA is more compact than an extended linear DNA of the same nt length, that doesn't necessarily mean that it has an easier time working its way through the network.
For example, a linear piece of DNA can orient itself so it goes "end first" through the mesh. Once the end of the DNA goes through a pore, it's relatively easy to pull the rest of the DNA through the same pore, as compared to trying to bend the DNA and pull it "sideways" through the pore - you have to remember that on molecular scales, DNA is rather stiff. You can't kink it in half very easily, so a piece of DNA that has to go through the pore "sideways" takes much more space than one that can be threaded through end-wise, even if you bend it as much as possible into a hairpin.
With a relaxed circular DNA, there's no end, so it's always going through the pores "sideways" so it's limited to the larger pores. In addition, it's large and floppy, so it takes quite a while to go through the pores that are there. When you add supercoiling, you don't fix the issue with going through pores "sideways", but you do limit the flopping around it does, so once you do find a pore of a usable size, you get the rest of the DNA through faster. In fact, with enough supercoiling you reduce the time spent flopping around enough that it goes through the agarose even faster than the linear DNA, which - while it can fit through smaller pores - still spends a bunch of time flopping around instead of going through the pore that it's started to go through.


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What sea animal is this?
I am in a remote village and a young boy (second pic holding tail) says this thing is his friend. This creature is safe, we held it for pictures and released it after. None of us know what this is and we do not know who to contact. The young boy plays with it every day so it is safe but it still is strange.
These are salt water shores, not fresh water.
Someone mentioned a dugong but it is far too skinny I think. I didn't get pictures of the head as we didn't know if it had sharp teeth.
Image is taken in a remote village in Kavieng, Papua New Guinea.

The creature's head looked like this.
Link:
 polartrec.com/files/members/cara-pekarcik/images/dsc_0160.jpg
I'm no expert, but I don't believe seals are in Papua New Guinea, it's almost a hybrid of few things.

Clearly a merman :p.

It is sure something that looks like a mammal... check any dolphin species or something like a sirenid... manate amybe? or something like seal.

The vertebral column is so pronounced! Doesn't appear like a dorsal fin.

Do you have a picture of its face?

I wish we did but all of us were too scared in case it might've had sharp teeth, it wasn't aggressive at all but since we have no medical nearby it was too risky

If you have any additional photos, please provide them.

Also, please orient us. We are looking at the dorsal (i.e. back) side of the animal, aren't we?? (Or is the animal upside down?)

Did you notice whether it had a blow hole?

Hi sorry it's 1am so my replies are slack, but yes you're looking at the dorsal side, and it did not have a blow hole. If I were to describe the head it looked awfully similar to a leopard seal but that's just a comparison. There weren't any other fins visible either. Such a strange thing we saw! Funnily enough, mermaids are huge in this culture and it was suggested by locals haha

@Jude Thanks for the responses. If possible, please take additional photos of this animal. Since you said it comes to play with the kid every day, I assume you'll have more opportunities to photograph?

What on earth is happening here??? This animal isn't any kind of seal (because of the dorsal fins) and it isn't any kind of dolphin because it doesn't have blow-hole and a find on his spine.... I strongly recommend that it is a sirenid... like sea-cows, but it is small. Because as you mentioned it plays with kids it maybe be a juvenile sea-cow... that's my opinion and I am not 100% sure :). Very interesting case by the way.

Will definitely be taking more pictures this afternoon, it's raining today but I don't think that will make a difference. Im a little worried as villagers believe this is genuinely a siren/mermaid/sea spirit in their culture and want to kill it as it brings death - very hard to persuade them and it sucks because it's a gentle little guy. Keep in mind this is a very isolated village and they were brought up on these beliefs unfortunately. The spine also was naturally pronounced - in the first pic we didn't hold up the tail

I also don't know how to link pictures but the creature head looked like this https://www.polartrec.com/files/members/cara-pekarcik/images/dsc_0160.jpg   And I'm no expert but I don't believe seals are in Papua New Guinea... its almost a hybrid of a few things. I'd also like to apologise to the person who edited my post, thank you! English is my third language so you helped me out

It would be interesting to know how long this animal has been around, and if it has been observed feeding, whether it looks healthy or not. I believe the provided answer is right (dugong). I read on wikipedia: "The dugong is a national animal of Papua New Guinea, which bans all except traditional hunting." -> Killing "mermaids" is not permitted, and I hope the animal will be treated with due respect.

This is off topic, but could you contact the Wildlife authorities and bring this creature to their notice. I think this is the best thing to do when one finds an unidentified animal and there's risk of death. @Jude

Could it just be a dead Pacific sleeper shark? On its back, given the colouration size, and the fin is set as a fish not a mammal they are twisting is!

It's probably a dugong, based on the location, lack of a dorsal fin, split tail, lack of a blowhole, and narrowing of the snout.
The prominent vertebral column looks unusual, but that might come from the strange posture it is being held in or from malnutrition.
This publication from the Australian government shows necropsy of several dugongs (note, this PDF contains graphic necropsy photographs), including one that was malnourished (see page 53). This individual shows some of the characteristics of the OP, including pronounced vertebral column and a clearly visible neck. The text notes the presence of these features as well.

Adult dugongs showing signs of malnutrition: a) with neck becoming visible
  and prominent backbone

Sadly, the other dugong pictures I found that look most like this specimen are also ones from news sources that are often dead or injured or needing some other human assistance. Some other examples:

Queensland couple come to rescue of beached dugong
Dugong dies from propeller wounds
Trang fishermen asked to help slow-moving male dugong
Rare Dugong saved in Maliangin Community Marine Sanctuary

Some pictures do show a prominent vertebral column near the tail in animals that seem otherwise healthy, but those images don't show the rest of the animal well (thanks to @theforestecologist):
http://www.oceanwideimages.com/images/11147/large/dugong-58M1444-20D.jpg
http://www.oceanwideimages.com/images/11144/large/dugong-58M1444-17D.jpg
As an extra piece of trivia, dugongs and their manatee cousins have been closely associated with mermaid legends.
Of course, a better picture of the animal's head, especially in profile, would make identification much more clear.

I knew it was a dugong... but a juvenile, since it doesn't have so much fat tissue that adults dugongs have... I believe that the unusual spine is because of the lack of food. Maybe because it is young its mother didn't learn to it the main seaweed nutrition that dugongs have.

Most pictures I can find from dugongs have more moon like shaped tails whereas the OP's picture clearly shows a strong split. Based on which pictures did you think that these tails were similair?

I agree about the tail, but perhaps this is really just an illusion from the way the animal is being held in the OP's pictures? I did find two pictures (here and here) that show a strongly pronounced spinal ridge leading from dugong taild like in the OP's photos.

I'm going to withhold an upvote for the time being due to the strangeness of the OP's specimen. Though I think you're likely ultimately correct that this is a dugong, I'd like to see you present a stronger case (e.g., address the following: skin color, ridge along back [feel free to use my photos], Rick Beeloo's comment about the tail, the narrow neck, the pointed nose, etc.).. I also don't think your photos are at all convincing :p

@theforestecologist Thanks for the extra pictures, I'll add them, and some as well as some more argument. I may wait a bit, though, for OP to post some more pictures, I think they will be quite helpful and the only way to make this definitive. Partly this is just a matter of process of elimination. There is no way this thing can be a seal, there is no seal with a tail like that (and no seals that live where OP is, though that's less convincing). There is no way it can be a dolphin/porpoise/etc because there is no blowhole. Etc..

@RickBeeloo In the linked Wikipedia article and many other (somewhat more reputable sources), one of the best differentiating features of dugongs versus manatees is the shape of their tail; dugongs have a fluked tail, manatees do not. I think the "fluke" is exaggerated in the pictures because of how the tail is held, like theforestecologist mentions.

Great find with that necropsy paper. You've convinced me. +1 for the effort! :D. Perhaps request to reproduce the malnourished dugong photo here?

@theforestecologist Thanks for the cleanup edits, much appreciated. This answer sort of ballooned into quite a mess. I think I won't bother requesting to reproduce the photo, unfortunately; it's an official Australian government publication, not a scientific one, that reserves all rights and requests written requests in the post for reproduction.

After looking over the links you included, I'm certain your answer is the right one. The prominent spinal ridge on this specimen seems to indicate starvation.

I know you said there was no blowhole on this animal but is it possible that the blowhole was closed and just a slit so not noticed?
The tail looks very much like a dolphin species but the low crest along the spine and no dorsal fin in sight is very puzzling. Your description of the head and your region of the world made me think of the Australian snubfin dolphin (Orcaella heinsohni) that's a recent discovered dolphin species near Papua New Guinea.
From New Guinea's Newly Discovered Species (from 2011)

In the waters south of New Guinea, an unexpected discovery was made in 2005. The snub-fin dolphin, Orcaella heinsohni, was once thought to be a member of the Irrawaddy species of dolphin. However, researchers found that snub-fins have different coloration, skull, fin and flipper measurements. That makes them the first new dolphin species recorded for at least 30 years. A skull of the new dolphin species was collected from Daru, Papua New Guinea. Scientists believe these dolphins occur mainly in protected, shallow, coastal waters, specially adjacent to river and creek mouths. The expected range of O. heinsohni is the coastal zones of Australia and Papua New Guinea.

Here's an image of the head shape.

Courtesy Daniele Cagnazzi
(from Support Our Snubfin Dolphin)

Could it possibly be a steller's sea cow
Well by the looks of it

spinal cord
the mouth
the fork tail
grass which it feeds on if u see the water in the photos
Well i could just be wrong but who knows

I think is blackchin guitarfish. Like that. But this picture not enought.

I completely disagree. It isn't a Blackchin guitarfish.

Please add support/citations for your answer. As of now, this appears to be an unsupported guess and will likely be downvoted. Please improve/expand upon your answer . Thanks.


text:
How is the breakdown of lactose regulated at the gene level?
How is the breakdown of lactose regulated at the gene level?
This is my answer: Without lactose in the cell, the repressor protein binds to the operator and prevents the read through of RNA polymerase into the three structural genes. When there is lactose in the cell, lactose binds to the repressor. This causes a structural change in the repressor and it loses its affinity for the operator. Thus, RNA polymerase can then bind to the promoter and transcribe the structural genes.
But I'm not sure if this is right...

Welcome to Bio. Homework questions are warmly welcomed here at Bio, barred you show your research efforts so far. We are not here to simply do the homework for you. If you can provide us with the things you do know, we can fill in the gaps for you. Good luck! I'm putting this question on hold for now. After you've made edits to this post we can re-open it for you. Please don't make another separate question out of it, because then other users cannot see the question history.


text:
Can you identify this Illinois wasp?
I live in northern Illinois and had these guys appearing in my room. No facial markings and they seem non agressive.
About 2cm in length with off white u shaped markings below it's waist and a single white line a few segments down.

It looks to me as Potter Wasp (or mason wasps), the Eumeninae, are a cosmopolitan wasp group presently treated as a subfamily of Vespidae, but sometimes recognized in the past as a separate family, Eumenidae.
Since there is no more info provided and image is not sharp I cannot be 100% sure.

The post displays info about its size now which was previously hidden due to improper usage of markdown.

The online Canadian Journal of Arthropod Identification has an issue covering the Vespidae of northeastern North America (PDF available here: http://biologicalsurvey.ca/ejournal/bmc_05/pdf/bmc05.pdf), with Illinois as a limital point; if you have a stereoscope available and are willing to take a specimen (freezing will work, if you don't want to use poisons), you will get a species name from that work.


text:
Why are these trees leaning, but no trees around them are?

This was observed in Florida.The trees on the left have a distinct lean to them, but none of the other trees in the area are leaning, why is this?
I'm not sure what other information is pertinent or what else I should look for.

Could it be that this location is in close proximity to the sea and that the sea (or a large lake) is located to the right of the picture?

How far away from the ocean are these trees?

@kmm Not close to the ocean. There is a small lake not terribly close (800ft). I'll have to check how much it aligns with direction of leaning.

Related: http://biology.stackexchange.com/questions/35622/what-could-cause-a-forest-of-bent-trees/35627#35627

There are several reasons as to why a tree might lean. Normally, it is a combination of some/all of the points below:

Weight distribution: Depending on the diameter of the trunk and especially the height of a tree, gravity can create problems. So the main question is how the weight of the crown is distributed over the tree's trunk.
Species variability: Different species of trees have different root systems, some go deeper and others don't. The depth and width of the root system are factors to consider when assessing a leaning tree.
Environmental factors: There are a variety of environmental factors that will contribute to a tree leaning. For example, a
tree that leans because it has grown towards the sun often has a curved trunk. The trunk curves due to the tree's ability to adapt over time to the changing
availability of sunlight. Its root system will grow to accommodate the “off center” weight distribution, up to a point. Additionally, storms or constant wind can obviously cause a tree to lean.
Structural damage: Leaning trees that don’t have a “sweep” (caused by wind) but tend to have a fairly straight trunk generally have a history
of structural damage to the root system or storm damage that has
caused the root system to slip, break, sink or simply fail to support the
tree in some fashion. If the trunk appears to enter the ground without
a mound of soil on the side away from the lean, then the root system
has sunk, either from rot, mechanical fracture, physical cutting of the root plate or soil subsidence. If the mound does exist on the back side of the lean, that's a sign that the root plate is being tipped
out of the ground and the roots have failed - either through mechanical wounding or structural failure. As roots break under stress from wind or off center crown weight pushing the trunk away from the soil holding the roots, the up-wind side of the root plate will tip out of the ground.

In addition, it may be worth mentioning that time plays an important role here too. Older trees will have been exposed to the forces of nature and plant pathogens for longer than younger ones so it certainly makes sense to take the life cycle of a tree into consideration, some live longer than others and thus may have been subject to wind while the other surrounding trees weren't "tall" enough to shield off any of the wind etc.
Sources: Georgia Forestry Commission - Leaning Trees - What's up with that

Interesting stuff, I'll have to look at the ages of trees nearby. What really struck me is how spatially localized the phenomenon is though, maybe some sort of localized weather effect.


text:
Hardy Weinberg equilibrium

Hardy Weinberg would predict that the frequency of normal females, to carrier females,
  to affected females for colorblindness is equal to p$^2$ + 2pq + q$^2$=1. You
  were told that q=freq of the recessive allele. If p+q =1 (frequency of the dominant allele +
  frequency of the recessive allele=1 or 100%) and q=.08, what is the frequency of the
  normal allele in the population? What is the frequency of carrier females in the
  population (ie heterozygous females)?

I get that the frequency of the normal allele is p = 1 - .08 so 0.92. However the frequency of carrier females is giving me an unrealistic number. Using p$^2$ + 2pq + q$^2$ =1, the value for pq comes out to be a negative value. Is it safe to just multiply p and q since that is what we're essentially solving for using the full HW equation? This would make the value (.08*.92) = 0.0736. Would that be the way to approach the problem even though it asks for females only?

Welcome to Biology.SE. Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy.

Btw, although the question is quite clear, the phrasing is a bit inaccurate and misleading. Is it the question as written for your homework?

Yes, that is the exact wording of the problem!

check your math, the value for pq comes out to be a negative value is incorrect

Thank you, got the value to be .0736. Would this be correct as to being the frequency of carrier females?

Carrier females= 2pq= 2 x .08 x 0.92
Because carriers say with genotype  Aa (A=dominant, a=recessive)  can arise due to two types of inheritances;one when A is from father and a is from mother and the other when it is just opposite.


text:
Why does double vision when drinking happen?
Why do you see double sometimes when you're drunk?  Its weird because it seems to happen more when you try to focus.

Try to look at something when you're drinking and it barely seems to double up
Try to focus on it more than just immediately, and slowly the image seems to separate
Refocusing on new object seems to re-focus and lets you not see double

Why does this happen?
Edit:
http://www.esquire.com/news-politics/q-and-a/a5711/double-vision-causes-0509/ This seems to imply an inability to focus, however, if I try to refocus on a new object it works out

I don't think it has anything to do with alcohol. Its related with eyes and refocusing from far to near object (and vice-versa). You should change the tags.

I have experienced same thing while practicing mindfulness. When I just look at a flame I could see it as I normally do but trying to focus on it more will cause the flame to double up and yet refocusing will bring normal vision. As @another'Homosapien' said I think it has something to do with vision.


text:
Aspirin - does it inhibit enzyme of thromboxane?
This is a diagram a friend showed me about the drug aspirin, where we were arguing which enzyme it prevents.

Aspirin is known to inhibit the production of prostaglandins. However, it also serves fit as a purpose to inhibit production of thromboxane.
My question is, does the drug inhibit enzyme a to prevent the production of both thromboxane and prostaglandins, or only enzyme B?

Aspirin and some other NSAIDs inhibit cyclooxygenase which is the first enzyme in the prostaglandin/thromboxane biosynthesis pathway if you consider first substance is arachidonic acid (a fatty acid). Generally, arachidonic acid is present in the form of a phospholipid, and if you consider that in the pathway, substance-Y is arachidonic acid and enzyme-A is cyclooxygenase.

From: Heckmann, Lars-Henrik, et al. "Outlining eicosanoid biosynthesis in the crustacean Daphnia." Front. Zool 5.11 (2008).


text:
What kind of "size" does SDS-PAGE separate by?
What is the exact property of the protein that affects migration of bands in SDS-PAGE; is it length, volume, or mass?
For example, will GGGGGGGGGG (glycine 10-mer; mw <600) migrate more or less than WWWWW (tryptophan 5-mer; mw >900)?

The protocol for SDS-PAGE uses a solution of sodium dodecyl sulfate (SDS, also known as lauryl sulfate) to solubilize and linearize folded protein molecules and give them a negative charge that is approximately proportional to the length (and more or less to the mass) of the protein, depending on its sequence. Some sequences may bind the SDS more readily, while others may not, so the relationship between charge and mass/length is not perfect.
The linearized (and often reduced, typically with DTT or β-mercaptoethanol) protein solution is separated by polyacrylamide gel electrophoresis (PAGE), wherein the negatively-charged protein(s) migrate though the pores in a gel due to an electrical field applied across the gel. Smaller proteins run faster, and are visualized (by many different methods) nearer to the bottom of the gel, whereas larger proteins are closer to the top. Typically, a standard molecular weight marker is run alongside the samples of interest so that approximate molecular mass can be gauged. A number of situations may cause the samples to not migrate exactly according to their calculated molecular mass, including high levels of glycosylation, phosphorylation, or other post-translational modifications, as well as variable binding to the SDS as discussed above.

Can you also focus on OP's specific example? Assuming that molecules of SDS is proportional to the length, G₁₀ will bind 2x more SDS than W₅. If you calculate m/z then it is higher for W₅. Since the mw of SDS is higher than average amino acid mw, should the binding of SDS basically overwhelm the effect of the peptide's molecular weight thereby making the separation purely length dependent?

@WYSIWYG no problem, I'll try to get to it later today. It's going to be rather hectic at work.


text:
immune response towards sperm cells
Question 1: Why does the immune system not act on sperm cells as sperm cells are developed after puberty?
Question 2: Does immune response occur when a person's own cells are injected inside their bodies?

Q1: Immune system recognizes gametes as self. Q2: Do you mean filling a syringe with ejaculate and injecting it back into the donor? That would be weird and likely unadvisable, mainly because the proteins, carbohydrates, and lipids found in ejaculate would likely cause an inflammatory response as they are accessing areas, (subcutaneous or intramuscular) that are generally sterile. Also ejaculate can carry bacteria and viruses that could also cause an infection.

@AMR OP is not asking for an advise but presenting a hypothetical situation.

@WYSIWYG Your edit for question two is over specific. Original:  "Question 2: when own cells are injected to same person then strong immune system occurs?" That in no way implies an intravenous injection. That would be an even worse idea as it would likely cause an embolism that would kill you before the immune system had a chance to figure out what was happening.

@WYSIWYG And my comment was not intended for advice. It was to say that it is a bad question to ask. and even if you were looking at it from an actual experimental design perspective, it would be almost impossible to get the permission of an ethics review panel to conduct the experiment. If is also bad in the sense that you could not ascertain what the antigen was even if you did go ahead with the experiment. You would need to isolate individual plasma membrane proteins, lipids and carbohydrates and test each separately to determine what if any antigen was producing an immune response.

@WYSIWYG As there is likely no modern literature published to elucidate question 2, and there would likely not be any ethically acceptable experiments that could determine the outcome. That question should be deleted. Question 1 is simply that the testes are immune privileged parts of the body. While the Wikipedia article speculates that they are immunogenic due to delayed development, the more likely reason is that sperm puts up fewer HLA surface proteins than somatic cells, which would make them a target for NK-cells, as NK's perform quorum sensing to determine whether to kill.

As for immune response elicited in the female http://biology.stackexchange.com/questions/28164/why-white-blood-cells-wbcs-do-not-react-to-foreign-bodies-like-sperm

Body does not act against sperms because the testes are isolated immunologically by the blood testis barrier.
In mumps due to this barrier becoming ineffective due to inflammation, orchiditis (inflammation of testis) may occur and this may render the person infertile in some cases.
Such antigens which are not exposed to body's immune system are called cryptic antigens.
One more example of cryptic antigen is the antigens of the cornea.
For more information see here.
For more you can search for blood testis barrier.
For the second question, immune reaction will occur if the injected cell contains cryptic antigens. If there are no cryptic antigens then there will be no reaction.
For cryptic antigens see here.


text:
Thickness / size / volume of a macrophage
What is the thickness of a macrophage? From some available literature it looks like a macrophage has a 'circular' shape of radius ~10 microns. But I need the thickness to calculate its volume.

volume is a function of r?

BioNumbers is a good database for different values (numbers) in biological systems. From BioNumbers*:
Volume of an alveolar macrophage ( Homo sapiens ) = 4990 (±174) µm3
Diameter of an alveolar macrophage ( Homo sapiens ) = 21.2 (±0.3)  µm
So, your thickness should be (assuming a circular shape of the cell):
Volume/(pi×(0.5×diameter)2) = 14.15 (±1.52) µm
Apparently, the size of the alveolar macrophages varies a lot between different species.

The AM from humans were significantly larger (p < 0.05) than those
  from all other species studied, corresponding to a 4-fold larger cell
  volume of human AM (4990 +/- 174 microns 3) compared to hamster (1328
  +/- 123 microns 3) and rat (1166 +/- 42 microns 3) AM

*
The paper that BioNumber refers to is this:
Krombach, Fritz, et al. "Cell size of alveolar macrophages: an interspecies comparison." Environmental health perspectives 105.Suppl 5 (1997): 1261.


text:
Why are female not competitive for reproduction like males?
I have wondered if competition for mate among males and the race among sperm cells would result in healthy offspring,
why no such mechanisms exist among females and egg cells?
(Even females are genetically responsible for the offspring.)

And generate an oocyte arms race... how? How to outrun a sperm cell as fast as possible?

You are asking two very different things. One is a social, group dynamics construct and one is regarding developmental biology. Decide which of the two you want answered and formulate that single question.

I think the question has been poorly executed, please think carefully about your question(s) and edit to make it clearer

are you talking about humans or sexual species in general? and are you asking about sperm/egg competition or organism competition becasue there are very diffrent?

As @Dexter said, there are examples of species where female compete for the access to the males but most often it is the other way around; males compete for the access to the females.
The reason for this discrepancy is mainly explained by Bateman's principle. Citing wikipedia:

Bateman's principle suggests that in most species, variability in reproductive success, or "reproductive variance," is greater in males than in females. This is ultimately a consequent of anisogamy. Females, especially mammalian females, almost always invest more energy into producing offspring than males invest. Bateman's principle anticipated and is consistent with Robert Trivers's theory of Parental investment—in most species females are a limiting factor over which males will compete. This competition results in some males being more successful than others, leading to greater reproductive variance among males than females

At first, I misread as Batman's Principle and got excited :P

@Dexter It might be the martini, but that made me laugh.

Actually there are lot of examples in which females are competing for mating which also have evolutionary consequences. It is also widely spread in nature. This competition may arise at cellular, molecular, genetic, behavioral level. Quoting from (Stockley and Bro-Jørgensen 2011)

female competition is associated with many diverse adaptations, from overtly aggressive behaviour, weaponry, and conspicuous sexual signals to subtle and often complex social behaviour involving olfactory signalling, alliance formation, altruism and spite, and even cases where individuals appear to inhibit their own reproduction.

Following table taken from (Gwynne 1991) which shows lot of examples in which females are competing

There are many more you can find by just searching on pubmed!

Males in monogamous species don't compete much for females. According to "The selfish gene", monogamy is an evolutionary stable strategy. They tend to only produce the number of kids they can get enough food to rear because those that produce more kids almost certainly can't rear all of them and maybe even 2 of them will starve because of the extra energy of producing the extra kid and of the kids fighting with each other for food. If any of them fight for more than their fair share of food, those who fight back those who fight for more than their fair share will be selected for because there's nothing to lose in fighting back for more than their fair share let alone their fair share. After that, those that start a fight for more than their fair share will be selected against because of the possibility of losing the fight and getting even less food, which is why they don't start a fight for more than their fair share of food in the first. At an evolutionary stable population size, each individual can on average get enough food to rear 2 offspring. It's an evolutionary advantage for a female to pick a male that doesn't already have another mate because if she picks a male who already has another mate, there will be 3 parents so they can get enough food to rear 3 offspring but each one will only have a 50% chance of being her own, making it pretty impossible for a male to get a second mate. Since there are about the same number of males as females, almost all males get one mate with almost no left over males or females. Males who fight against any male who tries to take their mate away from them are selected for which in turn causes males of a monogamous species who fight another male for a second mate to be selected against.
According to https://www.dailymotion.com/video/x1e19qg_bonobo-ape-our-closest-relative-nature-documentary_tech, bonobos are also peaceful. All the members of a group have sex with each other all the time and no male knows which baby is his removing the advantage in males fighting. They're probably also peaceful for a similar reason, that those that fight back to not get less than their fair share of food are selected for which in turn causes those that fight to get more than their fair share to be selected against.


text:
Is there a maximum limit of connections between a pair of neurons?
As neurons fire and work together, their connections strengthen. I was wondering if there was a limit on how connected neurons can be. If these neurons were constantly connecting then surely there would be an overload of connections at some point?

There's several ways neuronal connections can strengthen: growing the spine, increasing the amount of vesicles that carry neurotransmitters at the synapse, sensitizing and increasing the amount of receptors and yes creating more spines and synapses also.
Roughly, neurons can make tens of thousands of connections to multiple neurons the size of each spine is estimated to be between 0.01 µm3 to 0.8 µm3.
You are correct in saying that as life happens the connection would tend to grow to max and not encode anything anymore, however the brain seems to re-normalize all of its connections during sleep through special membrane channels.
Check out:
https://en.wikipedia.org/wiki/Neuron (especially the connectivity part)
https://en.wikipedia.org/wiki/Long-term_potentiation
https://en.wikipedia.org/wiki/Long-term_depression
https://en.wikipedia.org/wiki/Ion_channel