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Why do animals only eat some parts of their food?
For example monkeys/apes only eat part of a fruit and then throw the rest. Cats (big and small species) only eat some parts of their prey and then they abandon it.
Humans on the contrary leave as few leftover as possible.
What do we know about the parts that animals eat ? and how do we know it ?

Humans leave as few leftovers as possible? No, they definitely do not. They throw away a lot of good edible food.

Animals that abandon some food certainly have quite a lot of food at their disposal and they can be choosy and eat only the best. I'd be surprised that an animal that is starving would throw away some good food. If this is the case, it is probably a case where the animal is not adapted to its environment and do not recognize the good quality food as being good quality food.

It all depends on hunger. As in comment (@Remi.b), it has been mentioned, an animal won't throw if they are starving.

For example monkeys/apes only eat part of a fruit and then throw the rest.

Monkeys and apes can differentiate between good and bad part of the fruits. So, they eat what they can and if the color looks different (or however they differentiate them) they will throw the rest of them.

Cats (big and small species) only eat some parts of their prey and then they abandon it.

Cats in general are very picky eaters. They actually have a very short digestive tract, so, they need something easy to breakdown into energy rather than complex processes of digestion. Their main food consist of meat, they leave the inner organs as such.
Source:

http://en.wikibooks.org/wiki/Wikijunior:Big_Cats/Complete_Edition
http://bigcatrescue.org/feed-cats/

Image Source:

http://wordpress.as.edu.au/rspiers/2013/05/22/comparing-animals-digestive-systems/
http://cats56971.wordpress.com/2012/10/30/eating-habits-of-a-african-lion/


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Haidinger's brush: Is this a by-product of the eye's physics, or are there any evolutionary grounds for it?
The human eye is, very subtly, sensitive to the polarization of light. This is  an effect known as Haidinger's brush (see Wikipedia article of this name).
What, if anything, is known or at least intelligently speculated about the evolutionary "grounding" for this effect?
Another way to put this question: Some cephalopods and the mantis shrimp have sight that is sensitive to polarization of light and this sense is clearly begotten by evolutionary forces as it helps these animals detect prey and predators. So, is our subtle ability to perceive polarized light a leftover from a genetic forebear that benefitted from this ability? Or is it simply an artifact of the physics of the eye? The physics of Haidinger's brush is quite different from the topology of retinal cells that confers this ability in cephalopods and others I have read about.
A second question and related is: what is our nearest common genetic forebear that is known to exploit polarization sensitivity of its sight?

According to the link you provided, the phenomenon Haidinger's Brush seems to be associated with the macula of the retina. The yellow color of the macula may explain the yellowness of Haidinger's Brush. This suggests to me that the brush may be an artifact of the structure of the eye, and others have claimed that Haidinger's brushes probably do not have any ecological significance (Greenwood et al. 2003). If the brushes do not have an ecological significance, then they are very unlikely to have any evolutionary significance.
The brushes may be visible to other primates, such as Macaques (Snodderly et al. 1984), as they have a macula structure very similar to the human macula. This leads me to think the phenomenon would also be potentially visible to other primates such as chimps and gorillas. If so, then our nearest ancestor (forebearer) that could potentially see the brushes would be the common ancestor of humans and chimps.
For a broader review of polarized vision and underlying evolutionary hypotheses, the paper you linked to by Cronin et al. (2003) is a good review. I also came across a book, Polarized Light in Animal Vision. Polarization Patterns in Nature. by Gábor Horváth and Deszö Varjú and published by Springer. The front matter and table of contents are available here.  It appears to be a very thorough review of polarization vision in animals.
Literature Cited
Cronin, T.W. et al. 2003. Polarization vision and its role in biological signaling. Integrative and Comparative Biology 43: 549-558.
Greenwood, V.J., et al. 2003. Behaviorial investigation of polarisation sensitivity in the Japanese quail (Coturnix coturnix japonica) and the European starling (Sturnus vulgaris). Journal of Experimental Biology 206: 3201-3210.
Snodderly, D.M., J.D. Auron and F.C. Delori. 1984. The macular pigmnent. II. Spatial distribution in primate retinas. Investigative Ophthalmology and Visual Science 25: 674-685

Many thanks 3Cat for some fantastic material.

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Are there any differences between qRT-PCR and GEO (microarray data from NCBI) regarding dealing with internal control genes?
As we know, when we do qRT-PCR, the two most commonly used methods are absolute quantification and relative quantification, both the methods are involved in dealing with normalization of house-keeping genes or internal control genes (like GAPDH, Actin). In the microarray experiments, the similar normalization should also be adopted (I did not have any experimence with this kind of experiment). But I do know that someone obtained GEO file from NCBI, and simply did t-test analysis to find differenced expressed genes without any operation with the internal control genes. So I wander whether this is the right way, if not, what should we do with internal control genes to normalize data?

did you find an answer to your question? If you did, it would be great if you could post it here for people having similar questions in future

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Removing Sugars Bound to a Protein
I recently purchased some Maltose Binding Protein and as the name suggests this protein binds to maltose. The problem I have is the protein arrive with maltose bound. I know this through native mass spectrometry analysis.
Is there a way of removing the maltose bound to my protein sample while also keeping the protein in its native state?
Examples of two states from the PDB can be seen here: Bound and unbound

It's not clear from the question what the biological source of the maltose binding protein (MBP) is. As you may know E. coli MBP is used as a fusion partner in an expression-purification system marketed by New England Biolabs (this becomes relevant below).
My initial thought upon reading your question was to suggest dialysis. However I found some hints online that this might be problematical and eventually found this on a FAQ at the New England Biolabs site. Looks like this may be your answer.

Question: In order to rebind MBP to the column, the maltose must be removed. Can this be done by dialysis?
Dialysis does not work very well to remove maltose from maltose-binding protein. This is a general phenomenon of binding protein/ligand interactions; after the free ligand is gone, ligand that is released from the binding site usually finds another binding site before it encounters the dialysis membrane (28). We have determined empirically that binding the fusion to a chromatography resin and then washing away the maltose is much more effective. We prefer standard chromatography (e.g. DEAE) as the separation step, since it can separate the Factor Xa and MBP from the protein of interest. In case MBP co-elutes with the protein of interest, we include a large volume washing step to remove the maltose before starting the salt gradient. This way, the mixture can be run over an amylose column afterward if necessary.

So, in summary they are suggesting that you bind the protein to an ion exchange column; wash with lots of buffer; then elute the cleaned-up protein (using salt or a change of pH  - you will have to know something about your protein's behaviour on the column to do this).


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How many plants are needed to survive in an airtight chamber?
How large a garden do you need if you are to survive on them producing enough oxygen in a closed chamber?
And which are the most effective plants?

According to this news article, in a NASA experiment one man survived for 15 days in a sealed chamber containing 30,000 small wheat plants. If you read the article you will find that this did not produce a completely balanced system - some excess oxygen had to be removed, and some extra CO2 had to be pumped in.


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RT-qPCR of selected differential expressed genes: which dilutions in calibration curve?
I've seen in MIQE guidelines that calibration curves a needed when performing RT-qPCR. I'll use genomic DNA to perform these calibration curves.
My question is that I don't know the range of concentrations to test.
The genes I will check for differential expression have logFC between 2-8 (base 2 log).
50 ng/μL is the sample concentration I will have when performing the Comparative CT Experiment, but 98% is ribosomal RNA.
Please let me know you suggestions and possible reference books/papers to revise.

I am not sure what you're trying to do. I think you want to measure gene expression level (amount of transcript), but then why would you use DNA as your reference? What do you want to calibrate with the DNA?

Are you doing a gene expression analysis by relative quantification of cDNA? Or are you looking for copy-numbers of a gene in genomic DNA?
In either case, you need the same type of template in both the standards and samples, and that your curve must cover the whole range of Ct's in the sample set for the most trustworthy results.
For cDNA, I usually get a purified and concentrated cDNA from the same cell/tissue/etc. and do 1/4 dilutions for 5 points (every dilution giving roughly +2Ct)


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Can juice have a higher sugar content after packaging?
It seems like the orange juice thats been sitting in the fridge for awhile always tastes sweeter than the juice just brought from the grocery store.
Can juice ripen in the container ? By that I mean, the concentration of fructose and other sugars increases.
I remember learning in Bio class that fruit releases a chemical that causes nearby fruit to also ripen faster. I'm not sure of the source of this chemical but my question leads me to believe that it is in the juice itself.


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How does the colinearity of the HOX genes determine the body plan of an organism?
I was recently reading about colinearity in the HOX genes that give an organism its high-level body plan (where the order of the HOX genes on the chromosome follow the head-to-tail order of body segments, such that the head gene comes before the thorax gene, comes before the abdomen gene, etc).
I'm really just a layman  interested in this stuff (only completed A & P I), but I was under the impression that the location of genes on a chromosome has no bearing on the expression of those genes or phenotype of the organism -- in other words, that genes can be anywhere on any chromosome.
Do we understand how the order of the HOX genes ends up being expressed as the order of the body segments? Do we know why the positioning of these genes matters when the order of other genes don't?

Have you read Sean Carroll's "Endless forms Most Beautiful" ?I think you will get a complete answer in that book.

By the way, the order of the other genes is also important .  If it were not so, translocations of bits of chromosomes won't be harmful. Have to confirm this though.....

@biogirl maybe you could provide a short synposis of Carroll's book in an answer?

To tell you the truth, I have not read it completely. So, it's really difficult for me to answer this.

I'm a Biologist, the book @biogirl is talking about is one of the greatest works to read. The HOX Genes is an extensive topic. You'd better read some articles.

@John It might help if you could provide a reference for your claim.

@Remi.b Take a look at the Wikipedia page: http://en.wikipedia.org/wiki/Hox_gene#Colinearity_of_Hox_genes

This reply is very late, but for the benefit of biogirl, chromosomal translocations can indeed be harmless, so long as they are gene-dose balanced, and their break-points don't disrupt genes or important regulatory regions.
For example, many people live normally with balanced translocations and only find out when they have some trouble conceiving children and receive genetic counselling. Many translocations have occurred in evolutionary time between chimps and humans. The strict collinearity of Hox genes really is something special in animals, I think.

Gene dosage is often extremely important and so unbalanced translocations that affect gene dose often lead to a disease phenotype.

I have suggested that the colinear arrangement of Hox genes is instrumental in a “segment counter” - a mechanism allowing cells in the embryonic mesoderm to determine in which segment a cell is located and to activate the genes according to the location along the body axis.1 I have also posted an animation explaining the process. ## Reference: ##
1: Kudlicki, A. (2019). Why a Constant Number of Vertebrae? Digital Control of Segmental Identity during Vertebrate Development. BioEssays.

You might be interested in this book
When writing Hox Gene collinearity (or colinearity as it is often misspelled as explain in wiki!) on Google scholar or WebOfKnowledge you will get many results on the subject. It is still today an ongoing debate.
Below are some sentences I pick up from these articles. It is certainly hard to understand as I hardly understood what I wrote! The best for you is to go through this review. It is not easy (at least for me but it is not at all my field) but I think it is the best source of information you can find on the subject.
This and this might also help you to understand the debate on the subject.

There are several types of collinearity:
Spatial collinearity is the sequential 3' to 5' expression of Hox Genes along a body axis. Spatial collinearity can be associated with time dependence where the most 3' is expressed first. This is defined as temporal collinearity.
There are two main models to explain the mechanisms hidden behind this ordering.

1) Collinearity is based on transcriptional regulation and specifically that is limited by the progressive 3' to 5' opening of Hox cluster chromatin and/or mediated by global control regions
2) Collinearity depends on interactions between the Hox genes themselves. These interactions include 'posterior prevalence', a negative interaction among Hox proteins that clearly relates to functional collinearity in Drosophila.

Evolution:
It is suggested that collinearity evolved by repeated tandem duplication of an ancestral ur-Hox Gene

Great, this is what I was looking for! It says I can award the bounty in 3 hours. You'll receive it as soon as SE lets me.

Quoting from some parts of Sean Carroll's book - Endless forms most beautiful, I have tried to provide you with an answer but, remember that this can never suffice for the reading of this great book.
Yes, we do understand how the hox genes' expression is regulated.
From page 126-127

......The establishment of these Hox zones and their subsequent action
  in sculpting the different forms of repeated parts is the fundamental
  genetic logic upon which the modular forms of large,biletarian animals
  is built.
The genetic logic relies on genetic switches at two levels. One set of
  switches belongs to the Hox genes themselves. these switches activate
  each Hox gene in different zones that will become different modules of
  the animal. Another set of switches contain signature sequences that
  are recognized by Hox proteins and that control how other genes are
  expressed in different modules.
In both arthropods and vertebrates, the Hox genes are developed in
  zones along the main body axis. The distinct zones of each Hox gene's
  expression domain are governed by genetic switches, and seperate
  switches control Hox gene patterns in different tissues such as the
  ...... Because of the logic of the genetic switches, the cells that
  belong to one module express different Hox proteins or combinations of
  Hox proteins than those in adjacent modules....

Let us take an example of Ubx gene which leads to formation of wings in the 2nd and 3rd thoracic segments of  drosophila. This gene is turned off in the first thoracic segment  but in the second and third segments, it is turned on. This regulation can be achieved because of the genetic switches which in turn can be switched on or off by activators and repressors. These activators and repressors are unevenly distributed in the embryo and so regulation of switches in different parts of the embryo is possible.

The question is complex and it is nice that you looked up to your book to find this out. But does it answer to "why the order of the HOX genes correspond to the order of the body parts?" ?

@Remi.b is right. While this is a well-researched answer, it doesn't address specifically the colinearity that I was inquiring about--why the order of these genes on the chromosome matter.

@John Well, I just answered the first part of the your question. " Do we understand how the order of the HOX genes ends up being expressed as the order of the body segments? ".

@Remi.b answers the second part in an excellent way !

I have suggested that collinearity of Hox genes is a mechanism to maximise physical segregation between active and inactive Hox genes within the Hox gene cluster. This is to minimise interference between Hox genes in these two states.  See 'The significance of Hox gene collinearity' in Int. J. Dev. Biol. 2015 Vol 59, pp 159-170. Or download from https://www.researchgate.net/profile/Stephen_Gaunt

Thx for your contribution, but your answer does not answer the question "HOW does the order of genes in a DNA string determine the body plan".

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Chills down the spine with certain music?
I am sure many of us know the feeling of that tingling chill down our spines when listening to certain music.
I experienced this most when my younger brother played an emotional piano piece for a talent show (brought me to tears).

What causes that?
Is music the only stimulus to elicit that spine-tingling?
And in terms of evolution, why?

It is called a frisson, and actually, there has been a study about it, available here.
The frisson is kind of the same you get from cold weather, fear, or... well, other things not suitable to discuss if not knowing how old people reading this might be.
Actually, they found that this works best if you include familiarity. In their case, asking study participants to bring their favourite emotional music, in you case hearing it played by your brother.
How this evolutionary came by is unclear. But as it resembles the shivers you would call "a tingling sense of danger" it might stem from a reaction to uncertainty or at least unclear danger. In this case, it is meant to enable you to concentrate on whatever is coming, and maybe (but that's one of my own theories) this is how it came to connect to pleasant emotions as well: You want to be able to concentrate, delve into the emotion. This could explain, why it works best with familiar pieces: you already know that you want to listen closely.

frisson! - will be saying that more often now, cheers for the insights @skymninge

Music and Emotions
The most difficult  problem in answering the question of how music creates emotions is likely to be the fact that assignments of musical elements and emotions can never be defined clearly. The solution of this problem is the Theory of Musical Equilibration. It says that music can't convey any emotion at all, but merely volitional processes, the music listener identifies with. Then in the process of identifying the volitional processes are colored with emotions. The same happens when we watch an exciting film and identify with the volitional processes of our favourite figures. Here, too, just the process of identification generates emotions.
An example: If you perceive a major chord, you normally identify with the will "Yes, I want to...". The experience of listening to a minor chord can be compared to the message conveyed when someone says, "No more." If someone were to say these words slowly and quietly, they would create the impression of being sad, whereas if they were to scream it quickly and loudly, they would be come across as furious. This distinction also applies for the emotional character of a minor chord: if a minor harmony is repeated faster and at greater volume, its sad nature appears to have suddenly turned into fury.
Because this detour of emotions via volitional processes was not detected, also all music psychological and neurological experiments, to answer the question of the origin of the emotions in the music, failed.
But how music can convey volitional processes? These volitional processes have something to do with the phenomena which early music theorists called "lead", "leading tone" or "striving effects". If we reverse this musical phenomena in imagination into its opposite (not the sound wants to change - but the listener identifies with a will not to change the sound) we have found the contents of will, the music listener identifies with. In practice, everything becomes a bit more complicated, so that even more sophisticated volitional processes can be represented musically.
Further information is available via the free download of my e-book "Music and Emotion - Research on the Theory of Musical Equilibration"
or on the online journal EUNOMIOS.


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Why isn't Rh disease present in other mammals?
I have read about Rhesus D Hemolytic Disease of the Newborn, sometimes called "Rh disease". It's rare, but it can happen when an Rh+ baby is conceived by an Rh- mother.  This raises many questions. I have heard this problem only happens with humans; if so, why doesn't it affect other mammals like Rhesus monkeys?  Where along the evolutionary time-line did Rh disease come about in the first place?

Have you read this ?

I have read it now. It is a similar issue. A newborn has issues with a mother's antibodies that are in the mother's milk that they were not immunized to during pregnancy. These antibodies were brought about by sensitization (the same process that triggers RH disease). The difference being the antibodies do not crossover the placenta barrier during pregnancy. Although similar, it is not RH disease in mammals other than humans.

@biogirl essentially the difference is that one occurs during pregnancy the other during nursing.

Rh is just a proteinous(antigenic) factor in red blood cells; not a DISEASE.If it is present in blood you are Rh positive. If not Rh negative.An Rh negative person if exposed to Rh positive blood will form specific antibodies against the Rh antigens. In case of pregnancy, Rh antigens of the foetus do not get exposed to the Rh negative blood of the mother during first pregnancyas the two bloods are well separated by the placenta.
However during the delivery of the first child there is a possibility of the exposure of maternal blood to small amounts of Rh positive blood of the foetus.In such cases the mother starts preparing antibodies against Rh antigens in her blood.
In case of her subsequent pregnancies, the Rh antibodies from the Rh negative mother can leak into the blood of the Rh positive foetus and destroy the foetal RBCs. THis could be fatal to the foetus or could cause severe anaemia and jaundice to the baby.A condition called erythroblastosis foetalis arises.
This condition can be avoided by administering ant- Rh antibodies to the mother immediately after her first delivery.
This is not a disease but is just as a result of antigen- antibody reaction.As far as Rhesus monkeys are concerned, it is an innate factor in them, common to all.It is quite similar to the case of Bacillus thuringiensis in biotechnology. When inserted into plant cells these bacterial phytotoxins cause havoc as an insecticidal agent; whereas they seem to have exactly no effect inside bacteria.You may also consider the case of Penicillium notatum.These organisms are capable of causing harm to other living organisms but are not affected themselves.
Similar is the case with Rhesus monkeys.

will need references..

For just the basics on Rh factor you may check out NCERT Biology for class XI.You may check this site out: http://en.wikipedia.org/wiki/Rh_blood_group_system           You may also go through: http://www.nhlbi.nih.gov/health/health-topics/topics/rh/

This being an international forum, many would not be able to access the NCERT class XI textbook for biology. Please do include proper online links to scientific papers and articles in the body of the answer next time.

@The Last Word I provided links with the comment.Sorry for not including them with the answer. However you may check the links out, now that I have provided them.

It may not be a true disease so to speak, but essentially we are seeing children dying from naturally occurring differences in the blood types between that of the mother and of the infant. My question is why would this exist at all in the first place? What would the evolutionary benefit of such be? And why can this specific condition/occurrence not be found in other apes or other mammals?


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Organisms with the most extreme sensory capabilities? (sight, smell, sound)
Background
It is quite mind boggling to imagine what it would be like to be missing sight, sound, touch, smell, taste etc.
Question

Which organism holds the record for most extreme sensory limits for: sight, smell and sound? (one for each)

This would help give an idea of the "biological limits" of sense.

I believe this is too broad. There is a plethora of various kinds of neural sensors in animals, ranging from electric impulses to ultraviolet vision. Listing them all down might not be feasible.

hmm well this in itself was insightful thank you, I suppose if people list some nice sources to learn this kind of information would still be so helpful... in any case who says there is a limit to how many answers there can be...

@hello_there_andy Please read through this section of the Help Center - particularly "Your questions should be reasonably scoped. If you can imagine an entire book that answers your question, you’re asking too much."

@MattDMo I see, cheers for that clarification I will edit it right away then


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How easy is it to carry out de novo sequence assembly?
Today a colleague of mine asked the following question:

" Assuming I need to build from 0, a chromosome of a fish, with short reads
but no other reference whatsoever [de novo assembly]:

how much work is that?
Is there a generic software (like SAMtools) that will align the reads in a
scaffold one can use?
Basically, given a reasonably clear pipeline in terms of software, is it still blood sweat and tears or is it just a matter of getting it on a cluster?"

Very grateful for any suggestions, sources of information, software etc.

tl;dr: It’s blood, sweat and tears. I haven’t been involved in this myself yet but I know people who are. Depending on the complexity of the genome, you’ll get tons (they got in the order of 1M) non-overlapping contigs.

would it really be necessary to use 30bp reads? that's very short.

cheers guys, actually I pressumed ~30bp to give an idea but perhaps it is more flexible what lengths do you have in mind @ThomasIngalls? Hmm I wonder what the blood sweat and tears would be caused by? I presumed there would be some standard pipelines to automat the whole shebang?

De novo sequencing without using some long-read techniques for cleanup (like Sanger sequencing) requires a lot of coverage, and you still end up with substantial uncertainty in the results, due to the large amount of repetitive sequences that are longer than 30bp in most genomes. The reply by @bitwise gives a great idea of what I was thinking.

If you only want to use only sequencing techniques, you have a problem.
To get a feeling of what kind of results to expect, consider this paper published recently in Nature Genetics. They tried to assemble a whale genome de novo. They had 7 (!) paired-end libraries with different insert lengths ranging from 170bp to 20kb. Read lengths were mostly 100bp and in some cases 49bp. Average genome coverage was 91x.
Assembling this extensive data, they end up with over 100,000 contigs when the assembly is done.
So you really can't get a high-quality complex (i.e. large) genome assembled from only short-read sequencing data using the standard techniques.
That said, recent approaches such as libraries with much longer reads lengths (here) or the use of Hi-C data (here and here) do offer a way of getting high-quality complex genome assemblies using only sequencing data.

"If you only want to use only sequencing techniques, you have a problem." -- Do you mean resequencing techniques, or high-throughput sequencing techniques?

@ThomasIngalls I mean assembling a complex genome de novo using high-throughput sequencing. Resequencing assembly is not de novo assembly.

You can try looking around biostars.org, which is like stackexchange, but for bioinformatics.
Velvet is one example of a de novo assembler.
But 30 bp is really short, and animals have big genomes (not as tough as lots of plants and fungi, but still tough)
What you would get is a bazillion short contigs.  It would not be pretty.

cheers for the Velvet recommendation

I really like the genious software suite. It can multithread and really use the performance of your computer. Even complicated things like De Novo assembly are very very intuitive.


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How common is complete heterochromia?
How common is complete heterochromia? (One iris is a different color from the other)
Are there any statistics available for this? If no, why not?

Note: not my area of expertise

First of all, heterochromia can be congenital (found at birth) or acquired, and from your question it is not clear if you are asking about one specific type or the overall frequency (if so, at what age?). Since acquired heterochromia is often due to injury or disease, the overall frequency is likely to increase with age. Also see answers to the question "Is it biologically possible for an adult's eye color to change?" for more on reasons for acquired heterochromia.
According to an Austrian study (Stelzer, 1979), the overall frequency in the Vienna population was 0.26% (males: 0.16; females: 0.37). However, Medicine.net reports a frequency of 0.6% for only congenial heterochromia, but this number lacks a clear reference. A thorough review of different reasons for heterochomia can be found in Rennie (2012).


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DIfference between diversification and differentiation
In Adaptive dynamic :
what is the difference between Ecological Differentiation and Ecological Divergence ?

I would say that ecological divergence emphasizes on the process of speciation by niche differentiation while ecological differentiation emphasizes on the process of niche differentiation due to overlapping niche of non-necessarily closely related species. But it's no more than a guess! What do you think?

As already said in a comment: I would guess that ecological divergence emphasizes on the process of speciation by niche differentiation while ecological differentiation emphasizes on the process of niche differentiation due to overlapping niche of non-necessarily closely related species.
But looking to some articles, it seems that they use both term without making any difference. As found on this article for example.
Therefore, I would rather advice to no consider too much difference in meaning between ecological divergence and differentiation. But take time to define accurately the words you're using, especially if you talk about cases that fall on the border of two concepts!


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Why do some women have menstruation-like spotting throughout their pregnancy?
An interesting question that was asked during a lecture about human reproduction: what is the biological mechanism behind some pregnant women getting monthly spotting that they mistake for a regular period? I've found articles and research papers about bleeding during zygote implantation, ectopic pregnancies and problems with the placement of the placenta, but nothing regarding menses-like bleeding during otherwise unproblematic pregnancies.

Related: How common is it to be pregnant with periods?

Here are some causes of bleeding during pregnancy:

early pregnancy (first trimester):

implantation bleeding [1]
infection [1]
after intercourse [1]
miscarriage [2]
ectopic pregnancy [2]
cervical changes [3]

second part of pregnancy:

abruptio placentae [1, 2]
placenta previa [1, 2]
miscarriage [2]
vasa previa [2]
preterm labour [1]

References:

American Pregnancy Association. Bleeding During Pregnancy. Available from http://americanpregnancy.org/pregnancycomplications/bleedingduringpreg.html (accessed 29.07.2014)
U.S. National Library of Medicine. A.D.A.M. Medical Encyclopedia. Vaginal bleeding in pregnancy. Available from http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0003748/ (accessed 29.07.2014)
WebMD, LLC. Bleeding During Pregnancy. Available from http://www.webmd.com/baby/guide/bleeding-during-pregnancy (accessed 29.07.2014)


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How do proteins get into the blood stream?
So I'm asking this in reference to the injection of insulin, which is commonly done subcutaneously (in the hypodermis, a fatty part of skin). Now I know proteins usually get into the blood when digested through the stomach/intestines - but I was wondering how they manage to get into the blood when injected into muscles/fat? I know there are capillaries pretty much everywhere, but from what I've researched proteins are too large to get through capillary walls.
That begs the question then, how do proteins manage to get into the blood stream when injected? I can't really envisage large capillaries, because surely they'd have huge holes in them or whatever to allow large proteins like insulin in. Any help on this one? Cheers

maybe from lymphatic capillaries(they have larger pores) ... I am not sure....

Found the answer - the lymph capillaries. I've not researched them too in depth but from what I've read thus far, their job is to essentially pick up fluids not picked up by the blood capillaries. They have walls that allow proteins to enter but make it very hard for fluid to flow out.
Wiki states that an average of 20 litres of blood gets processed each day by the blood, with roughly 17 litres through the blood capillaries/system (1), with the remaining 3 litres through the lymphatic system.
These are also prevalent around skin. 70% of lymph capillaries are found near the skin (2).
1) http://en.wikipedia.org/wiki/Lymphatic_system
2) http://www.lymphnotes.com/article.php/id/151/

Could you expand on this slightly to make it more useful for people viewing it in the future?

Apologies, didn't see the comment above suggesting the lymphatic system, and have done a bit more research so edited.


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Does Lucid Dreaming decrease the regenerative effect of sleep?
After watching this SciShow video on sleep, I wonder about lucid dreaming.
Specifically: Does lucid dreaming and associated directed agency within Lucid Dreaming decrease the regenerative effect of sleep?
That is, if I gained the skill of lucid dreaming - would I be negatively tampering with the brain's autonomous healing processes for the period that I had conscious control or even simply objective awareness during sleep?

I am not sure about biology, but from what I feel of lucid dreaming, I, contrary to decreasing the regenerative effect on sleep, can increase it, since I am able to choose what dream states are the most refreshing. I have also noticed that sometimes it is enough to reach a particular states and dream and see particular things to get the tiredness load off in just a few seconds (of experiencing a particular dream). That never frees you from the requirement of the full-scale normal sleeping, but comes handy in some situations

It's possible that they do, depending on the intensity of the dream and the amount of brain activity.
For example, if the dreamer is thinking too much or is having a dream that's way too intense, the brain activity goes up and they're not as rested.  However, lucid dreaming can be good for sleep if the dreamer creates a more relaxed dream.  This can possibly be better for the sleeper, especially if they're someone who experiences nightmares every night.
Basically, it just depends on what you're dreaming about.  The calmer and more relaxing the dream is, the better.
Source:
-www.world-of-lucid-dreaming.com

Welcome to Biology. It would be great if you could add some references to your answer.

A scholarly source would be preferred to fan site / infomercial.

That's true.  Should I just take my answer down, then?

You could edit it?

If you can't edit it, you could make a comment out of the answer. Those kind of comments can be very helpful.

Yes, when you are dreaming, brain activity increases ( called the REM phase because of the effect of the increased neural activity: rapid eye movements ).
You can tell this by looking at the EEG, from witch we can state that our brain is more active and therefore is consuming more energy, making the regenerative effect of the sleeping less efficient.
https://en.wikipedia.org/wiki/Rapid_eye_movement_sleep#Electrical_activity_in_brain


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What is the evolutionary advantage of regret?
Some motivational speakers may say that regrets are only useful to learn something from.
What are the other advantages?

Regrets (as an Emotion) have fair equally it's disadvantages. And in this question of your's, did you intentionally avoided talking about it's disadvantages? Please make it clear. Also regret on a long-term leads to self loathing, chronic stress. it's a negative emotion, isn't it?

Very interesting question.
First I'd like to highlight that this question relates to a very hypothetical field of evolutionary biology which is evolutionary psychology. This wikipedia article on evolutionary approaches to depression might be of interest as well. One sentence says: "Feelings of regret associated with depression also cause individuals to reflect and analyze past events in order to determine why they happened and how they could have been prevented". It basically says the same thing than you said in your question.
What other advantages might "regrets" have? Before trying to answer it, I'd like to ask : is it necessary that it has advantages? A behavior or a feeling might as well be a by-product of selection for big brains. It might therefore not be selected for but it exists only because there is not much selection against this by-product trait.
Our brain are often considered to have evolved for social purposes. I would hypothesize that if someone express "regrets", he might benefit from other's care and pity. And the best way to express "regrets" is to feel the "regrets". Robert Trivers would maybe say that in order to fool someone else (make someone else think we regret) the best thing to do is to fool ourself (make ourself feel "regrets"). See his book, the folly of fools.

Very good. I am thinking of regrets for things we do to ourself.

Besides encouraging thought which leads to strategies that avoid behaviors that lead to regret, could regret also be involved in a kind of catharsis, perhaps draining feelings of anxiety (brought by a negative event)? Persistent anxiety would tend to have negative consequences, so having a way to mute that response could have advantages even if the mind did not learn or reinforce any behaviors that reduce the bad events (or their bad effects).


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Identification of this plant?
Photographed in Rocky Point, Mexico. Any ideas about this plant? Thank you!

Could you give an indication of its size? It is hard to judge with no reference. Also, when was the picture taken?

The horizontal-looking axis is notable. please provide much better descriptions (including was it a tree? or small herb?).

It  looks to me like some gymnosperm tree. Looking like Araucaria and Cryptomeria . Araucariaceae is common in southern hemisphere. Wiki article on Araucaria https://en.wikipedia.org/wiki/Araucaria

Was it a big tree or small herb or a young tree or a shrub? Were those leaves and axis soft or stout? What's about the size of these twigs? From at-a-glance looking the picture it looks much like Araucaria, a tall tree.

May be related one : http://biology.stackexchange.com/questions/35653/what-is-the-scientific-name-of-this-evergreen-plant

[Not really a precise answer (and I'm not a botanist after all).]
It's likely a lycopodiophyte. Looks like a Huperzia species, but it's impossible to tell exactly from the provided photo [if the species is not familiar, of course]. Of great help would be general appearance of the plant and form of sporangia.
You can try this key: Lycopodiaceae of North America.

Lycopodiophyta was definitely my first idea as well, but beyond that I have no clue.

Looks to me like a gymnosperm like Araucaria and Cryptomeria


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Why doesn't T5 exonuclease have endonuclease activity in Gibson assembly?
Gibson assembly uses T5 exonuclease to chew back the 5' end of dsDNA to generate overhangs. However, T5 exonuclease, in contrast to lambda exonuclease, is reported to have ssDNA endonuclease activity (https://www.neb.com/products/m0363-t5-exonuclease#tabselect0). Why doesn't his cause problems during gibson assembly? Is it just because these don't yield viable assemblies? Or is it because this activity is inhibited somehow, such as the T5 concentration is too low?

The buffer conditions used in the reaction also mitigate against the endonuclease reaction, so it should not be a problem if you stick to the protocols exactly. I've worked on this enzyme since 1988 and was the original "cloner' of the overproducer see http://www.sayers.staff.shef.ac.uk/fen/   for more information on these enzymes
Jon Sayers, University of Sheffield.

I've never actually done a Gibson assembly, but looking over the protocols at the New England Biolabs website, I think the answer must be that the ssDNA exposed by the T5 exonuclease is quickly protected from the ssDNA-endonuclease activity because it (the exposed DNA) anneals with the complementary sequence on the other component of the assembly reaction. Following that, any gaps are repaired and sealed by DNA polymerase and DNA ligase. All of these enzymes are of, course, present at the same time in the one-step assembly reaction.
In summary, under the conditions of the assembly reaction, the low-level ssDNA endonuclease activity of the T5 exonuclease is simply outcompeted by the other reactions taking place.

This idea is supported by the paper that originally discovered the endonuclease activity of T5 exonuclease: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC328551/?page=1 . They report the level of endonuclease activity is low compared to exonuclease activity.

Yes, I found that too, and set off on a search expecting to find that the low Mg suppression of endo- activity would be the key, but apparently not.


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Why would a single celled organism evolve to be multi-celled?
I read a story this week on Richard Lenski who has been 'evolving' E. coli for more than 50,000 generations now.  One comment I read was from someone who doesn't accept Evolution who pointed out that we haven't seen a single celled organism 'evolve' into a multi-celled organism.  Another person responded and said that a bacteria is not going to evolve into something that isn't a bacteria.
So, if Evolution created single celled organisms and then multi-celled organisms how might that change have happened?  And is it possible to recreate that set of driving forces to make a bacteria something other than a bacteria?
To that end, what advantage does being multi-cellular have over being unicellular (if that's even a word)?

There are quite a lot of books addressing this question. Here are some few examples: Major transitions, levels of selection and Major transitions revisited. Note concerning the question of level of selection versus kin selection one might be interested by this article

Two things:

Although there are a number of hypotheses, as others have pointed out, this is not an entirely solved problem. Attempting to figure out which hypothesis (or hypotheses) are most plausible is an ongoing area of research.
2.Clearly, saying that "a bacteria is not going to evolve into something that isn't a bacteria" is an oversimplification. Eventually this is possible. But it would take orders of magnitude longer than we can test in a laboratory - even with such impressive experiments as Lenski's.

@seaotternerd, If we use 20 years as a human generational time period then 50,000 generations is 1,000,000 years.  Looking at the 'conventional' timeline for human evolution we have progressed quite a bit in the last 1,000,000 years - easily changing 'species' more than once.  Given that, why do you say that 'orders of magnitude' more generations are required to see a change in bacteria?

@CramerTV - While it's true that the lineage that lead to humans has transitioned between "species" multiple times within the past 1,000,000 years, the evolutionary distance between two different species (say Homo sapiens and Homo erectus) is orders of magnitude smaller than the evolutionary distance between two different kingdoms (bacteria vs. non-bacteria). Bacteria would have to undergo multitudes of changes in order to be considered something other than bacteria.

Take a look at the social amoeba, Dictyostelium discoideum to see an example of how a single celled Eukaryotic protist can exhibit social, cooperative behavior that leads to the formation of a cooperative multicellular spore that allows for species survival under starvation conditions.

The question suggests that you might want to have a look at Understanding Evolution (UC Berkeley), a free online introductory course to evolutionary biology

How did multicellularity evolved?

It is an ongoing field of research - Some insights about the origin of multicellularity
This is a big ongoing field of research. To start with an example, there was relatively recently (2012) an important article by Ratcliff et al. that shows that yeast can quickly evolve multicellularity under selection on the speed they sink to lower water layers. This article is one among many others and is far from being able to explain everything we would like to understand about the evolution of multicellularity. Typically, I think that this yeast species had a multicellular ancestor and we might think that this species would already have fixed alleles (=variants of genes that is fixed meaning that the whole population is carrying this variant today) in the population predisposing this species to easily (re-)evolve multicellularity. Also, they may have kept some standing additive genetic variance in their genome from their past and they would therefore very quickly respond to selection as they don't need de novo mutations. (Sorry if this last sentence was slightly technical).
One of the first traits that we usually refer to when talking about the evolution of multicellularity is the presence of sticky proteins allowing individual cells to paste to each other.
Some insights about the evolution from simple multicellular to more complex multicellular
Then, we could talk about more complex multicellular and argue how do these simple multicellular evolve into some more complex organisms. A common argument is that multicellular can have specialized cells are very could at doing what they're doing as they are specialized. Also, some level of complexity is thought to have raised due to the fact that multicellular organisms tend to have smaller population size than unicellular (see Lynch and Conery, 2003). It is important not to confuse evolution of complexity with the evolution of multicellularity although these two notions are somehow related.
What do you mean by multicellularity?
The evolution of multicellularity can be discussed in the context where sister cells form an organism together or when unrelated cells (among the same species or even cells from different species) come together to form an organism. Also, the multicellularity can be discussed at a different level depending on how we want to define multicellularity. Is a stack of cells reproducing individually, working for their own benefit a multicellular? Do we need a division of labor? Do we need a division between germline (reproductive caste) and soma line (non-reproductive case)?
How many times did multicellularity evolve independently?
Some people consider that there are multicellular bacteria (biofilms) but we will avoid discussions that are based on limit-case definitions. Let's talk about eukaryotes. Most Eukaryotes are unicellular and multicellularity evolved many times independently in eukaryotes. To my knowledge, complex multicellularity however evolved only (only?) 6 times independently in eukaryotes.

Metazoa (animals)
Ascomyceta (fungi)
Basidiomyceta (fungi)
Viridiplantae (green plants)
Florideophyceae (red algae)
Laminariales (brown algae)

Model organisms and interesting cases to study multicellularity
There are a bunch of specific clades that are particularly interested in studying multicellularity because they present transition states. For example Volvox is a chlorophyte genus and the species in this clade present different stages of multicellularity; Some species are exclusively multicellular, some form small groups, some create big colonies, some have some division of labor and some even have separation between the germline and the soma (Some castes don't reproduce). (ref1, ref2, ref3, ref4, ref5, ref6). Yeasts are also a good model organism for studying the evolution of multicellularity.

Not trying to quibble, but there are multicellular green algae, are they included in Embryophyta for the purpose of the list, or are they independently multicellular too? Or are they not complex?

Good point. I think I was no inclusive enough when saying Embryophyta. According to tolweb.org (here), charales (who are multicellular) aren't Embryophyta. I think it would be correct to say Streptophyta. However, because the phylogeny doesn't seem to be perfectly solved yet (and because I don't know if groups such as ulvophycae are multicellular or) I just edited my answer to say viridiplantae (green plants).

As you say though, the level of complexity of the non-embryophita, green plants might be low enough to not be considered but I am not quite sure how complex is their multicellularity compared to the brown algea typically, so I'll just go safe and include everybody! Thank you

A model organism used for the study of cell signaling that transforms from a vegetative state to a cooperative multicellular spore is Dictyostelium discoideum in the absence of food. This organism demonstrates how simple cell signaling can lead to cellular aggregation and cooperation, in order to insure the propagation of the species, even to the point where some cells are sacrificed to form the stalk of the spore, which elevates the spore above the surface to where it is more likely to encounter food.

For one thing, larger organisms are much more energy efficient.  This is what is known as Kleiber's Law where the caloric requirement scales as the 3/4 power to the body mass.
Another thing is that when all the cells cooperate to form a multicellular organism, each given individual is more likely to reproduce and less likely to die due to environmental variation because cooperation creates stability.
There are several theories about how this came about,but those are the elements of why.  Collaboration and efficiency improve the chances of survival, which is to say that selection will favor multicellular organisms however they came to be.

Disclaimer: Not my field of research, and not a field where I know the litterature well. See it as a complement to the other answers.

A distinct advantage of multicellularity is specialized functions of different cells. This can allow for higher efficiency of e.g. metabolic processes, and also that redundant functions can be removed from some cell lines, since they can be handled by other cells. Therefore, the constituent parts can become simpler, while the resulting organism becomes more complex at the same time. Mathematical modelling of cellular systems have shown how this type of division of labour can evolve from unicellular lines (Ispolatov et al. 2011), through the steps of aggregation and differentiation from preexisting functions.
An interesting intermediate step that can provide some clues to how multicellularity can evolve, is in cyanobacteria, where some unicellular species can show partial specialization e.g. when part of cellular biofilms. A phylogenetic study of cyanobacteria has also shown that they have reversed from multicellularity to unicellularity at least five times, and most extant cyanobacteria seem to descend from multicellular ancestors (Schirrmeister et al. 2011). This means that the evolution of multicellularity is not a one-way process, but seems to be a much more complex process.

I STRONGLY encourage to read work from the lab of Nicole King - she studies Choanoflagellates, which are the "out-group" for animals - they are, in some sense, the most animal-like single-celled organism that exists.
Chaonos are also amazing because they go through a single to multicellular transition in there own life cycle, so they provide an amazing opportunity to understand when it is more beneficial to be single-celled vs. multi-celled. Currently, one of the working hypotheses of the group is that one of the main drivers of the push towards multicellularity may have just been simple fluid dynamics: the flows around a spherical multicellular "rosette" of chaonos bring more food to them.
If you are interested in the evolutionary transition to multicellularity you must read work from the King Group.

If single cells are capable of surviving on their own then why did multicellularity evolve?

This situation can be compared with the evolution of family and society, in a way; during the time of crisis, the survival chances increase when someone stays in a group.
Similar conditions would have resulted in the evolution of multicellularity. The difference between being truly multicellular and just being a group of cells is that in multicellularity, the individual cells cannot survive in the absence of the other. Moreover, different cells in a multicellular organism perform different kinds of functions. However, it is certainly likely that grouping without a strong dependence would have constituted the early stages in the evolution of multicellularity.
One of the complex kinds of microbial colonies is biofilm. In a biofilm different "regions" of the colony have different kinds of functional roles; the "outer" cells take up nutrients for the colony from the surroundings whereas the inner cells reproduce and keep the colony thriving. Bacteria have also evolved a way of signalling (or "talking") to other bacteria (of the same species) by a mechanism known as quorum sensing, which in a way changes the behaviour of the bacteria when then stay in a group.
Dictyostelium or slime mold (or affectionately called dicty :) ) is an example of early evolution of multicellularity in eukaryotes. When there is plenty of food, dicty stays as unicellular amoeba. However, when there is a shortage of food, the dicty amoebae start grouping up and give rise to a multicellular "slug". The dicty slug roams around and when it encounters right conditions (such as humidity), it differentiates to give rise to a "fruiting body", which more or less looks like a fungal spore. In a fruiting body some cells form the spores (which will produce new dicties) whereas some cells form the stalk (which supports the spores). Apparently, the choice of what part will a cell become, is random and at this stage the individual dicty amoebae are no more selfish. The aggregation of dicty amoebae is co-ordinated by a signalling molecule called cAMP and this works in a way similar to quorum sensing.

 Taken from Wikipedia

Volvox is another example of an early stage of multicellular evolution.
To sum up, as you said single cells can very well survive on their own. However, in some situations being multicellular would have given the organism some survival advantages. You should understand that this is just one of the survival strategies and not all organisms needed to adopt this. In fact, there are many more unicellular species in the planet compared to the multicellular ones.
I would reiterate Remi's suggestion that you should have a look at this site called Understanding Evolution, hosted by UC Berkeley.
You can also look at this post on our site about a recurrent doubt faced by many students and non-experts in the area of evolution: "Why do some bad traits evolve, and good ones don't?"

For the same reason that sociality evolved so many times among animals. There are lots of advantages in having similar fellows. And multicellular organisms are, after all, just a colony, sometimes a society, of individual cells.

Interesting perspective.  I never equated multi-cellular evolution with symbiosis.

Thanks, @CramerTV. I remember coming to this conclusion after studying Volvox algae.

The eucaryote that became the modern organelle mitochondria, combined with procaryotes. This probably occurred as a result of the mitochondria being absorbed by the parent cell but not destroyed as it usefully created energy rich ATP molecules using Oxygen and Water through respiration.
These were the first Eukaryotic cells, they went on to become Eukaryotic, multicellular life.

Various benefits to Eucaryotes becoming multicellular include:

The volume to surface area of a cell gives cells a natural size of a few micrometers. Larger single cells find it increasingly difficult to absorb enough nutrients or oxygen for the volume of there cytoplasm.
Amoebas can be larger due to being so irregular in shape, this ensures that so nowhere inside the cell is it too far from the cells surface. Various more spherical centimetre scale single celled life also exists in nutrient rich parts of the deep ocean, such as the Valonia Ventricosa.
https://en.m.wikipedia.org/wiki/Valonia_ventricosa

Another advantage is that structures can form between cells, outside of the cell walls, that can still be protected inside the creatures body. Such a connective network in animals called the extracellular matrix.
https://www.khanacademy.org/test-prep/mcat/cells/cytoskeleton/v/introduction-to-cytoskeleton

Note that creatures like the sea sponge are multicellular, but do not have distinct areas of the body such as organs in the same way as animals do.
"The genes I discuss in my article were not present in the common ancestor of all life on Earth. They do not exist in bacteria, for example. They do not even exist (as far as scientists know) in sponges. Only after the ancestors of cnidarians and bilaterians diverged from sponges did they emerge." (A planet of viruses, Carl Zimmer) This is the quote I could find, as I remember, relating to "bodybuilding" in many creatures, but not the sea sponge.

Why the downvote?

There is no obligation to give feedback with a downvote. Given the frequency of your posts getting downvoted I'd suggest you read on how to write good answers in the help pages, look at some well received answers on other posts etc. Also given that you have previously been confrontational and defensive in the face of comments and criticism then perhaps downvoters are less inclined to comment (it would be a waste of time).

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


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Where does all the carbon go?
I found it hard to get numbers on global primary production, but apparently it's somewhere around 50-60 $Gt / year$ for carbon content in the terrestrial production, and a similar figure for the oceans. Global oil and coal extraction together are around 10 $Gt/year$, only a part of which is pure carbon (iirc, around 80%). Since carbon in the air actually increases, does that mean that most or all of the carbon fixed in Net Primary Productivity go back into the atmosphere through consumption and destruction of the biomass?
I was assuming that the biosphere in total was fixing more carbon that it emitted, and that the surplus was what turned into oil and coal. But with these figures it looks a lot more like a full circle that nets to zero input / output. Which is true, or is that unknown?

NPP? Gt/a? it's good practice to expand abbreviations

@GriffinEvo probably $Gt/a$=gigatons/acre and $NPP$ is Net primary productivity.I am not sure enough to edit the question to include this.

@satwik pasani I am sure about the second one, edited in the question.

I believe most of it goes into the oceans

... where it causes acidification H2O + CO2 <-> CO3H2 carbonic acid.

Good question! The way that the carbon budget stays balanced was a bit of a mystery until recently. The amount of carbon in the atmosphere (and the rate at which it was increasing) was lower than models suggested that it should be, given rates of photosynthesis, respiration, and other carbon releasing processes. Somewhere, there was a "missing carbon sink" that wasn't being accounted for. After many years of debating whether the sink was terrestrial or aquatic, it turned out to be a little of both (which is the conclusion to just about every debate in ecology), although somewhat skewed towards the terrestrial (I think). Forests were sequestering more carbon than had been thought, and so were oceans to some extent (although ocean sequestration relied on a chemical reaction that is in danger of reversing if the water warms up too much). For a thorough account, see this article.
But it sounded like you weren't wondering what the missing sink was so much as how there continues to be enough carbon in the air for plants to photosynthesize (if I'm interpreting your question correctly). Carbon gets back into the air for the most part because of cellular respiration, which all organisms, including plants, do. Net primary productivity takes plant cellular respiration into account, but there are still tons of living things on earth eating plants (and thus taking in their carbon) and then breathing it back out after they break down the carbon-containing molecules for energy. There is also natural combustion and volcanoes and such putting carbon back into the air.
EDIT (to address the new part of your question): Oil and coal were produced when large quantities of carbon were buried deep under ground (and thus subjected to lots of pressure) for thousands of years. This is suspected to have happened during the aptly name Carboniferous era, which featured giant plants and, scientists hypothesize, no decomposers to break them down. Since we have much decomposers now, and much smaller plants, oil and carbon are not currently being produced. This is why we call them non-renewable resources. By extracting them from the ground and burning them, we are taken carbon that had effectively been removed from the pool of actively cycling carbon and adding it back in.
The carbon cycle doesn't really have input or output (except the occasional carbon exchange with outer space), because it is defined as already including standing sinks like oil and coal. When we take carbon out of a sink, like oil or coal, it needs to go somewhere else. Terrestrial and aquatic sinks can store some of the additional carbon that we're adding to the not-underground part of the cycle. However, they can't store all of it, so some is staying in the atmosphere instead.

So is the biosphere overall a carbon sink, or is it exactly balanced without anthropogenic emissions?

There are sinks and sources within the biosphere. Overall, the sinks are not enough to balance anthropogenic emissions, hence the rising CO2 content of the atmosphere. The mystery was just over why CO2 content was not rising more quickly than it already is, and the answer was that the biosphere contains more sinks than we had initially realized.


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Hypothetically, what is the smallest functional form of human?
Since the my first encounter with doraemon manga, I've been wondering many things, one of them is the small light.
Assuming we had an instrument, such as small light, which enabled people to grow and shrink as they wanted to, what would be the smallest and the most compact functional form of a person?
First, I can rule out that we couldn't be as small as an atom because we couldn't be function as human being if we were compressed into 1 atom. So did 1 molecule. and so did 1 cell.
Second, you need more than 1 cell to construct organs, i.e. I couldn't imagine an eye which consists only several atoms or molecules.
Therefore, there should be a limit to the the size of human organs in order to fully retain their functions and thence, there should also be a limit to the minimum size of human organs.
What are the limits of size of each of human organs?
What are the limits of size of human then?

Not a real answer, but the smallest known primate appears to be the Phillipine Tarsier at 3.4" tall http://en.wikipedia.org/wiki/Philippine_tarsier  I would be surprised if there isn't a smaller primate hanging out somewhere.  If we were that small I doubt we would be able to drive a car or write television shows.  The brain case is quite small, so it kinda depends on your definition of humans.  eukaryotic cells don't shrink well. Hard question!

"Chandra Bahadur Dangi is the shortest man in history for whom there is irrefutable evidence, measuring 0.546 m (1 ft 9 1⁄2 in)."

This question is for Doctor Frankenstein!
The answer would depend on what you would accept to consider being a human.

Does it still need to be able to make simple calculation in order to be a human?
Yes, because otherwise we would have lost some functions. But then you may ask…
Does it need to have big enough hands in order to fulfill the social function of hand shaking.
Does it has to be attractive to the other sex?
Does it need a heart or is it fine if oxygen diffusion through tissue only is enough for this creature to live?

I guess that if you change the number of cells you will necessarily change the functionality. I am not saying that small guys are not as functional as big guys. For example, big guys are better runner, while small guys are better climber.

Are we allowed to shrink the cells to have minimal sized cells?
Are we allowed to shorten the DNA in order to shrink the cells?

Notes:

There are approximatively 200 different cell types in a human

My reference is not a peer-reviewed article (ref). Wikipedia lists cell types and it doesn't seem to go over 200. However, it is important to realize that it probably very much depend on how you define cell types.

Terminologica Anatomica lists over 7,500 names parts of the human body
There are 13 or 14 (depending on the gender) gland types
This article provides an estimation of the number of cells in the human body
Here (wikipedia) is a discussion on the concept of the minimal cell
Here and here (biology.SE) are discussions on the minimum number of genes/amino acid to sustain life
Here (biology.SE) is a discussion on which species has been found to have the smallest genome

Great answer. But only 200 cell types? I think that's a vast underestimation...

Thanks. I added a comment in my answer to explain why I picked 200 and clarify that this number might be subject to semantic issues.


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Does the existence of one species imply the existence of many other?
Reading one of Sir Arthur Clarke's scifi stories, I came across a statement something to the effect of, existence of a single species automatically implies the existence of many other species. So considering multi-cellular organisms, something more complex than a virus/bacteria, if we know for a fact that there is one species (plant/animal whatever) then without directly observing any other species or any obvious evidence, can we deduce that there must be other species? Assume we are in a completely new environment like a brand new planet discovered with life on it. Does the existence of a  species imply existence of many other species?
Thanks.

I am not sure I'm providing the kind of answer you would expect.
Your question is very conceptual. For such question it is important to very well define the concepts you're using. For example, the concept of species is not well defined (and will certainly never be well defined as it does not represent a natural category to my point of view). Also, the separation you do between complex and non-complex species might not be obvious. For example, you create two categories which are bacteria/virus and multicellular. But you kind of forget the many of the eukaryotes which belong to non of these two categories. Or some bacteria that might almost be considered as multicellular.
I think it would help answering your question if we had the arguments of Sir Arthur Clark for saying such things. Below are two arguments I could use to defend your statement.
Speciation:
If you consider than one population rarely (or virtually never) go under sufficiently major changes before undergoing speciation, then you would never have only one species which is very different from the others.
Ecology:
One might consider that one species cannot by itself be responsible of a whole cycle of elements. Therefore, if the species we observe can theoretically live forever (equilibrium), then, it implies that other species must exist to recycle their wastes. But this hypothesis has nothing to do with the separation of species per complexity that you do.

Update:
Following your comment: So what you had in mind seem roughly the same than my "Ecology" argument. The difference is that I emphasized on the fact that one species alone cannot live for ever because they degrade their resources through time. I did not want to say that one individual of one species cannot live without the presence of another individual of another species. This individual would need the presence of the other species not for himself but rather but its great-great-grand-children when one resource would have been totally consumed by the ancestors.
For your curiosity, here is base of the tree of life. What is eukarotic but not plants, animals or fungi are called protista and are all (or almost all?!) unicellular. You'll notice that viruses/viroid and prions does not belong to this tree. It would be a bit long to explain why they are no represented and it would have nothing to do with your question :D

I don't have much of a biology background at all so I just assumed naively that viruses/bacterias are "simple". I read all of his short stories back to back so I don't specifically remember which story it was. But if I remember correctly, humans see some giant whale-like creatures on Jupiter and a character remarks about how there must be many other species here. I myself interpreted it to mean like how we humans have a symbiotic relationship and need help like for metabolism, etc.

If complexity correlates with specialization, then it seems that complexity would correlate to some degree with ecological specialization. The speciation argument presumably also includes survival of simpler organisms/species while complexity develops. (By the way, even the definition of organism might be a bit fuzzy. E.g., when, if ever, did a mitochondrion ancestor stop being a symbiote/separate organism? Or how is a colony of clones distinguished from a single organism?)


text:
What is the difference between SNP and STR?
I thought that these were just different format of the same data.
But it seems there isn't a way to convert SNP (single nucleotide polymorphism) data to STR (short tandem repeat) data. Am I right?
As I understand SNPs is basically a "diff" between some base human dna (parts that never change) and given dna. While STRs are strands of dna that differs between individuls.
But if there are enough SNPs (i.e. all of them), it would be trivial to deduce STRs, right?
For example, currently 23andMe tests the whole mitochondrial genome. Does it mean that one can easily deduce STRs?

STRs/SSRs/microsatellites are just short repeats, whereas SNPs refer to a single nucleotide that is swapped out.  Both can easily be different between humans, but in STRs the issue is mainly the length of the repeat whereas the SNP is the actual base in that spot.

It's single nucleotide polymorphism, not polymerase

@Amory, so basically STRs are some kind of insertions/deletions of multiple nucleotides?

If you want to call it that, sure.  It's repeat number, basically.

The solution is in the name!
SNP: single nucleotide polymorphism
The name tells us that it is a change that affect one single nucleotide and that there can be multiple of these (polymorphism could be rewritten as multiple forms)
From the SNP Wikipedia page:

[A SNP] is a DNA sequence variation occurring when a single nucleotide — A, T, C or G — in the genome (or other shared sequence) differs between members of a biological species or paired chromosomes in a human.

So, for instance, if you take 8 individuals and sequence their gene XYZ, you may find, at a certain locus (=position) on the gene:
Individual 1: AAGGTG C AGCAGTC
Individual 2: AAGGTG T AGCAGTC
Individual 3: AAGGTG T AGCAGTC
Individual 4: AAGGTG T AGCAGTC
Individual 5: AAGGTG C AGCAGTC
Individual 6: AAGGTG C AGCAGTC
Individual 7: AAGGTG T AGCAGTC
Individual 8: AAGGTG T AGCAGTC
The position highlighted in bold is a SNP. In this case we only have either C or T (and this produces 2 different alleles for gene XYZ).
This page from University of Utah has a very clear animation on SNPs.
STR: short tandem repeat
These are short repeated sequences. They're in tandem, that is, one after the other.
STR consist of a few (2-6) nucleotides that are repeated several (5-100) times.
For instance this page from the University of Arizona gives the example of D7S280, one STR with sequence (GATA)n (that is, GATA repeated n times)
  1 aatttttgta ttttttttag agacggggtt tcaccatgtt ggtcaggctg actatggagt
 61 tattttaagg ttaatatata taaagggtat gatagaacac ttgtcatagt ttagaacgaa
121 ctaacgatag atagatagat agatagatag atagatagat agatagatag atagacagat
181 tgatagtttt tttttatctc actaaatagt ctatagtaaa catttaatta ccaatatttg
241 gtgcaattct gtcaatgagg ataaatgtgg aatcgttata attcttaaga atatatattc
301 cctctgagtt tttgatacct cagattttaa ggcc

In this case, variations between individuals reside in the number of times the sequence is repeated.

Still don't understand. Do you mean to say that each person has a different sequence length? It is reasonable, but wouldn't that be represented as corresponding SNP insertions and deletions?

Could you please make an STR example  for multiple individuals, like you did for SNP?

Exactly, one could have CACT CACT CACT (3 times) and someone else CACT CACT CACT CACT (4 times). SNPs, are mutations in one single base.


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For the human head, which direction is anterior, and which direction is ventral?
I read the wikipedia entry and I am sort of confused.
In dog, the nose is toward the front. That's anterior. So I conclude that human nose is anterior.
In dog, the head is on the back. So that's dorsal. So I concluded that humans' top head is dorsal.
Yet that's not how things seem to work on anatomy.
We call humans' top head anterior. We also call human nose direction as ventral.
How could that be?
The whole system of anterior, dorsal, ventral, posterior is there so we can see humans like we see dogs (at least anatomically).
Yet it changes again.
So which one is right?
Let me put it this way
Dog's chin is ventral from the eye
In humans, is humans' chin ventral from the eye too? or posterior?
What about the nose? Dog's nose is it's anterior most organ.
In humans, is the nose anterior too?
I mean, if we're going to have different terms for humans and dogs, might as well use words like up, down, front, back right?

It's simple - anterior = ventral and posterior = dorsal for humans.

I thought anterior posterior axis are always perpendicular to ventral dorsal axis on any area of interests?

These terms are determined for "horizontal" animals.

In other word, for humans the nose is anterior? That means the chin is dorsal then. We just need to put humans into horizontal position?

Humans are are upright in their anatomical position - fig. 1 - from which all directions and terminology stems.

Figure 1: Anatomical Position
Because of this, anterior is normally the same direction as ventral and posterior normally the same as dorsal - fig. 2.

Figure 2: Normal directions in humans
Cranial anatomy is a special case, however, as the entire axis of the body bends round during embryonic development as seen in fig. 3.

Figure 3: Bending of the developmental axis
This leads to the cranium being a little odd, where dorsal is equivalent to superior and ventral to anterior in this area of the body only

Figure 4: Resultant difference in neuroanatomy conventions
However, for convenience, anterior and posterior retain their original directions even in this area.  Therefore you could eliminate a large amount of your difficulties by just using these terms instead for most of the body.

To answer your specific questions:

So I conclude that human nose is anterior

Yes

So I concluded that humans' top head is dorsal. Yet ...We call humans' top head anterior

The top of the head is technically dorsal, however in practice would never really be referred to as such, instead being superior.

In humans, is humans' chin ventral from the eye too? or posterior?

The human chin is both inferior to the eye (looking straight at the face in the coronal plane) and anterior to the eye (but only marginally).  It's more obvious if we look at the tip of the nose instead, which again is both inferior and anterior to the eye.

In humans, is the nose anterior too?

Yes, the nose is anterior.

Is the nose ventral? So top of head is not anterior.

So that means dogs will be different than humans then?

No, the top of the head is superior not anterior and yes, in most animals other than humans the directions will be different as the majority don't walk upright so dorsal wont be the same as posterior and ventral wont be in the same direction as anterior.


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How has the use and subsequent ban of DDT affected insect populations?
Living in Australia there were less ticks for example during the use of DDT, now there are more ticks prevalent here. I am wondering if any insect species have declined permanently as the result of the DDT use, and if some have repopulated disproportionately (compared to populations prior to the use of DDT- if there is such data) since it's cessation of use.
How has the use and subsequent ban of DDT (dichlorodiphenyltrichloroethane) affected insect populations?
Are there any studies on this?

affected them in what context?

@GriffinEvo edited , hopefully this is clear, pls advise

yes good thanks, so comparisons of species diversity/richness, before during and after the use and subsequent ban of ddt.

The most thorough study on the matter appears to be entitled "Anthropogenic impacts on mosquito populations in North America over the past century". Their broad conclusion is that various mosquito populations decreased in abundance and variety during heavy DDT usage years. However they have revived in the past few decades. The only species that seemed to have a permanent decline is Ae. Stimulans.  While this study was only on mosquitos, it may be representative of wider insects - most revived but a small fraction faced permanent damage.
There is a large amount of more associative evidence that observes a large decline in insect biomass and can only predict pesticides, such as DDT, as the culprit. The NYTimes had a good article on this.


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What limits our ability to grow enamel rods?
From what I've understood from what I've read (which might be wrong), enamel rods extend away from the dentin in our teeth. As young people grow, the rods are thickened.
What are the technical limitations and/or problems/challenges of trying to extend/grow the rods/crystals while the teeth are in the mouth?
One issue I guess could be that the enamel is porous, and so chemicals could affect the other parts of the teeth.
But one example of trying to improve the quality of tooth enamel is Novamin, which some manufacturers have claimed creates a glass on the tooth. But I don't understand what that means.

Chandra's Textbook of Dental and Oral Histology and Embryology with MCQs p40-42 explains the complexity of enamel, and provides diagrams and images of real enamel.
What I didn't know before was that the hydroxyapatite is in the form of very small crystallites packed inside the key-like structure of the rods. The rods are packed together with a cement-like material. The rods themselves are segmented.
This small design and lack of vital parts suggest to me that bioglasses like Novamin would at least not recreate the natural enamel structure.
What isn't so easy to guess is whether crystallites from the components of the bioglass are formed on the existing crystallites, and if so, whether this can continue indefinitely, and with what qualities.


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What are these flitting sea worms?
I filmed the creatures below this August in the Mediterranean (specifically, the port of Fornells in Minorca of the Balleares). The images were taken from a boat moored just outside the harbor and floating above a field of posidonia in case that is relevant.
There were many of them and they were whizzing about at high speed:

This is to give you an idea of the scale. The jellyfish on the right was about the size of half a tennis ball.

They were a very strange sight since there were so many of them and moving so fast. You can see a video of them in motion here:
http://www.youtube.com/watch?v=GJCzjXALRJ0
The image quality is not very good but you can see how fast the things were moving. So, any idea what these are? I am assuming they are larvae of something or other but what?


text:
How predictably will RNA polymerase not transcribe repetitive sequences?
I am working on an (expensive) synthetic construct, which happens to have many "repetitive" sequences within it that are integral to its function. Primarily, the two sequences that are worrying me are:

A long polyA (about 15 nucleotides).
A consecutive sequence of two nucleotides: GGGUUUGGUUGU, etc.

I've heard from many some of the transcription horrors they've been through because of similar sequences with similar nucleotides. However, some advise that transcribing it shouldn't be a problem.
How predictably can RNA polymerase transcribe these sorts of sequences in E.coli?

I don't think repetitive sequences are intrinsically problematic to an E coli. Bacteria also deal with things like polyadenylation. Basically, you have nothing to lose from trying -- E coli is one of the more robust expression platforms, and it's difficult to predict whether the sequence will fold into some tertiary structure (which can easily impede translation.)
So I think the predictability should be set at the baseline for E coli RNA polymerase error rate, which is about $10^{-5}$.

Yes, transcription of a polyA sequence will be unreliable: for a repetition of 15 times the same nucleotide, the rate of transcription errors will be huge.
For example in E. coli, this paper http://www.ncbi.nlm.nih.gov/pmc/articles/PMC331007/ gives some order of magnitude of transcription errors caused by repeats of nucleotides. According to their data, for a run of 11 A (so shorter than yours), their are more than one third of transcripts with a frame-shift (deletion or insertion of one nucleotide).
In addition you may have bigger problems than transcription errors: your construct will also be extremely prone to frame-shift mutations. For example according to the data on figure 3 of http://www.ncbi.nlm.nih.gov/pubmed/22991466 by extrapolating to a run of 15 A, you can expect an indel rate higher than 10^-2 per base pair per generations. Because you have 15 target nucleotides it means that more than 10% of the cells will have a frameshift mutation leading to your gene not being functional.
I do not have data for 'A consecutive sequence of two nucleotides'.

Welcome to Biology SE! Your answer is welcomed, but we prefer more detailed answers where things are explained, statements are supported with references. Simply posting links to articles may not necessarily the best practice (while it is a good way to support your claims). Please elaborate your answer by processing the papers you linked, extract useful and relevant information from them, use your on words, quote if necessary. Feel free to visit our help center on guidelines for posting good answers. In this form it is rather a comment than a full answer.

I am not sure why 'This does not provide an answer'? I edited the post to add more precisions, but my answer remains the same: a polyA sequence of 15 nucleotides is a problem if it is 'integral to [the] function' as the author says.

I've seen mRNA delivery papers that make their mRNA using a plasmid with up to 150 As on the 3' end of the gene so they don't have to add the tail through a separate enzymatic reaction. However, being on the 3' end would probably prevent frameshift problems. I don't know how they get the As into the plasmid, I tried to order a 100 A DNA oligo from IDT so I could try to add it to a plasmid, but they wouldn't synthesize anything longer than a 30 As in a row.

@AliceD 's comment was before you edited your answer which by the was looks much better!

Great answer. +1 thanks for editing. Writing up the answer and answering the question is something else here at Bio.SE :)


text:
3' or 5' DNA capping protein
Does anyone know of a protein/molecule that can be attached to one end of the DNAs temporarily ? eg. i would like to only to allow one strand of DNA be ligated to another DNA molecule to either it's 3' or 5' but not both. thanks

Could you explain what you're hoping to accomplish a bit more? Why wouldn't it be possible just to put RE sites at one end of your DNA and the correct end of the piece to be ligated, digest with the RE and then ligate the digest?

Alternatively, you could do fusion PCR/Polymerase Cycling Assembly: http://en.wikipedia.org/wiki/Polymerase_cycling_assembly . PCR up your fragments with additions to the primers complementary to the other piece you want to connect to, then combine the two pieces (now with short complementary regions) and do another PCR to make the full product.

Thanks A. Kennard for giving me the answer. you are right.


text:
Why is this dry pepper fruit still "powered"?
Check out this photo of my pepper plant this cloudy morning: (click for full res)

Usually (and this can be seen on 2 and a half of the 4 fruits in this pic) the fruits are "disconnected" from the plant's juice flow when they're ripe. Then the fruit starts to dry. Yet the middle one in the pic is dry while its "cord" is still green (literally). Why does it not become dry like his fellows do?
There's also another interesting situation going on with the lower right fruit's "cord", which is half-dry. I wonder why it has been like this for a little over a month now without change.
The lighting conditions are pretty poor for this plant, so I use a 40 watt incandescent lamp for it and 4 other plants 24/7.
Please, excuse my poor vocabulary :)

The fruit in the middle had his "cord" completely dried out this week, but the weird lower-right half-powered pepper is still like this. I decided to remove them all and I didn't take a pic, which I regret now. It could have been an interesting visual addition.

probably because of the way sunlight falls on them.. the part that receives more sunlight dries out faster than the others. Please check if the sunlight received is uniform all over.

@TheLastWord  makes sense. The sun is blocked by a few leaves for the left peppers. I suppose it must be the reason.

that is the obvious reason.. might be some   biological processes too, but this could be the major contributor.

It might be a potential reason, but certainly not the obvious reason.


text:
Do people often blow out the air from their lungs a lot when living in the cold condition to keep their lungs warm?
Do people often blow out the air from their lungs when living in cold climatic conditions to keep their lungs warm?
I ask this question because it could connect to how people in different areas construct linguistic sounds.
For example, the Germanic families of Language (German, English,...) use a lot of air from the lungs to construct the sound?
Is that because the Europeans living in cold climate often blow out a lot of air from the lung to keep warm and as a result gradually they construct air-driven linguistic sounds?
For people living in warm climates (ex: Sino-Tibetan language like Chinese, Thai), we mostly use the tongue to construct sounds, and we use very little air from our lungs to make sound.
I posted this question to some forums & some people said it’s baloney. However, there's one thing for sure, the environment shapes how local people construct sound. People construct the sound like that because it is constrained by something. One thing can not stand alone, it must be the karma or outcome of something else.

There's warm parts of Europe and cold parts of China... a more proper way to test it would be to test the same language in hot and cold areas and/or at different seasons

Heat loss hypothesis:
I would rather think that blowing while speaking means that one has to inspire often and therefore he would lose much heat by convection. According this hypothesis, I would rather expect to see southern people blowing lots while speaking.
Metabolism hypothesis:
We might say that at low temperature the metabolism increases and therefore the consumption of oxygen should increase. As shown here for example. This would make blowing much air more profitable for people living in cold environments.
Articulation hypothesis:
One might as well hypothesize that the cold would tend to make articulation more complex and using much air would help to be well understood.
Note: It would be interesting to look at many local scales if it is indeed true that the colder the more air people use. At global scale, I am afraid that the observations are quite dependent and statistically speaking, there is not much evidence that cold environment correlates with blowing much air while speaking

But in warm, particularly in tropic climates, you don't loose as much heat by breathing as with cold (and therefore also dry) air: the incoming air is warm and moist already. And I suspect that loud and clear pronounciation of Germanic does not need more breath, but rather better resonance and other techniques that probably do not lead to more breathing (otherwise, how could one survive a long monologue on a theatre stage without hyperventilation)

@cbeleites Well, in my answer I assumed (as did the OP) that germanic languages need more breath. But I have no idea if this is true. In your answer you criticize this assumption and I agree with you.

I guess the main point is that 'blowing out air' doesn't help to 'keep the[ir] lungs warm' anyways as you explain in your 1st paragraph. I just added "experimental" hints that the things one does do to save heat in cold air anyways do not include speaking...

In a cold climate, do people often blow out the air from their lungs a lot when living in the cold condition to keep their lungs warm?

No, and it wouldn't make any sense: breathing more means inhaling more cold air that needs to be warmed up, so the result is a heat loss. The more so, as cold air (< 0°C) has a low water vapor pressure, while the lung likes to have the air at body temperature and well moistened. Which means that you also loose the vaporization heat of the water.
The function of moistening and heating the cold and dry air as well as recollecting some of the heat and water when breathing out is done by the nose. So the sensible (and done) thing in cold weather is to avoid breathing by mouth and instead keep your mouth shut and breathe by nose.
Nevertheless, neither German nor English, nor any of the Scandinavian Germanic languages is spoken through the nose.
My experience is that cold air (personal minimum: -40 °C) in the mouth is very unpleasant, and makes me cough as it is still cold when it arrives in the throat, but of course breathing out by mouth is less of a problem. But breathing out by mouth and in by nose means that the nose cannot recollect the heat and moisture from the outgoing air.
In any case, the amount of breathing is linked rather to oxygen demand and $CO_2$ to be gotten rid of), and even the fastest speaking people I know do not get close to hyperventilation by speaking, not even speaking German or English.
Which means that speaking Germanic languages needs less breath to produce the sounds than what you need to breathe for physilogical reasons even at not much above base rate metabolism (sitting while talking) anyways. Which would imply that the breathing difference between Germanic and Sino-Tibetan languages would not cause an important driving force in language evolution.
A side point is that I don't agree with your concept of cold climate. Both Germany and England are counted as temperate climate. Actually, Frankfurt has higher minimum temperature all year round than Lhasa (as you mentioned Tibetan in your language family).
Also note that the Indo-Germanic language family covers a range of climates from tropic to polar just as the Sino-Tibetan covers some cold regions as well), so maybe language families that are spoken only in polar regions vs. such that are spoken only in tropic regions would be better to look at (see e.g. the Wikipedia language family map).
However, there are probably some confounding influences that need to be taken into account. In cold weather, you do not sit or stand around chatting with people as much. And in the polar climates, historically farming has hardly been possible. So you have populations where hunting has been very important for survival, and regions with very low population density. Both mean that on average, you'll be silent instead of talking. As for having a chat with someone, you'd ask them in - or the length of the chat is limited by temperature.
Which means that if cold is a driving force for the type of pronouciation that evolves, it would be a rather weak link. And in any case, speaking less will overcompensate all these breathing differences.

I personally agree with the OP since taking slower, deeper breaths lowers the minute volume (because of dead space), so it would actually slow the rate of cooling.


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Where can I get yeast mutants?
I want to use some yeast mutants to conduct gene functional analysis, and the gene was isolated from plants. Can anybody give me some information regarding the websites or agencies from which I can purchase the yeast mutants?

see this answer http://biology.stackexchange.com/questions/10917/sources-for-common-laboratory-saccharomyces-strains

as an addition to the above I'd add: the yeast deletion collection at Stanford http://www-sequence.stanford.edu/group/yeast_deletion_project/downloads.html#strainsavail  and this list of brewer's yeasts just for completeness: http://byo.com/resources/yeast


text:
Is ability to easily pollinate desirable?
In Mendel's crosses was it desirable for the plants to be able to cross-pollinate and self pollinate easily ?

Yes, the fact that pea plants were easy to pollinate was desirable and helpful in understanding the effects of Mendelian factors (genes) but for the proper study of the factors expressed CROSS POLLINATION of homozygous plants having different phenotype and genotype ( e.g. cross between RR and rr) was preffered rather than self pollination.


text:
Order of events in hibernation

Arrange this in sequence :
i. Heat loss exceeds heat production.
ii.As body temperature falls, heat loss decreases.
iii.Body temperature equals environmental temperature.
iv.Metabolic activities fall to the basal level.

I am confused between i,iii,ii,iv and iv,i,ii,iii.

@satwik you have answered my question. Just for the sake of our question to answer ratio why don't you " answer " it ?

I think the order i,ii,iii should be correct, since the fall in temperature occurs after the heat loss exceeds production and will continue only till the temperature equals the ambient temperature. iv is the reason for i. Hence iv,i,ii,iii sounds pretty convincing to me.
With i,iii,ii,iv , the main problem is that there can not be any appreciable fall in temperature ii after the temperature equals the environmental temperature iii. And iv seems more probably to be the reason for i rather than the reverse