text:
Why do the deoxyribonucleotides use T and ribonucleotides use U?
We all know deoxyribonucleotides form DNA while ribonucleotides form RNA, DNA is double stranded while RNA is single stranded, and RNA can transcribe from DNA. We also know that DNA use A, G, C, T, while RNA use A, G, C, U and that it's the DNA that stores genetics information, not RNA.
My question is: how does the lost oxygen atom on deoxyribonucleotides 2' site of the sugar (turning it into a ribonucleotide), make such a large difference in function? It just an oxygen atom. Why don't they just all use U or all use T?

Why deoxyribose for DNA and ribose for RNA?
This answer may solve the question why is DNA double strand, RNA single strand, but it doesnt explain why does RNA uses U instead of T.

The question isn't really the same, but the (excellent) answer to the linked question probably answers this one.

RNA can and does form double helices, either through intrastrand base pairs or between strands. http://biology.stackexchange.com/questions/19115/what-makes-dna-helical/19119#19119

"My question is, all the different is due to the deoxyribonucleotides lose an oxygen atom on the 2' site of the sugar, how could be so much different? It just an oxygen atom." Hydroxyl groups are more reactive than a hydride group. The 2' -OH can be deprotonated and react with the Phosphate in the backbone of the RNA molecule and break the phosphodiester bond and cyclize with the phosphate attached to the 3' carbon. The 2' -H cannot react with the phosphate group, so the phosphate backbone of DNA is more stable than an equivalent RNA molecule in that regard

The difference between the T and the U likely has more to do with the enzyme catalyzing the synthesis reaction https://en.wikipedia.org/wiki/Nucleotide#Synthesis and is not directly related to the 2' - hydroxyl.

"It just an oxygen atom". Umm... If you remove an oxygen atom from water, you get a highly flammable gas and not something you would drink to quench your thirst. There's no such thing as "it's just a single atom". Changing an atom is a huge difference.

For the switch from thymine (T) to uracil (U), it actually doesn't have anything to do with the sugar backbone of the nucleotides. This article on Science Daily explains that U is more cost efficient to produce than T because it can be easily gotten from a chemical degradation of cytosine (C). Since RNA has a short life span and because the cell needs a lot of RNA it uses U. DNA, on the other hand, undergoes a lot of checks and repairs. If it were to use U, it wouldn't know if the U was really a U or if it was a C that got damaged. Since it is important to keep the number of mutations to a minimum, DNA uses the more costly T to ensure fidelity.
I would also like to point out @AMR's comment. It isn't just an oxygen atom. An oxygen atom is the difference between the air we breath and ozone that can kill you. It's the difference between water and highly flammable hydrogen gas.

RNA forms double stranded structures!

dsRNA is thermodynamically more stable than dsDNA, actually.

@canadianer The A, B, and Z forms of ds helicies is an artifact of in vitro preparation of the molecule related to the the salt content and consistency of the humidity during the crystallization process. This does not mean that we actually see these structures in vivo, though for DNA, our best model if B. And as I asked on a different thread, is the thermodynamic stability related to the hybridization and thus melt temps needed to open dsRNA or is the relationship actually referring to the stability of the molecules sugar-phosphate backbone.

2'-OH can and does get deprotonated and can then attack the phosphate,  breaking its bond with the 5' carbon of the next nucleotide it the chain. The phosphate and 2'-OH cyclize and the backbone is broken and broken chromosomes lead to apoptosis and cell death, so using an RNA double helix for chromatin would be riskier. Also, it may not be an advantage in larger genomes to have a molecule that is thermodynamically more stable, as this would likely slow and/or increase the energy required to replicate that genome.

@AMR There is a difference in Tm. See, for example, this paper: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC331958/pdf/nar00044-0318.pdf

@canadianer Thank you for the link. It might be a bit difficult to draw genome wide conclusions from 24bp strands, but I am sure that the results are accurate. Adding to my comment above, I also wonder how ribonucleotides interact with histones or if they can, as packing becomes a very important and highly conserved chromosomal element as genome size increases.

@AMR The only conclusion I'm drawing is that dsRNA is thermodynamically more stable than dsDNA.

@canadianer Your observation is correct, and in retrospect I think that the meaning of the last sentence of the answer is unnecessarily vague. Your point regards hybridization stability and I can see where SolarLinux comparison may not be valid from that perspective, however, RNA molecules degrade more rapidly in the sense that their backbones are prone to breakage because of the mechanism I mentioned before. In that respect, DNA is a more stable molecule as it will not break in this manner, making it more suitable for information storage than dsRNA.


text:
Most human-like teratoma ever recorded?
I'm curious to learn about the 'most human' teratoma ever recorded. By that I mean a teratoma which most resembles the form of a human being.
I suppose there are several factors which would contribute to this criteria:
-Most organs, and components found in a human (e.g. brain, teeth, organs, etc.)
-Most closely organized structurally like a developing human.
Also I was wondering. Given the right conditions could a teratoma grow into a living being? Could they theoretically develop the necessary organs to be excised from their host and sustain the functions necessary for survival.
Basically I am curious to learn about the possibility of teratoma maturing into a bonafide organism.

There's a 2003 paper published in the Journal of Korean Medical Science describing a case of a 'homunculus' within a teratoma: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3055135/
It contained some hair, brain tissues, cranial and other bones, but no internal organs.

Way cool. This is the best example I've seen thus far. Thanks for bringing it up.

source: Stack Exchange

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

sort: votes


text:
Why do chameleons move back and forth?
I was always curious, why do chameleons have this strange gait?

could you post a link to a video of the behaviour?

https://www.youtube.com/watch?v=KNsjrokwr-E - hmm they claim that it tries to imitate a leaf. but there is no wind :D

same with walking sticks I guess. They seem to try to blend in with the trees.

The movement you observed serves two functions:

Imitation of leaves to protect against predators
Improved stereoscopic vision while scanning for their own prey

Imitation of leaves (mimesis)
Chameleons in the wild live in trees and are surrounded by leaves. In order to protect themselves from predators they move forth and back to blend with leaves moving in the wind.
Also note that their torso shape resembles a leaf:

Why do they move like this even when there is no wind and they are not sitting on a tree? I suppose they just follow their instincts. Evolution "did not prepare" them for sitting in a cage. The lack of ability to know when to move and when not was not a evolutionary disadvantage so there was not pressure to get rid of it.
Improved stereoscopic vision
Chameleons are predators that use their tongue to catch prey e.g. grasshoppers. While they are looking for their next target, they scan their surroundings with both eyes independently, i.e. one scans the left hemisphere, the other eye scans the right hemisphere, thus during this time they have no stereoscopic vision.
Moving forth and back helps alleviating this. They can estimate the distance to their distance better through the use of motion parallax (closer objects seem to move more than object further away when we move sideways). Once they found a target they turn in its direction and then use both eyes to focus on it, preparing to shoot out their tongue.
(Disclaimer: I am not a biologist. This is from my own reasoning and the German Wikipedia article about Chameleons)

Predators are very good at spotting moving targets, as movements will easily stand out from inanimate objects and vegetation.
Most prey will prefer to hide or just run if they are spotted by predators.
But the chameleons prefer to blend in with the vegetation instead. This gives them the advantage that they may move in plain sight, and still not be recognized as prey.

I don't understand this explanation at all. Are you categorizing chameleons as prey or predators?

They go back and forth for the same reason that stick insects and caterpillars do. to imitate wind and foliage, leaf trembling, to ward of their predators. A possible additional reason is to gain added perspective of their environment.
Here is example of same principle in stick insects:
https://www.youtube.com/watch?v=EAIRjpaOXKs
https://youtu.be/gHoDKY8jL1g
https://www.youtube.com/watch?v=Rq7-BPuLXLo
They don't have the physiology or habitat where they can escape or hide from predators hence the open air hiding tactic.
They don't have running muscles and skeleton. They couldn't run if they wanted to (slower than a snake or bird) and they couldn't hide because trees also don't offer crevices like cliffs and walls do. Their behavior is good for catching more prey and for staying hidden.
They are related to Iguanadons, which are adapted to moving in the sea (cold). Chameleons often live in the shadows, 130 of 171 species are forest dwellers, and most of the others live in trees of savannas and steppes, only a few live on the floor.
They don't need to be warm to hunt, their tongue is still one of the fastest things in vertebrates, so they can hunt when they are cold.
Their prey is not very intelligent: birds, snakes and more rarely mammals. because they are too slow to run away, they don't have hiding places except for the branches, they have a very cautious walk which is disguised, with slow head movements, very active eyes, and ability to keep head still in between steps. hunters will tell you that animals are very oblivious when their head is moving, they generally need to stop to see you, and chameleons stop constantly. there was research to understand their slow muscles, the muscles have slow fibers, they have a heart which is not as capable as fast lizards. http://onlinelibrary.wiley.com/doi/10.1002/jez.1402630102/abstract

How does this answer the question?

Why do they use mimicry is tacitly the same question ... omitting stuff too simple to care to memtion .. as in what do the mimic... we know... why they do so is less trivial. The imitate leaves because of limited matbolism... the suck energetocally like a stock insect. To cut a lomg story short. They dont oscillate due to physiological processes do they... based on a broad look at species habits.

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


text:
Telomeres and daughter strands
How is the primer present in the daughter, leading strand replaced? I've circled the primer in question.

I don't see how this primer can be replaced by DNA polymerase; there is no free 3' end for DNA pol to act on.
My book, however, says there is no telomere problem with the leading strand.
Other sources say there is a telomere problem.
So what is it?

Replication doesn't start at the very end of a chromosome, so there is no problem with leading strand synthesis. It's probably easiest to see if the other half of the image was there:

Forgive the lion; plain white paper seems to be in short supply. Also my writing. Too much tea this morning. Hopefully you can see that leading strand synthesis can continue right to of the end of the chromosome as the fork progresses. The leading primers at the replication origin can be replaced once the first Okazaki fragment from the other replication fork is synthesized.
There is, however, a problem, aptly termed the end replication problem, with lagging stand synthesis:

The dots just mean the chromosome continues in that direction. Important to notice is the lagging strand RNA primer at the end of the chromosome. When this is removed, there is apparently no way to synthesize DNA there. Repeated replication cycles progressively shorten the chromosome and cause the Hayflick limit to cell division (the number of times a cell can divide before dying). To solve this problem, some cell types express an enzyme called telomerase. This is an RNA directed DNA polymerase that adds deoxyribonucleotide repeats to the 3' end of a DNA strand, using its own internal RNA template, to prevent information loss.

Actually, the lion is positioned pretty well to be a topoisomerase. Just about to cut…

thank you so much for this helpful answer. I think I see it now. You are saying that the primers for leading strand synthesis are always sandwiched between DNA segments, while one primer for lagging strand synthesis is unfortunately found alone and un-sandwiched? And that it is these sandwiched primers, that, upon removal, can be replaced by DNA because there is a free -OH end on one side of the sandwich?

@Dissenter You're welcome and yes I think you've got it.

Cells need not die, the will enter into senescence when their telomeres get too short. Also, this may confuse the issue slightly, but the 5' end, though synthesized to the end of the chromosome, is processed to create a 3' overhang. Both ends need a 3'overhang in order to strand invade the telomere to form the T-loops at their respective ends of the chromosome. If the T-loop does not form, this can lead to chromosomal translocations or it can cause the cellular repair mechanisms to recognize the ends as DS breaks and that can trigger the apoptotic pathway.

I think the confusion is coming from the way this picture is drawn. The leading strand does not begin at the end of a chromosome, there is in fact more DNA to the right of your picture that is not shown. This picture is showing the left half of a replication bubble.

I think I understand this. Replication will occur bidirectionally from the the origin inside the replication bubble. If we focus just on 1 parent strand being replicated, on one side of the origin, the daughter stand replication will be continuous. However, on the other side of the same parent strand, the replication will require Okazaki fragments.
So for the same daughter strand, on one side of the replication origin, it will be leading, and on the other side of the origin it will be lagging!
Back to the telomere shortening (end replication problem), this will mean that each daughter strand will end up too short on it's 5' end after the RNA primer (Okazaki fragment) is removed.

Welcome to Bio. We encourage the use of references and sources to allow people to read the backgrounds of your answer.


text:
Incomplete Dominance and Probability
I have a follow-up question about an in-lecture question (this is not a homework question). As you can see I have already answered the question and the question is closed to further submissions.

In any case, this is my reasoning.
The male has the genotype Gg and BB. Fur color is incompletely dominant so to have black fur this implies the male has the genotype BB not Bb (which would likely be gray).
The female has genotype Gg and Bb because as the question states, the female is doubly heterozygotic.
The two have a FEMALE offspring - this is critical. This means that the male "donates" a copy of his X chromosome to the offspring. Now if the question had asked about a male offspring, then that would mean the male had donated a copy of his Y chromosome instead, and the male would have no "say" in the male progeny's eye color.
So the probability of green eyes between a cross of Gg with Gg is 3/4.
The probability of black fur between a cross of BB and Bb is 1/2 given that there is incomplete dominance.
So the probability of both events occurring simultaneously is 3/4 * 1/2 = 3/8 = 0.375.
Is this correct? Or should I account for the "female" offspring part and half the answer?

The male has a phenotype XGY BB, and the female, XGXg Bb. Thus the probability is 0.25.

Eye color is sex-linked. So a green-eyed male has genotype G- (only one X chromosome) for eye color and BB for fur color. The female has genotype GgBb. For the offspring to be female, 1/2 probability, to have green eyes 1/1 probability (G is dominant and it will receive the G from the father), and for gray fur 1/2 (1/2 chance it will receive b from the mother). So 1/2 * 1/1 * 1/2 = 1/4


text:
What are non-heritable changes to genomes?
I am told that mutations are heritable changes to the genome.
So this begs the question - what are non-heritable changes to genome?

Mutations are not necesarily heritable changes to the genome. Think of newly acquired mutations that lead to cancer. These are not heritable. Only mutations which are present in the sperm or egg cells are heritable, no matter whether these are old or newly acquired. Non-heritable changes in the genome occur anywhere else, for example in your skin after prolonged sun exposure.

@Chris "Mutations Are Heritable
Changes in DNA"

I don't see it like this. A mutation is a change in the DNA code.

To my point of view the expression "heritable change in DNA" is extremely misleading of even a non-sense. OR it uses a definition of heritability that is close to the one of inheritance. The concept of inheritance then depends on whether we look at multicellular inheritance or unicellular inheritance.

What is your textbook btw?

@Remi.b "Principles of Life" By Hillis ... piece of crap if you ask me. I prefer Campbell.

The passage says mutations are changes in the DNA sequence that are passed on from one cell or organism to another. Their definition of heritable seems to be how a layman would perceive it, not necessarily how am evolutionary biologist would.

Also what is your definition of changes to the genome? Sequence changes, epigenetic changes, regulatory changes?

Regardless of the use of "heritable", the later part of the quoted paragraph is not true: "we can state that mutations are changes in the nucleotide sequence of DNA that are passed on from one cell, or organism, to another". It should be "that may be passed on". As many pointed out mutations are not necessarily passed on.

Somatic mutations are "heritable" by the daughter cells of the somatic cell. It is indeed heritable in the cellular level; doesn't mean that it will always be inherited (what if the cell dies/doesn't divide)

Mutations in Cancer cells are heritable @Chris - they pass from one generation of cancer cells to the next, not heritable in the germ-line of the organism but still inherited within lineages of cells.

@GriffinEvo Using this definition every mutation would be heritable as long as the cell which acquired it is still dividing.

The definition above states "from one cell, or organism, to another" @Chris

I don't know what you really mean by "heritable changes to the genome". I think you will understand why this sentence makes no sense after reading what follows. I start with some background and then try to address directly what confuses you.
Short introduction to the concept of heritability
The concept of heritability may have two meanings.
Heritability is a concept defined at the population level for one given trait. The heritability ($h_B^2$) (in the broad sense) is the ratio of the genetic variance $V_p$ over the phenotypic variance $V_p$, where the phenotypic variance can itself be decomposed into environmental $V_e$ and genetic variance $V_g$ (and their covariance that we will neglect for the purpose of this question).
$$h_B^2 = \frac{V_{g}}{V_{p}} = \frac{V_{g}}{V_{e} + V_{g}}$$
When saying environmental variance $V_e$, we don't refer to the total variance in the environment (such as the variance in temperature for example) but we refer to the phenotypic variance (in a given population of a given trait of interest) that is caused by environmental variance. The same logic is true for the genetic variance.
Inheritence
While the concept of heritability applies to phenotypic traits, the concept of inheritence can apply to DNA material. A mutation is inherited if the offspring receives the sequence from his/her mother or from his/her father (assuming we are talking about a species that have sexual reproduction with 2 genders).
Somatic versus germline mutations
As pointed by @Chris in the comments. In multicellular organisms, not all mutations can be transmitted to the multicellular offspring. Most of the cells do not give rise to any other multicellular organisms. For example, imagine that while the biceps is under development at very low age, a mutation occurs that will be inherited by the daughter cells but not to the multicellular offspring. we call the line of cells that do not give rise to gametes (sperm and ovules), the soma line, by opposition to the germ line which gives rise to the gametes.
To answer your question
As soon as a given locus (position on the DNA) has some variance and that this variance explains some phenotypic variance, then the phenotypic trait it influences has a heritability greater than zero. If the variance at this locus has no effect on the phenotype, then it's heritability is zero (because $V_g = 0$, although there is some variance in the actual sequence). If the phenotypic trait of interest does not show any variance (in the population considered), then the concept of heritability is undefined for this trait!
I think you may have a confusion between "inherited trait" and "heritable trait". A mutation will necessarily be transmissible to the offspring (except if it happen to be in the somatic line in such case it will only be transmitted to daughter cells but not to the multicellular offspring) but it doesn't mean that this mutation will necessarily explain some variance in a phenotypic trait. A new much is necessarily heritable (pay attention to the soma vs germ line) but does not mean that a phenotypic will have higher heritability thanks to this mutation.

it's what my book tells me; "Mutations Are Heritable
Changes in DNA."

See my update. Hope that will help you. I think you got messed up by the concepts of heritability and inheritance. The answer is maybe complciated I am a bit scared to have just render things even more complicated. But I hope it will help you. I've got to go now, so I cannot give you further answers today! Sorry

@Dissenter yes, mutations are heritable i.e. they can be inherited but they don't necessarily get inherited since during meiosis you have processes such as independent assortment and chromosomal cross over, which means the gamete won't necessarily have the mutation of the parents!

Most mutations to the DNA are heritable, but not all are inherited.
Mutations occur in the DNA, DNA is then replicated and transmitted to offspring (cells or organisms). Generally all mutations are heritable because they can be inherited, but some aren't - either by random chance (drift) or deleterious fitness effects (selection). Any mutation which makes the cell less fit has a reduced chance of being inherited, but even mutations leading to cancer are inherited at some level (from mother cancer cell to daughter cancer cells) but at some point this lineage of inheritance will stop because it will kill the host (but this is no different to species/lineages of organism going extinct - if I carried a new novel mutation but didn't have children then that mutation is not inherited).
*I suppose a mutation which stops DNA from being replicated could be classed as not-heritable because the DNA is not going to be replicated, but that depends on there being no other sources of replication machinery (other cells perhaps) - a process I don't know well enough to offer any firm conclusions on.
Non-heritable changes to the genome
DNA can be altered beyond just sequence mutation, for example methylation- but this can be used as a heritable change to the genome (genomic imprinting). Perhaps gene expression with strong environmental effects on gene expression could be considered as not heritable (because if the environment is not "inherited" then parent-offspring regression would be 0) but maybe that's a change to the transcriptome rather than genome.


text:
How can antibiotics damage the ear?
What is the mechanism by which aminoglycoside antibiotics (such as streptomycin and gentamicin) damage the mechano-sensory hair cells of the auditory and vestibular system? (Could this be seen as evidence for Lynn Margulis' theory that these cilia are descended from bacteria?)

Thanks, I added two links (but it doesn't allow new users to add more).  Maybe it will let me add another one here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2728278/

The article does describe the mechanism.  I just didn't know if it is similar to the way it affects gram negative bacteria?        "When exposed to aminoglycosides, hair cells demonstrate both morphologic and molecular features of apoptotic cell death, including condensed, marginated chromatin, and positive terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling staining (Forge and Fradis 1985; Li et al. 1995; Lang and Liu 1997; Nakagawa et al. 1998; Forge and Li 2000; Matsui et al. 2002; Mangiardi et al. 2004)."

"In addition, aminoglycoside-induced hair cell apoptosis is mediated by c-Jun N-terminal kinase (JNK), a member of the mitogen-activated protein kinase family...Furthermore, aminoglycoside exposure results in cytochrome c release from the mitochondria and caspase activation in hair cells (Cheng et al. 2002; Cunningham et al. 2002; Matsui et al. 2004; Sugahara et al. 2006)."

This phenomenon is called Ototoxicity, which literally means "toxic for the ear". Mostly the cochlea or the auditory nerve are affected and almost all these cases are connected to medications as gentamicin or cisplatin.
The reasons for this are that the cells are either driven into apoptosis or necrosis. This is caused by destroying mitochondria and releasing calcium and cytochrome c which triggers apoptosis or by deregulating the the JNK-signal transduction pathway and causing necrosis. This image gives a nice overview:

For further reading you can start with the Wikipedia page on ototoxicity and then also read these two papers which are both freely available (the figure above is from the first):

Intracellular mechanisms of aminoglycoside-induced cytotoxicity.
Gentamicin rapidly inhibits mitochondrial metabolism in
high-frequency cochlear outer hair cells.

To answer the question why this occurs in the ear, it seems that there is some genetic predisposition for this, see this paper: "Aminoglycoside-induced ototoxicity." Mitochondrial damages leading to hearing loss is also not uncommin, see here. Noise seems to play an additional role here and is probably the "last drop" to cause hearing loss.

Thank you for your very clear answer and great references!  One thing that I still don't quite understand is why the hair cells would be disproportionately affected.  Don't all cells contain mitochondria?  And if so why isn't apoptosis triggered in all cells?

Thats a good question for which I have no answer at the moment. I will look into it.

It seems that there is some genetic predisposition for this, see this paper: Aminoglycoside-induced ototoxicity.


text:
Property of E.coli harboring F element
From Genetics by Ursula Goodenough

E.coli harboring an F element are endowed with a number of phenotypic
  traits :
1.They are sensitive to infection by ssRNA phages and certain ssDNA phages.
2.They resist the growth of female specific phages as T3 and T7.

What is the molecular mechanism behind this sensitivity and resistance ?

Some bacteriophages adsorb on the pili. So the individuals carrying the F-element will be susceptible to these.
F-plasmid encoded membrane protein PifA is responsible for the T7 resistance [See here]. The exact mechanism is not known

If you see the list of references in the textbook chapter you will be able to trace the reference for a certain quoted fact


text:
What I can do in order to improve the folding of the protein?
I am struggling with the expression of the certain protein. It seems that it is not properly folded and thus, it is not active. I tried to express it at the lower temperature and for the longer time, but it did not help. Can anyone give me a clue what I can try to do?
The size of the protein is around 55 kDa. I know that I have some soluble protein as I run western blot. The protein contain His-taq on the C-terminus so I started with Ni-NTA column chromatography. Steps of purification:

Incubation the lysate with resin (30 min/4°C)
Unbound proteins were collected as the ‘Flow-through’ fraction
Wash 1 with buffer: 50 mM NaH2PO4, 1M NaCl, 10 mM Imidazole
Wash 2 with 10% buffer B in buffer A
Elution with buffer B: 50 mM NaH2PO4, 1M NaCl, 250 mM Imidazole

Because the protein is co-purified with something else in size around 57 kDa (which might be a chaperone protein) I tried also:
1. add ATP to first wash in concentartion of 2.5 mM and incubate column for 1h/4C
2. add ATP to first wash in concentartion of 2.5 mM and incubate column overnight in 4C
3. add ATP to first wash in concentartion of 2.5 mM and incubate column overnight in room temperature
4. add ATP and glycerol to first wash in concentartion of 2.5 mM for ATP and  4M for glycerol and incubate column for 2h in 4add ATP to first wash in concentartion of 2.5 mM and incubate column overnight in 4C
All the method end up with two close to each other bands (only one of them is my protein) and protein is not active.

What kind of protein? Is this a membrane proteine? Probably even a helical? Or is it toxic? What conditions did you try?

DNA binding protein. I tried express it in 37°C /4 hrs, 20°C/4hrs and 20°C /overnight

You'll have to add a lot more detail if you want to have a chance for any proper advice. All the known properties of the protein as well as your exact expression and purification protocols at minimum. Otherwise you'll only get some guesses and vague advice.

If you have over-expressed an eukaryotic full length protein or the enzymatic part, then E. coli does not necessarily provide a good environment for its folding so you need to express it in the same system which the original protein came from, e.g. mammalian or Drosophila etc. E. coli over expression is mostly used to generate wast amounts of protein for the purposes of protein sequence based Ab generation amongst other things. Look at this review for some of the solutions it offers for proteins not folding correctly in E. coli when over-expressed (http://www.biomedcentral.com/1472-6750/4/32).
The remainder of your question is a duplicate of this question (Ni-NTA purification, problem with the chaperone protein), which I have provided an extensive answer/comments to!
In addition, since the lack of enzyme functionality is a potential indication of errors in its state/3D structure, it is however not a definitive reason. Could you provide some explanations as to what experiments you have conducted to reach that conclusion and how this second point about chaperone eluding with your protein relevant to the first and the last section of your question?

Also, to make it easier on yourself. If it is a soluble protein, use a leader sequence that translocates out of the cell. Then there will be no need for lysis


text:
What species of butterfly is this?
This big fellow came to visit my kitchen (in Hong Kong) a bit earlier.
It is brown with some longitudinal white stripes, banana/boomerang-shaped patterns towards the middle, and an eye-like marking on each forewing tip. Picture below.
What kind of butterfly is it?

I helped it find the exit in the meantime, not before taking a lot more pictures.

Can you please add where your kitchen is located?

People can't search by image very easily. Could you please add a text description of it to help people find it?

@HighlyIrregular I'm not sure how to describe it.. brown butterfly (well.. moth) with white stripes? Any suggestions?

@aditsu, something like that is good. The marking on the front tip of the wing looks a little like an eye too. I'd describe some of the other markings as boomerang or banana shaped, and v-shaped.

@HighlyIrregular I added a description, you can suggest changes if you want.

It isn't a butterfly, it's a saturnid moth -  Samia canningi, also known as the wild eri silkworm moth.
There is a good image on Flickr here, and some more information here.

Oh wow, something about its coloring and behavior seemed to say "moth", but I couldn't believe that a moth could be so big and so beautiful.

It's related to the largest sprcies of moth - the Atlas moth.

A lot of those Samia look alike, I'm impressed that you could identify the exact one.


text:
Datasets of aligned nucleotide sequences
Where can I find some datasets of aligned nucleotide sequences? And what should I assume about the accuracy of the alignments there?
(I would like to use such datasets for training the alignment model I am working on. In particular, to help me get an estimate on some parameters such as the frequency of single nt INDEL at some locations.)

What do you want to do with this aligned sequences? Test algorithms? Actually your question is a bit unclear.

I would like to use such a dataset for training, i.e. to help me infer some parameters for the alignment tool I am working on. Thank you for your comment; I will edit my question to clarify.

I agree with @Chris! do you mean if the alignment itself can be trusted based on the algorithm used or the sequences themselves can be trusted. Are you worried about the semi-conserved sequences being aligned in a variable manner depending on the algorithm used? For different alignment algorithms please see this post (http://biology.stackexchange.com/questions/20075/what-is-the-state-of-the-art-algorithm-for-multiple-sequence-alignment). I could be totally wrong but multiple alignment and semi-conserved sequences is mostly an issue for AA not nucleotides since they either match or they don't

Thank you for your comment. Amino Acid alignment wouldn't work for my purpose (I think), because I am trying to infer the probability of a single nt INDEL at a given location.

So the alignment has to be trusted in the sense that the nucleotide INDELs predicted by the alignment are correct.

Well.. Indels are read by your sequencer.. There are machine errors and sample prep errors. You have to set up controls in your machine and train your set.. I haven't really understood your question, however.

I haven't really understood your comment but that is probably because I'm relatively new to this world. What I'm trying to do: A pair of aligned nt sequences can have regions that are conserved, it can also have insertions/deletions. Those insertions/deletions can be of full codons, but there can also be insertions/deletions of single nucleotides (Am I right so far?). My purpose from a dataset of aligned nt sequences is to study those insertions/deletions (and infer parameters based on them for the alignment tool I'm working on).

@AnasElghafari.. I would suggest that you use some diagram to make your question clear.

Okay, let's forget about the "goldstandard" and "absolutely correct" business. I edited the question so now I am only asking for the datasets of aligned nt sequences.

Hey guys, I edited my question into something which -I hope- is clearer. Can you please remove the hold?

what do you mean by aligned nucleotide sequences: pairwise alignment or MSA?

pairwise would be enough for my purpose.

There are some manually curated HIV alignments at LANL. HIV is quite variable in length so you will find many indels in these alignments.

You can find 46-way multiz alignment from UCSC genome browser, it is down on comparative genomics part and labelled as "cons 46-way", which is a genome alignment of 46 vertebrate species. You can use data on their genome browser on the site, or get download information here.
If you are interested in pair-wise alignments, I don't know of any pair-wise alignment database, but in fact you don't need one. You can search for nucleotide sequences from NCBI nucleotide database and align them using BLAST on their website. BLAST is maybe the most common tool for pair-wise alignments and also for database alignment searches, where a single query sequence is searched for matches throughout a database of sequences. If you want to do a large number of alignments, you can download BLAST to your computer to do them faster.


text:
where to find the relative frequency distribution of synonymous codons
Most amino acids can be encoded by more than one codon. For example, Serine can be encoded by any one of {UCU, UCC, UCA, UCG, AGU, AGC}.
My question is in two parts:
1) what are the relative frequencies of those codons? This question can be equivalently phrased in probabilistic terms: What is the probability that a given amino acid was encoded by particular codon?
2) Is this probability dependent on the context (the neighboring codons/amino acids)?

The phenomenon of using different codons with different probabilities is called codon usage bias. How the different codons are used is sometimes pretty different between species and requires some care. This is especially true when you want to overexpress sequences in bacteria to produce protein, which may need codon optimization to ensure an optimal codon usage (otherwise rare tRNAs can slow down the translation process). There is a database (based on the NCBI Genbank) which gives you the codon probabilities for different species:

Codon Usage Database

Additionally, these papers might be interesting:

Synonymous codon usage in bacteria.
An evaluation of measures of synonymous codon usage bias.

Regarding your second question, I don't think (and I haven't found any evidence either) that the codon usage is dependent on the neighbours.

The codon usage biases are species-dependant, so you may have to measure it for the genome or set of genes you are interested in.
This bias is at least in some cases correlated to the genome composition in terms of A, T, G and C (see figure 3 of this paper about cyanobacteria). So in a sense, it is indeed dependent on the context if you include nucleotide composition in what you call "context".


text:
Blood pressure difference while seated and laid down
My blood pressure readings differ a lot when I read them while seated and while I lay down on a bed.
I tie the strap in both cases to my left bicep and rest for a minute before noting the readings down.
For example, one reading I took was:
Seated: 130-85
Laying on bed: 115-75
These were noted down one after the other.
I am not sure if there should be this much difference in the readings and is this something to be worried about.

Do you have any symptoms?

No. I don't have any. Any specific symptoms?

It is expected that BP would be higher when laying on the bed than when seated.  Is the cuff at the same height relative to the heart in both of your measurements?  Also have you tried measuring BP when standing?

If blood pressure increases on standing, you may have some degree of orthostatic hypertension (not to be confused with orthostatic hypotension which is more common).  This link might be of use:  http://www.medscape.com/viewarticle/543590_2

Thanks Chris. While standing and having the cuff position at the same position relative to my heart when I took the other two readings gave a fall of around 5.

I can't offer specific advice as to your personal readings, but it is normal to expect a difference in blood pressure between sitting & supine (lying down) positions.
I have taken this quote from the Department of Health Care Sciences at Wayne State University website.

Effects of body position on blood pressure
Blood pressure is commonly measured in the seated or supine position; however, the two positions give different measurement values. With that in mind, any time a value is recorded, body position should also be recorded. It is widely accepted that diastolic pressures while sitting are higher than when a patient is supine by as much as 5 mmHg. When the arm is at the level of the heart, systolic pressure can be 8 mmHg higher, such as when a patient is in the supine position rather than sitting. A patient supporting their own arm (isometric exercise) may increase the pressure readings. If the patient’s back is not supported (i.e., when a patient is seated on an exam table instead of a chair) the diastolic pressure may be increased by 6 mmHg. Crossing the legs also may raise systolic pressure by 2-8 mmHg. Arm position plays a dramatic role in value errors as well. If the arm is below the level of the heart, values will be too high; if the arm is above the level of the heart, values will be underestimated. For every inch the arm is above or below the level of the heart, a 2 mmHg difference will be found (Pickering et al. Circ 2005;111:697-716).

So if you are comparing your own blood pressure day-to-day, make sure you keep a consistent position.
Additionally, if you are reading guidelines for healthy/risk blood pressures, make sure you take this into account.

Thanks for the valuable inputs Luke. I did take a few readings this morning in different positions and they are totally different than yesterday. Now while laying down the reading is more than while seated.
Supine: 125-80
Sitting: 109-72
Standing: 102-70
So I guess my cuff position was not at the same position relative to my heart yesterday and that gave this difference in reading.
Also, as normal reading is said to be between 100-60 & 120-80, when I saw 125-80, I was a little worried.

125/80 is nothing to worry about really.  Over 140 and I'd start to worry.  So if you're taking BP medication, it's working so keep doing it, but otherwise you don't need to start taking it for 125.


text:
Is love biologically useful?
I thought about this statement a while ago:

Natural selection sucks, it says those who love too much (or too many) will die the easiest and fastest. Sad but true.

Only family (biologically of course) should be loved. This isn't rather an ethics question but whether those who love too many or too much die easiest. true?
NEW QUESTION: What about if you love your subject, mathematics, to death? You'll give up meditating, personality, gym, friends, goldfish, everything just to find out new theorems. What is the take on this?
Surely you'll take a bird's eye view right after the accomplishment (or perhaps failure sometimes) and see what you've accumulated in losses (or in earnings). But Is it in the right path of the true purpose?
Given the person is highly into itself, such that it operates on an ideology instead of what the current trends are (in this case, stay healthy^^), it would be great to love. Nothing else would matter.
Biologically, it wouldn't make sense. If I loved something like mathematics, how in the world could I produce babies? Geniuses like Erdos never had children but, my god take a look at his work.
^^I'm not sure if my claim is correct, which is the matter of this question:
Should we stay healthy or go beyond our health (as the Curie's did) to discover science?

Completely false.  Natural selection is a process by which traits that hurt reproductive success can become less common while traits that improve reproductive success can become more common.  In complex organisms, altruistic behavior and society can be a huge fitness benefit for all creatures in the population.  The ability to love is probably one of the best traits a species can possess.

Also, depending on what exactly you mean by love, the exact opposite may be true. Those who reproduce promiscuously, for example, will be the most selected.

Sometimes fitness may be improved by short lifespan, I'm thinking trade offs between reproductive success and somatic maintenance

@Amory that is very irrelevant. Does it inspire reproduction of genes familiar to the individual?

some animals find that monogamy and small groups and tending to their offspring works for them, others find that having lots of offspring and eating the ones that can't get away fast enough works best.  Biology has a tremendous number of solutions to the one problem.  love is just one of them.

Natural selection deals more with populations and not so much individuals. Its not really accurate to say natural selection says this person will die young if they do X. Its more looking at which traits will proliferate in a population. Obviously since love exists, the quote is not true.

the behavior of individuals are often observed in ethology and the effects of selection/evolution still discussed.  i think the question, to be fair doesn't focus specifically on individuals

@DonLarynx I'm feeling somewhat indebted since I wrote most of the answer before the bounty was put up.  If there's anything I can add or clarify for you, please let me know.

The idea that we only love our family according to biology is not true, but its also not clear what people mean by the word 'love'.  There are many ways to interpret that word!
Hope this doesn't totally suck any romantic ideas out of you, but metaphysical concepts of love and romantic ideas of love are not always relevant when you talk about biology.  A case for the universal human family and world peace can be made.
In evolutionary biology love usually has a different meaning than most people mean, but maybe one similar to what you refer to here; Love is often considered to be the bond with one's offspring to help ensure that they succeed and reproduce.
This idea is most often expressed in terms of "kin selection".  A theory that an individual is helpful to your reproductive success if they carry genes similar to you.  In particular ant colonies may be entirely built around the solidarity of the family unit: all the workers are birthed from the queen and they themselves do not reproduce, but they do work together because, to put it plainly, helping the hive is helping themselves reproduce.
The biologist Sarah Hrdy has written an excellent book that looks at the biological origins and variety of ways that motherhood creates social and emotional relationships, which is not entirely a human idea of motherhood, but biological and mind expanding for the evolutionary take.
However, the idea that only close relatives should be loved is not quite right. Even intuitively we see adults adopting children distinctly unlike them in appearance, people devoting their lives to the general good, etc etc. Biology cannot pretend that this sort of behavior doesn't exist - it can only try to explain it within the framework of what we understand.
Its well understood that cooperation and social cohesion are also the result of evolutionary forces.  The primary reference for this is the iterated Prisoner's Dilemma experiment; in systems where individuals are interacting over and over again, helping others creates a system of cooperation where reciprocity where everyone benefits because the payoffs are stability, security, safety etc.
Again this might not sound like 'love', but in human social, cooperative situations it can be professed as love. Love of country, profession, causes etc if you will.
There is a big debate about whether altruism exists: many biologists believe that an extended from of kin selection is in play - that we're all one sort of human family.  This is essentially an argument that all our energies are self interested on some level - we're just trying to further the interests of the human race because it will help our own offspring do well.
I think it might go further than that - we also care for non human and even ugly very distant forms of life if you look at some people's lives.  One can argue that the realization that caring about the ecosystem is self-interest and not altruistic.  The distance at which this extends kin selection is pretty far, but anyway the argument goes on.
Additional Points: Lots of human interests like science, are a sort of love? They don't seem to help reproduction.
This is a pretty deep point, really.  I'd say it can help to understand question to start with uncles and grandmothers.  Lots of animals do not reproduce, and this is considered okay by kin selection.  Take a look at wolf packs.  The alpha male is the only animal to mate, the other males seem to be hanging out.  First of all the wolves may be closely related, so the avuncular role of taking care of cousins and nephew/nieces is one kin selection argument.  But even if they weren't, there is the fact that pack structure is not biologically altruistic; the other males and females who do not mate may still do so in the future.  In the meantime, the pack cooperation creates a more secure condition where offspring can have a better chance of success.  Lots of creative, cultural, scientific work is similar as far as I can see.  We can adopt non-reproductive pursuits and still feel that we are doing something worthwhile.  I guess the same can be said for adoption, social causes, religion and just about anything else people do which is not having children.
How can this be a selective advantage - included by evolution into the human instinct?  I'd cite the grandmother effect here.  There is some evidence to support the idea that women live longer after menopause because it creates more successful grandchildren.  While this is not a direct effect, any mutation that extends the caregiving instinct would be sustained in the gene pool.  Its possible that if such a caregiving instinct of uncles and grandmothers were to extend to other people, even beyond the family, that it would be sustained in the gene pool.
Indeed being smart and or rich usually doesn't increase the number of children humans have.  In fact the opposite is the case for both statistical and anecdotal evidence.  Few would say that this is a bad thing.  Human being are getting a better deal when they spend energy on better quality offspring, not quantity.  You can look at the r/K selection theory for a better understanding of this argument, but some animals have chosen cheap offspring and many of them - think cockroach or guppy.  These animals would rather eat their offspring than try to feed it.  Humans, more than nearly any other animal i believe, spend their lives caring for helpless offspring until they are ready for life.  Modern life has only extended this from a few years to nearly 20 years.  But it certainly works - the only animal that can compete with human beings is other human beings.
Hope that makes sense.  There's some speculating here, but its hard to dispute that people devote their time and energy to all sorts of things besides mating.  In the end biology has to accommodate such behavior.  Biological theories we call laws don't change the behavior of living things;  its always the other way around.

Shigeta brings up the question of altruism which Richard Dawkins famously explains in the context of evolution in The Selfish Gene. This is probably the easiest way to translate feelings of love into biology.
EO Wilson has also addressed the idea of kinship and  altruism, providing arguments on both sides of the issue at this point. He was an early champion of kinship as a basis for altruism, but has more recently suggested that it requires too much mathematics for the individual to decipher without any real data (I mean you would need a lot of data and some time to figure out whether to save your cousin or your niece and have to make assumptions about your own risk). I think Dawkins ideas make a lot of sense even if they do assume some unconscious math, after all, we can catch baseballs - something that requires a lot of math to solve on paper, but we do it in an instant in our head.
It may be helpful to consider the tribal nature of humans throughout much of our evolution. Who needs math when the real question is merely,'Is this person a member of my tribe or not?'
If we need to consider romantic love, consider couching it in similar language. 'Can I form a strong bond with this person so that we can successfully raise children?'


text:
How do cellphones calculate heart rate?
How do cellphones calculate heart rate ? I understand that the cameras there try to count undulation in blood flow, but is the method of calculation same as that of professional SpO2 monitors ?

I'm not sure this question is on topic here - it's about technology and apps. But assuming you mean how do apps like this one calculate HR. I believe it measures fluctuations in the colour of the skin (it will change as the quantity of blood varies in the capillaries with pulsing action) and it is simply a case of X beats in 10 seconds = 6*X bpm. SpO2 is a measure of oxygen saturation, not heart rate.

@GriffinEvo Thus us exactly how it is done. The "redness" of the skin changes with the heart rate and this is measured. See this reference. I would suggest you make it a real answer.

@GriffinEvo I was not sure where the question belonged, this looked the most relevant forum.

I asked a related question on Skeptics recently and was pointed to this work - it appears to be detecting changes in skin colour related to heart rate.

Wouldn't this work out only for people with a very fair complexion ??

@WYSIWYG: if you look at ~1:40 of the the Siggraph 2012 video you will see that the algorithm works for dark skin tones too.

@GriffinEvo I agree with Chris, try to make this into an answer. You can also incorporate information given by others.


text:
Human longevity interventions ranked by effectiveness
Generally living longer and with a better quality of life is considered a good thing, if not for ourselves then for our family and friends who care about us. Some factors that influence human longevity are outside our control or only currently exist in a research laboratory; others factors we can control but vary in their impact and effectiveness.
What interventions (preventative or curative) applied by individuals have been proven to increase human longevity, ranked by their effectiveness?
The interventions can be ranked by the ratio of Time Spent vs. Time Gained or Money Spent vs Time Gained. A centuries' worth of data driven medicine and longitudinal studies should provide some answer as to what works and what doesn't.
For purposes of this question, please exclude future interventions that have not yet or never been tested on a sizable portion of population.
Some of the biggest improvements in collective aggregate life expectancy in a society have been communal solutions such as elimination of pathogens. As these either exist or don't exist for a given community - I'd like to narrow the scope to interventions applied or chosen by individuals (such what they personally do or don't do). That is, interventions that supplement communal improvements.

Time Spent vs. Time Gained is not a concept I'm familiar with, because much of the time, the gain was an entire lifetime. I don't know that any studies have averaged it out for entire populations.
Four generations ago, the average Swede had the same probability of dying as a hunter-gatherer, but improvements in our living conditions through medicine, better sanitation and clean drinking water (considered "environmental" changes) decreased mortality rates to modern levels in just 100 years, researchers found.
The most significant advances which promoted health and longevity include (as mentioned above):

improved sanitation.
improved water quality.
vaccines.
antibiotics.
improved living conditions.
improved nutrition.

Since you posted a comment indicating a change in your question, I'll stop here.

My bad. I'll need to narrow the question to mean individual interventions that supplement overarching communal interventions.

Time Spent vs Time Gained is a way to attempt to remove nation-specific costing from an assessment of effectiveness. For instance, 1 hour of Intervention X every day adds 10 years if applied from Age Y. But then it removes a whole class of interventions that are not time based (excluding a Labor Theory of Value). In practice, studies that separate out communal interventions from individual interventions may or may not be common, depending on who's driving the report or research grant. Typically government studies aim for bang-for-buck on interventions they can directly apply (i.e. communal).

Woah! That is totally out of my league! Thanks for clearing that up before I got too deeply into my answer.

+1. Your answer was very useful in helping me clarify what I meant by longevity interventions.


text:
Why do peas change colour?
I am doing an experiment on preservation of peas.
The first notable change to the peas over a period of one week is that they have changed colour from bright green to a dull colour... Why is this so?
The only test tube which did not have peas which changed colour was the one which was kept at 4 degrees Celcius in a fridge, so it probably has some relation to temperature...
Many thanks
N.B.: I know that the bacteria reproduce and could use the pea as their source of food, but how do they have any relation to the colour of the pea? I also put the tag "bacteria" and "thermodynamics" as I couldn't find any other related tags.

Have you preserved them in a refrigerator ?

Might be interested in reading this

@biogirllajja Interesting, but I'll still have a look at the answers to this question...

I am tempted to post an answer, but I am not sure if it is ethical to do your homework for you completely. Do you have access to the full text of article biogirl lajja linked ? The introduction section, page 2, contains your answer.

One more keyword - chlorophyll.

its okay to post an answer Barbara.  homework questions are allowed

@Barbara I've done my homework, by using information on this site: http://faculty.weber.edu/coberg/class/3853/3853%20MOs%20and%20Food%20Spoilage%20notes.htm (though I can't write the answer myself as I'm not a proper biologist) Don't worry, if you answer this question, you will help the community and others who wish to know the answer to this question (and you'll get more rep). Thanks ;)

Chlorophyll is a dye that makes leaves green, it plays a key role in photosynthesis. It is present also in unripe fruits, young peas etc. Maybe I should say chlorophylls, because it is a group of similar chemicals. They get degraded by heat.
(No assistence of microbes needed).
Bonus: Chlorophyll contains magnesium at the molecule core, which facilitates the green color. There were some creative people, who were upset, that the canned cucumbers are not green enough, so they added some copper-containing molecule during canning. It replaced magnesium and was more stable, so beautiful bright green cucumbers were on the market for a while. However, they turned out to be slightly poisonous and are not sold anymore.
Bonus 2: Most varieties of peas change color also naturally as they rippen. The seeds become yellow. The chlorophyll gets degraded in plant metabolism. The chloroplasts, i.e. the cell organelles responsible for photosynthesis change function to become storage organelles called leucoplasts.
(Edit: Ooops, I first wrote that chlorophyll supposedly contains iron. That was wrong, it is magnesium. Iron is present in a similar die called heme, which makes blood red. Probably I am getting too old :-) )


text:
Reasons for strange heart rate graph following exercise (line going up and down)?
Following a 2 minute general jumping and movement exercise designed to involve the entire body, the pulse was taken every minute for ten seconds. Strangely, the graph appears to jump up and down, for which I have little understanding why.
The pulse was measured simply and crudely with the traditional "fingers on the wrist" method.
If it is not clear, time is on the x axis and no. of heartbeats per minute on the y.

Thanks in advance

If the graph were what I would consider to be "normal", the general motion of the line should be downwards, settling to the normal heart rate. Instead, the graph has decided to jump up and down yet there should be no or little error.

A possible answer to this question could be user AliceD's suggestion in the chat room that "If sampling rate is low, you get this jumpy behavior because variations result in these 'binary' jumps."

Given the manual way the heart rate was determined I question the accuracy of the data. I would suggest to repeat the experiment and check repeatability of the data. Accuracy can be increased by determining the pulse heart rate over a longer interval than 10 seconds.


text:
Why are siblings unidentical? (Which chromosome of the pair do gametes have?)
I know that a normal human cell has 23 pairs of chromosomes (total: 46).
On the other hand, a gamete has only 23 chromosomes.
Which chromosome does the gamete choose out of each pair?
And if "One of each pair of chromosomes comes from the mother, the other from the father.", then the chromosomes of a gamete could be an exact copy of the chromosomes in a grandfather's gamete?

Have you read the basic Mendelian genetics; check the law of independent assortment.

Therefore, there are many levels of variation.

The gamete doesn't "choose" one or the other.  Both are made and you get two gametes, one for each.
Also it's unlikely to be an "exact copy" due to recombination and random or independent assortment.  There are also smaller influences on genetic variation, and epigenetics, but at this level of question I think you should focus on those two.
Was this homework?  If so it should be tagged.

Also there is random assortment, so even without taking recombination into account there are 2^23 possible combinations for assortment, or about 8.5 million combinations. Throw recombination into the mix and you start to see why there is so much variety, even among siblings.

No this is not homework, just personal study, but thanks for your answer, it was well worth a read.

Great links as well!


text:
What shows how healthy someone is by their heart rate?
What shows how healthy someone is by their heart rate - how low it is at resting pulse or how low it is during exercise or how large the difference is between the resting rate and rate with load? Any ideas?
Clarification:
Essentially, how does the heart rate reflect healthiness and in which ways (is it the resting pulse, pulse during exercise, differences, etc.)
Thank you for your time and effort

As an additional note, Chris from the chat room says that "the time you need after an exercise to get to the complete resting pulse is a good indicator."

"Which questions are off-topic?: personal medical questions and health advice."

@fileunderwater I don't quite think that my question is off-topic since it is not listed under:
-> personal medical questions and health advice
-> philosophical or ethical questions related to biology
If you read the question carefully, this question is the relationship between heart rate and health, not "I go to the gym every week, what else should I do?"

In general, these types of health related questions are closed at BioSE, since they could 1) be a reformulated question on personal health advice or 2) be used to evaluate individual health. Both are off-topic for the site. Your Q is also not framed in terms of biological processes, but only asks about evaluation of health.

@fileunderwater "personal health advice" "individual health" - This is an entire field in biology on the research of fitness where graphs of heart rates (bpm) and breathing rates (metres cubed per hour) are used on a regular basis. User Chris has done some training in this field too. This question stems from research, not individual health interests and actually results from a team practical.

I'm simply stating my view and how I interpret the off-topic guidelines. See these three meta posts for earlier discussions: http://meta.biology.stackexchange.com/questions/556/policy-on-health-questions , http://meta.biology.stackexchange.com/q/139/3624 and http://meta.biology.stackexchange.com/questions/597/clarifying-our-scope-with-regards-to-medical-questions

@fileunderwater Don't worry, I don't mind a grudge here or there ;) It's part of life.
Anyway, in reference to your first link, [quote from answer:]
"As you say, questions that ask for mechanisms on e.g. how something will affect the body would still be on topic, if correctly phrased."
All I am asking for is how do scientists determine the healthiness (if that word exists) of a person from the heart rate and how reliable is it.

I can see myself the misreadings of the questions so I will hasten to edit it.

@fileunderwater For heaven's sake, my question has got NOTHING to do with personal health!

And now a whole load of closers have piled in

@TimTimmy Can you please leave out other persons from your questions/replies?

@TimTimmy I voted to close when I left my earlier comments, which should make my reasoning clear. BioSE is in general very restrictive towards medicine/health, especially if questions aren't phrased in terms of biological processes. You only mention 'health/healthiness', without any definition of what you mean with this, and do not include any reasoning on e.g. how different aspects of heart rate is related to oxygen uptake, immune response or other aspects of "health". I therefore find it off-topic, but others might see it differently.

@Mad Scientist I don't see any purpose to this question anymore due to the wide miscomprehension of it and it will just clutter the community. Could it please be possible if it could be deleted? Thank you

@fileunderwater I see what you mean, but I have to note that the purpose of this question will help me to write key points for a book on GCSE Biology. Truthfully, I don't see much of a point any more in arguing. Hopefully the moderator will delete the question

A healthy heart and cardiovascular system distributes oxygenated blood more efficiently than a less healthy one. Therefore, for a given level of exertion, a healthy heart will need to pump fewer times than a less healthy one to provide the same quantity of oxygenated blood to the rest of the body.
It's pretty much that simple.
However, the whole patient has to be considered. A low heart rate in and of itself doesn't mean someone is fit since there are many drugs and medical conditions that can create a low heart rate. Person A sitting in front of you appears fit and healthy, is on no relevant medications, and has a heart rate of 50? Fitness almost certainly explains it. Person B sitting in front of you is overweight, on several meds and not very fit? Fitness almost certainly doesn't explain it.

Is there also a relationship with the difference between the heart rate during excise and during rest?
e.g. I did a team experiment and Will had a lower heart rate than Harry. However, when it came two exercise, the difference between the exercise heart rate and normal heart rate was larger than Harry's. Is this an error, mere coincidence or something that can tell us more about his health?

@TimTimmy Not an error unless the measurements were in error, but I don't know how to interpret the results you pose. Someone who is more fit should start with a lower heart rate and end up with a lower heart rate for the same level of exertion than someone who is less fit. But that's a huge generalization. Individuals respond very differently to the same levels of exertion.


text:
Can a plant be programmed to produce any arbitrary object?
I'm wondering if a plant can be programmed (by modifying its genes) to grow into any shape that it's programming instructs.
I understand that a plants genes are its instructions of how to convert the nutrients in the soil into the plant we see. So, instead of producing an apple tree or a giant sequoia, couldn't a plant be programmed to shape itself into a house, desk, or even at a stretch of the imagination, a bioship?
I'm looking for any links, or explanations of why this could/couldn't be done by anyone with more experience than I that could guide my research.
I am hoping that a plant behaves just like any other system. That it has inputs (nutrients, sunlight etc.) a function that describes it (its genes) and an output, the plant that grows. With this in mind, I suppose it would only be a matter of modifying the genes to produce the desired output (with the constraint being the available input).
Thank you,
Paul

Certainly this should be possible, however our knowledge of genetics is not advanced enough to actualise it

It could not fit in a comment...
1) Any material have some physical limitations and living tissue are not exceptions. A plant cannot resist to very high pressure without changing shape for example. Outside of these problems of material sciences I think the major considerations are technical…
2) It is possible to influence the shape of a plant by changing its DNA code, changing its physical and chemical environment (micro or macro environment) or by injecting some substance. Today we might be able to influence the number of branching of certain plants species for example. But we are terribly far from having enough knowledge in biology (in genotype-phenotype map, in biochemical pathway) in order to transform a dandelion into a shopping mall! Even we had already described all chemical pathway linking genes to phenotypic traits, it is immensely more complex to think of which kind of DNA sequence might transform a plant into something that is so different.
I don't know if anyone has ever created a totally synthetic (and not copied from already existing sequences) DNA sequence and could predict the impact it would have on the organism phenotype. Some people were able to create a totally artificial self replicating RNA though.
Note: Some people play with the properties of the DNA molecule in order to create various tissues. This might interest you as well.
One can highly improve this answer by giving some results of studies on synthetic life.

From your comments I understand that theoretically it seems possible to do this sort of thing (apart from the physical strength etc. of a material that a plant can produce from the given resources) but that current understanding is not up to the task. The translation from code to results (genotype to phenotype mapping) is what most interests me and I will look it up. Thanks for the ideas. And if anyone has anything else to add I would love to hear it.

For instance, there is Mycoplasma laboratorium

@Paul I guess the most interesting things you may find are not with the keywords "genotype-phenotype mapping" but rather with "synthetic biology" and "bioengineering". I should have used these words above!

Thanks Remi, I looked up these topics and found many interesting articles, even one about a line detection algorithm using bacteria that respond to light. Anyway, probably the main use I can see for synthetic biology is for recycling, imagine when you want to refurbish your house, instead of knocking down the unwanted part, carting away the debris and building a new section, we could reprogram the genes of the house so that a new section forms out of the existing materials. I think it even though it sounds far-fetched, it's a realistic dream.

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


text:
Could random male-only-offspring mutation wipe out a species?
If we can engineer the extinction of a whole species of mosquitos with male-only-offspring genetic mutation, how come such scenario never happened naturally in the past to other species? Or has it?

What do you mean exactly by engineering a species with male-only-offspring genetic mutation?

I don't think you can make the population extinct this way.  Individuals whose genetics allow them to have female offspring would be hugely favored evolutionary.  You might drastically reduce the population, you might drastically reduce the incidence of mosquitoes biting humans, but I don't think you'll achieve extinction.

@swbarnes2 what mechanism would favour the unmodified individuals?Your comment is not answering this.

It has happened the R2D2 mutation in mice is famous for it, the mutation prevents or drastically reduces female offspring.  It can wipe out entire populations when it shows up, it doesn't wipe out the species becasue there are frankly too many mice, separated by too much distance, while breeding too fast for the gene to spread fast enough before the population crashes. If mice happened to live on only one island however they would be gone. These events are called selfish sweeps or selective sweeps that result from a transmission bias in a gene.
the opposite can also occur (female only) however this is slighly less likely to lead to instant extinction since a possible out exists. Lepidodactylus lugubris(a gecko) being a famous example and is a female only species that reproduced through parthenogenesis. These types of species are exceedingly rare and have problems however as they are very vulnerable to disease since they have low diversity. Species like this are driven extinct indirectly by the mutation that led to a female only species as their diversity sufferers drastically so disease or environmental change can wipe them out more easily.

The link appears to be broken.

@canadianer try it now.


text:
Why do Lapidaria margaretae look like stones?
Previous Research
I stumbled across a trending reddit post "Lapidaria margaretae looks like stones" (as of 3rd Februrary 2015); but I could not find discussions as to reasons behind why.
Question/s

Why do Lapidaria margaretae look like stones? I am interested in both the morphological/physiological reasons, as well as possible evolutionary mechanisms.
Or perhaps I am asking the wrong question, then what should it be?

I've never seen a stone that looks like that…

"Teleology is like a mistress to a biologist: he cannot live without her but he's unwilling to be seen with her in public." - J.B.S. Haldane (1892 - 1964)
I can't tell you why Lapidaria margaretae looks like 'stones'. But I can deduce something from the way this plant looks.
First and foremost, I can say this plant probably evolved in an arid region, possibly a desert (less than 10 inches of water per year), because it is a succulent, with a shape that comes pretty close to minimizing it's surface to volume area (decreased evaporation, decreased transpiration). Seeing as it's a dwarf and shaped as it is, I might hazard that it's windy and sandy where this plant evolved, also because of it's shape - low to the ground, sturdy, low surface area, able to resist the wind. Finally, the light color of the plant suggests a lot of bright sun (reflects sunlight more than some darker colors).
None of that is foolproof, but in this case, it turns out to be right; the plant comes from southern Namibia, and is commonly called the "Karoo rose".
This is one image of the Karoo region:

Stones come in all kinds of shapes and sizes, also influenced by water, wind and other environmental influences. That this plant looks like stones is mostly coincidental.

I'm struggling to understand the significance of the quote :/

ah.. well in your defence @anongoodnurse hmm step (2) of the  scientific method (at least the Pirsigian six step flavour) requires us to dream up hypotheses!


text:
Could murder be modeled as an infectious disease?
Background

"When swine flu hit the population it spiked in certain areas and
  tapered off in neighboring regions, it hits hardest where people have least protection and this pattern is more pronounced (here)"

Apparently incidences of murder spreads in a similar pattern to infectious diseases such as swine flu according to a 26-year study of the city of Newark, New Jersey (summary).
Questions
It would be interesting to hear your opinions, but some interesting questions I would like to ask are:

To what extent could murder and the epidemiology infectious disease
patterns resemble each other?
What factors could you suggest may lead to their apparent
similarities?
Given that murder could be modeled as an infectious disease could we
apply epidemiological interventions to murder?

Seems like murder would be a weird disease. maybe its like cancer,  everyone is a carrier for murder- we all have it.  It would break out at a rate modulated by environmental conditions.  some might claim you wouldn't have to actually model the individual experiences, but others would expect it.

Interesting! I was thinking along the lines of "if you kill my gang-member I will kill yours" and it spreads like that, coupled with desensitization to murder as more of it occurs nearby - but these kind of discussions are what I was hoping to spark :)

maybe in very small circles you could model it as a meme like disease, but I'm not sure it would model a statistical number of murders. Sociological and policy factors are still probably more likely to model crime in general -  just my opinion... but not without its proponents.  http://www.telegraph.co.uk/news/worldnews/northamerica/usa/10320691/US-crime-murders-and-manslaughters-by-state.html

While it's probably possible to create an epidemiological model that mimics the spread of murders, it would be ethically dangerous territory to study in a controlled way to get a dataset that points to causes (and not correlations).

@ThomasIngalls That objection is also true for infectious diseases, which is why we model in the first place.

@Fomite Good point. Also, nice answer.

Here's a very interesting TED talk for you, regarding violence instead of murder https://www.ted.com/talks/gary_slutkin_let_s_treat_violence_like_a_contagious_disease?language=en

Disclaimer: I'm an infectious disease modeler, and generally pretty skeptical of "We modeled X like an outbreak!" claims, because many are just an exercise in curve fitting.
Given that, the answer is both "Yes" and "No".
"No": Murder as an act really isn't transmissible, and if its not transmissible, it can't be modeled as an infectious disease.
"Yes": It is probably possible to model some things in the same way we model infectious diseases, because the underlying causes of murder may be somewhat 'transmissible'. Certain behaviors, cascading effects (if one family member is incarcerated it increases the likelihood that other members of that family will be incarcerated) etc. might give crime "disease-like" properties.
That's probably largely driven by underlying social networks and the like, which are also important to infectious diseases. But then you have a problem in reasoning. For example, did murder "spread" along a social network, or did we merely sample a group of people with a shared underlying cause (for example, poverty, membership in gangs, etc.)
It's probably useful to model some of these things, but it's more useful, in my mind, to model them as their own process, rather than trying to shoehorn them into being like a disease.

Also, pretty much all areas of modeling borrow heavily from each other such that it is quite possible to have components of a model that look very like components of another, but for very different reasons.


text:
Could mating/recombination be responsible for evolution of entirely novel features?
The diploid chromosomal architecture is rather interesting. For example, because of diploidy we Humans have to mate. Of course in that sense, because diploid organisms often have mate, this has led to emergence of sexual organs as novel features etc.
But, what I am interested in, is the prospect of recombination and mating being able to lead to drastically novel evolutionary traits.
For example, if a remote tribesman from the Pygmy peoples of Central Africa were to mate with an urban dweller, one theoretical example of a novel feature could emerge in the offspring are new inter-gene/protein interactions between these "never met before" sets of alleles. Recombination would then "seal the deal" by shuffling these allele sets between the maternal/paternal chromosomes, such an individual's offspring would now become a mosaic of their hybrid parent. Just imagine cross-over events occurring between two very divergent promoters of the same loci.
Questions:

Could the unison of such divergent sets of alleles theoretically lead to unique phenotype and features that bear little resemblance to any features belonging to the parents?
Are there any real examples of morphological/physiological features such as that I have tried to describe?

I doubt this will cause any problems or new features coming up, since humans are pretty homogenous genetically speaking. This will probably cause some problems in the future with isolated populations. But when they can not mate anymore with each other, then a new species evolved.

Could the unison of such divergent sets of alleles theoretically lead
  to unique phenotype and features that bear little resemblance to any
  features belonging to the parents?

Though it is possible that some unique characteristics may emerge but it is very less likely that the offspring will bear no resemblance to the parents. You start with an example of humans. In this case it is, in my opinion, very unlikely because there is not so much of genomic diversity yet that may lead to such an outcome as you ask about.
Some examples exist, such as the liger (offspring of a male lion and female tiger) that is bigger than both the species. This happens because of improper growth regulation because of interspecies differences. This could happen because the divergence between lion and tiger is much more than the intraspecific variations.
Just a speculation : perhaps the offspring of H.sapiens and H.neanderthalis could have had such a feature but it seems unlikely for the current population of H.sapiens


text:
How many transcription factors are there?
In molecular biology and genetics, a transcription factor is a protein that binds to specific DNA sequences, thereby controlling the flow (or transcription) of genetic information from DNA to messenger RNA.
My question is simply how many transcription factors are there in the genomes of:

Humans
Anopheles gambiae (or it's close taxonomic relatives)
Less prioritized: any other species

This is the Curated database of mouse and human transcription factors. And this is the paper in which they describe how they curated the database. In summary, there are 3230 putative mouse TF, 1200 of which are described in scientific papers.

As the number of human TFs have been discussed by the previous answers, I'll limit myself to Anopheles gambiae.
In the same issue of Science in which Holt et al. published a genome sequence for Anopheles gambiae (1), Zdobnov et al. published a comparison of the A. gambiae and Drosophila melanogaster genomes.(2) While the two species diverged about 250 million years ago, and the D. melanogaster genome is about twice the size of the A. gambiae genome, the two species still show broad similarities and a similar number of proteins.
The authors identified 6089 protein pairs as "clear orthologs", corresponding to 47% and 44% of the of the Anophelesand and Drosophila proteins respectively. One might thus be tempted to estimate the number of TFs in A. gambiae as similar to that in D. melanogaster. For the latter, the FlyTF database (http://www.mrc-lmb.cam.ac.uk/genomes/FlyTF/old_index.html) currently lists 753 putative site-specific TFs and 454 "well supported" candidates. More recently, Hammonds et al. identified 708 melanogaster genes "likely to encode sequence-specific DNA-binding TFs".(3)
Edit: You may also want to check out the following question on Biostars: http://www.biostars.org/p/53590/

Pretty interesting question. There are a few numbers out, I remember that round about 10% of the human genes are coding for transcription factors (unfortunately I don'T remember the source for that).
This paper from 2002 estimates between 2000 and 3000 factors:

Signal transduction and the control of gene expression.

This paper from 2009 states a number of 1391 manually curated factors and also speculates about a number of 2000 - 3000 factors in total. This is definitely interesting to read.

A census of human transcription factors: function, expression and
evolution.

Amos Bairoch, of SWISSProt/UniProt fame has set up the nextprot database, a manually curated repository of knowledge for human proteins. While that won't help you get a number for the mosquito, it does make it easy to retrieve a list of human proteins that are annotated as transcription factors.
Searching for "Transcription Factor" in the "Function" tab returns 1405 hits. You'll notice that most answers are in the same ball park despite small differences, but bear in mind that many of these are assumed TFs and it will be a while before all of them have been experimentally confirmed to act as such in vivo.


text:
Cats, Dogs and Bears - how are they related?
What is the ancestral relationship between cats, dogs and bears?
I presume they are more closely related to one another than other paraphyletic clades of mammal.

Which came first?
What did their common ancestors look like?
What are their geographical origins?

You'll like this: http://tolweb.org/tree/

and this: http://www.onezoom.org/mammals.htm

Clades are, by definition, monophyletic.

Cats, dogs and bears all belong to the Carnivora clade of mammals, but they are not the only ones belonging to this clade.
For instance, cats are more closely related to mongoose and hyenas than to dogs or bears, who in turn are more closely related to raccoons, weasels, and walruses.
Their common ancestors likely displayed various adaptations to a carnivorous diet, as the name of the clade suggests, and which are still present in many extant Carnivora (the panda being a well-known exception).
Together with many other groups of mammals, Carnivora are part of a clade named Laurasiatheria thus named because they may have originated in the Laurasia supercontinent, which comprises nowadays north America and Eurasia.


text:
Do animals suffer from "Human" mental disorders?
It is tragic, but apparently Killer whales and Dolphins can commit suicide too (e.g. here)...
This suggests they can become depressed. I wondered whether they were "clinically" depressed like many people are, and what other mental illnesses have been observed in animals in general.
Questions

Which mental disorders have been observed in animals? Which animals?
What is the prevalence of these mental disorders in those animals?
Are the causes and treatments of these disorders similar to Humans?

Strange thought
Organisms that have not evolved the ability to make "conscious choices" cannot decide to end their life.

We had a similar question, relating to suicide, before. The http://biology.stackexchange.com/questions/3478/is-there-any-documented-evidence-for-suicide-among-vertebrates-other-than-humans/8931#8931

You will be hard-pressed to find any scientific data on this question. Psychology in humans is already a difficult study, at times failing to demonstrate results with real scientific rigor. When studying animal psychology, you face another substantial barrier - language. Although some primates have been taught to communicate with sign language, the best of them are still far from the level of proficiency of a human. We can measure brain activity and observe behavior, which can lead us to strong suspicions about what is going on in an animal's mind, but very little can actually be proven.
Mostly, all we can do is speculate about such questions. You will find some veterinarians out there who treat pets for mental conditions, but you will find at least as many people calling them quacks as those who believe in the validity of their work. And certainly, they can't prove to you that a treatment has helped an animal. It's subjective.
If we see an animal do something which in a human might reliably be interpreted as a sign of depression, it's possible that this interpretation is appropriate for the animal as well. It's also possible that there is some totally foreign unrelated explanation. The problem we find when trying to scientifically discuss matters which cannot be proven scientifically is that scientists must be careful to state what they know and nothing more. So they might say "We cannot prove that the porpoise is depressed", or "Science cannot prove the existence of a God." This is often misinterpreted as evidence against the finding - that the porpoise is not depressed; that there is no God. This is a fallacy. Rather, we should recognize that we have different ways of exploring questions like these.
I can't prove it to you, but I know that my Beagle had a rich emotional life. I know this because I spent huge amounts of time with him. He was a close friend of mine. I would just as soon question whether my wife has real emotions as my dog. I can't prove that my wife's emotions are real either, but I don't have to. It would be silly to assume that everything she shares with me is some sort of evolutionary programming, and not real emotion. Now, when I extend this to cetaceans, I must admit that I don't have any friends in those circles. So I can only guess.

"You will be hard-pressed to find any scientific data on this question." This is untrue. There is a whole field of study on animal psychology and cognition called Ethology with a lot of high quality literature. You don't have to guess if your beagle has a rich emotional life; fMRI's can prove it thanks in part to Dr. Gregory Burns (human and animal neurobiologist).

@anongoodnurse I've seen the summaries and reports on some of these studies. While it's nice that someone is making these attempts, I find it very pale evidence next to the experience of having a pet. The point I'm making in this answer is that I am NOT guessing about my beagle's rich emotional life. I know it for certain. These studies' results did not add to my certainty. Science was never intended to be the only source of true knowledge. Mistake that, and you will find that for all the PhDs you can collect, your still an idiot.

You're the one making a mistake, not me. I take it you're not a scientist, nor have you ever been. Experience is subjective; research, while still limited, is much less so. You can believe with all your heart that your pet snake has a rich emotional life; that doesn't make it so. It really doesn't matter (to truth or fact) what you believe. It only matters to you, and maybe those who love you, work for you, etc.

@anongoodnurse I apologize for any offense taken. The statement was intended more generally, not personally. Nevertheless, I stand by it (other than the misspelling of "you're"). Science is one of many lenses through which truth can be observed. Refusal to look through any other lens is tantamount to willful blindness. On questions of emotion, science is not of zero worth, but it's a little bit like - I don't know - trying to use a thermometer to determine color. That's fine, but I hope you don't mind if I'm more interested in what I'm seeing with an optical spectrometer.

A functional MRI can tell you a lot more than your eyes can about your own feelings. People rationalixe, suppress, dissemble. FMRIs don't. Just the facts m'am. I was a person before I became a scientist, which was before I became a doctor. It's not that I don't use my eyes or my mind; it's that I know which is less subjective.

I know of at least one case, some social primates develop maladaptive behaviors similar to sociopathy if raised in isolation without the social contact with others of their species as they grow up. It appears they need to be socialized as children just like we do.

Source 1
Source 2

Good question: We know that prion diseases affect the psychology of animals (Scrapie, Mad Cow). But without a doubt genetic regulation of endocrine and neurotransmitter pathways is subject to the same folly as in Homo sapiens. Sorry I can't support that with links to publications...
update: There are many animal models: http://www.ncbi.nlm.nih.gov/pubmed/746371

Having an animal model of a disease does not prove that animals can have the same symptoms. An animal model will have the same chemical imbalances, that does not, however, necessarily mean that it will have the same psychological manifestations of said imbalances. It might, but there is no proof.

@terdon, I would still advocate Gent's answer, though, some users may not have realised the significance of a parasite/pathogen's ability to affect the cognate brain physiology of some organism. Deviations from normal decision-making, are often exploited by such parasites, towards their own fitness gains... quite an interesting angle of an answer IMHO.


text:
Is there any data to explore the heterozygosity of the South African lion over the last 18 years?
Background:
I need to find data on the heterozygosity of the south African lion over the last 18 years... and I'm struggling: so far I have found a single data point.
Question:
Where can I find data to help me explore changes in the heterozygosity of Lions living in South Africa?

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