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In protein-protein interactions what is the difference between a binding site and an interface?
I see binding site and interface used almost interchangeably in the literature, but I'm not sure if it is exactly the same thing or not - what is the difference?

By PPI do you mean protein-protein interactions? I see binding site more in the context of transcription factor binding sites (i.e. protein-DNA interactions; I may be biased here by my own experience though). It would help if you quote examples from the literature.

We can't give you an answer without more context. Neither of those terms is really standard, so what they mean will depend on context. Could you give some examples?

A protein-protein interaction (PPI) binding site is a type of interface. If it has been established that the interface is a PPI binding site, then the terms can from that point forward be used interchangeably. But the word "interface" is very generic and does not have any specific scientific meaning so the nature of the interface must be defined or else the term is fairly meaningless.

Just thought I'd add a dictionary entry. As you said, the term interface doesn't have a special meaning. http://dictionary.reference.com/browse/interface


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Is it easier to burn a calorie of fat or a calorie of a carbohydrate?
Say someone eats 100 calories of chocolate vs. 100 calories of carrots. Something tells me that eating the chocolate will lead to you generating more fat. Will it? Is it harder to burn the calories that you consumed from the chocolate?

It isn't burning of the calorie you should consider as once digested different calories are stored in the same manner, it is actually the digestion itself.
Proteins are by far the most energy requiring foods to digest such that around 20% of the calories in proteins are used in extracting them. In comparison carbohydrates are much easier at around 5-10% whilst fats are even easier to digest.
But think of it in simple terms, chewing a vegetable and digesting it down and the relatively sheer quantity of mass you need to make it calorifically the same value as chocolate means that yes 100 calories isn't 100 calories.
All then in terms of real life application, our bodies respond to how much we eat. If we eat a large volume of low calorie food we will eat less calories in total. This also plays an important role.
Source: http://www.ncbi.nlm.nih.gov/pubmed/20613890

So when you eat carbs, you really only have to "burn off" 90-95% of it (because the act of digesting it does some of the work for you), whereas fat you have to burn close to 100% of it?

AndroidPenguin, if you dont mind let me add a one liner summary for your answer: Nothing is burnt inside the body; it is either fixed, spent or excreted.

@user6035 yes. Although so many other factors apply!

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Why can't you just take a vitamin? Why you need a healthy diet on top of that?
From what I understand, your body needs certain amounts of vitamins and minerals to maintain health. Why can't we just take enough pills to obtain these vitamins and minerals?

Getting enough food as an energy source would be a problem.

I think the piece of missing information here is the distinction between macronutrients and micronutrients. The info from Mayo clinic quoted in the another answer addresses some reasons why whole foods might be better than pills for obtaining micronutrients (i.e. vitamins and minerals).  While this may be true, most of it remains to be conclusively demonstrated (arguably). However, one clear reason “why….you need a healthy diet on top of that” is (unarguably) to obtain the fat, protein, and carbohydrates that your body uses to create energy. Unlike the minerals that act as cofactors, these macronutrients are the substrate. They are broken down to create the ATP that keeps everything running and they are built up to create the very structure of the body.

The energy that is consumed in the form of food or drinks can either be stored in the body in the form of fat (the major energy store), glycogen (short-term energy/carbohydrate reserves), or protein. . . to be used by the body to fuel energy-requiring events. *

These are called macronutrients because they are required in gram quantities — hundreds or even thousands of times more massive than the requirements for most micronutrients. As such, they don’t fit in a pill. As tragic as it is, we must keep eating.

*Gibney, M. J., & Nutrition Society. (2009). Introduction to Human Nutrition. Chichester, West Sussex, U.K.: Wiley-Blackwell.

TL;DR : Food gives the human body much more than simply vitamins & minerals. A healthy diet is essential to overall healthiness, not just this one aspect of it.
Micronutrients
The component you're asking about - vitamins & minerals - are referred to as "micronutrients", and is only a quarter or so of what the body needs. Micronutrients are the vitamins like Vitamin A, Vitamin B, Vitamin C, etc. but it's also trace elements like zinc, iron, iodine, and many other metals that the body requires in very small quantities.
This is the part of the diet that most people actually overlook, and is what pills like the "once-a-day" vitamin are intended to supplement.
Macronutrients
Much of what we get from food falls in the category of "macronutrients". These nutrients are the actual building blocks of the body - things like fats, proteins, calcium, carbon, hydrogen, etc. A lot of macronutrients are required on a daily basis, and it would be difficult to condense these into a pill form. An average-sized pill would have to be taken 5-6 times a day in order to provide even a less-than-average amount of macronutrients for the average person.
Digestion
The human body is designed to be an engine. The act of eating is hard-coded into human physiology, and the act of digesting food kick-starts a great many processes throughout the body. Digestion is a rather efficient process, and it's one that only works properly when it has enough food to break down. A handful of pills could never fuel this process correctly, since they would simply dissolve in the stomach and never require any kind of breaking down.
Psychological
Lastly, food & drink have a psychological component to them as well. The human brain is wired so that it desires food on a psychological level. The physical act of eating something soothes that desire in a way that a pill never could. One of the greatest obstacles to someone trying to lose weight is this very component - even when their body technically has what it needs from vitamins, supplements, or shakes, this psychological aspect of hunger makes them want food anyway.

The Question: Why can't we just take enough pills to obtain these vitamins and minerals?
We don't know enough about nutrition.
There are about 45 essential nutrients, which you need to consume to be healthy and live. You can get all of them from food without thinking about them. I'm not sure if currently there are a lot of supplements on the market that contain all essential nutrients. Also, we may currently still not know which all nutrients are essential, so we may miss some when designing multivitamin/mineral pills.
Food is easier!
A healthy adult who regularly consumes both plant and animal foods in reasonable variety and amount does not really need any vitamin/mineral supplements. And you need to eat foods to get calories. Yes, you could make supplements to substitute calorific content; imagine some sort of carbohydrate powder. But why complicate this when food is readily available, much cheaper, and easier?

Why has this been down voted? It answers the question in a way the others don't: why bother? I've made some edits. Feel free to roll back.

Your answer is in Cellular Respiration which is the production of ATP (energy storage molecules). Food is Carbon and Hydrogen. The body needs carbon and hydrogen for cellular respiration. Carbon and Hydrogen are not in vitamin pills they are in food.

Please add some references. This is a great answer overall though!

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How do viruses or bacteria survive outside the body long enough to spread?
Say I cough on my table, then someone else touches it and picks up something I've got... how is it that these things can live outside the body, how long can they manage it, and how long is generally 'safe' to consider something no longer carrying these germs?

depends on the species and its constitution... Can you be a little more precise..

It depends entirely on the environment the virus or bacterium is in and also the size of it.
Virus
With regards to viruses, the most important thing is typically whether or not the virus has an outer membrane or envelope.
Non-enveloped viruses such as rhinoviruses, noroviruses and adenoviruses can in fact survive for long periods outside the host (up to several days) whereas viruses with membranes such as HIV, influenza and the herpes viruses which do well in the host survive for shorter time periods.
Experiments with rhinoviruses and influenza viruses have shown potential survival times ranging from a few minutes to 48 hours or more.  They remain active longer on stainless steel, plastic and similar hard surfaces than on fabric and other soft surfaces.
This is because many enveloped viruses rely on the proteins on the surface of the membrane to attach to the host cell, this envelope is generally sensitive to degradation to sunlight and normal cleaning procedures.
Outbreaks associated with the non-enveloped viruses can continue for many months due to their relative stability in the environment, think of winter vomiting outbreaks, hand foot and mouth in animals as good examples of this phenomenon.
Bacteria
Because bacteria can undergo metabolism, synthesise proteins etc. for themselves, their life span is usually longer. If we split them into gram positive and gram negative its easier to discuss. Gram positive bacteria have a protein coat that prevents drying allowing them to survive longer. An example is the bacteria Staphylococcus aureus, which is responsible for toxic shock syndrome, food poisoning, and wound infections. With its protein coat it can withstand temperature and humidity extremes. The spore may survive for weeks on dry clothing using sloughed skin cells for food. The Bacillus anthracis, the anthrax bacteria, can also form spores and survive tens to hundreds of years. This is in comparison to gram negative which need humidity. An infamous example is Escherichia coli which survives typically only a few hours at best.

Virus particles (virions) are not alive. They are just a Genome Delivery Vehicle. They are essentially like landmines. However like different types of landmines different types of viruses can remain "active" for longer or shorter.
Those depend as explained above on the virion structure but also on Humidity and temperature, the fomite (surface) and the ammount of virions. Some viruses need up to 10k Virons to cause disease. The higher this "Particle to PFU ratio" is the lower the chance they can remain active outside the body for long. So if the Virus in question needs few particles, is not enveloped then this one can in theory live for quite a while outside, Norovirus for example is one of those.

Viruses really take to heart the idea of "quantity, not quality." Like animals and plants, viruses and bacteria are a completely different ball game (even more so than animals and plants).
As you maybe know, you have bacteria floating around you in the air right now. Realistically, a single T4 bacteriophage (a type of virus) has a life cycle of about 20-30 minutes at 37 C°. However, in this time period, it often reproduces in a bacterium and creates tens if not hundreds more phage particles using the bacterium like a machine that was hacked to do its bidding.
The only way to prevent a virus from attacking is through vaccinations and other preemptive measures, as it is so difficult to prevent reproduction.
Bacteria are so different they, for all intents and purposes, cannot be approximated. For a rough approximation, somewhere from hours to weeks.

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Lysosome function
Does any cell have lysosomes in it? Or maybe there are other organelles that do the same function. I read about it a lot and I can't find a good answer.

Yes, lysosomes (note spelling) exist. see https://en.wikipedia.org/wiki/Lysosome

The very first sentence of the Wikipedia article on lysosomes: "A lysosome (derived from the Greek words lysis, meaning "to loosen", and soma, "body") is a membrane-bound cell organelle found in most animal cells (they are absent in red blood cells)." So yes, any cell except RBCs would have lysosomes, as they are essential to the function of a metabolizing cell (which RBCs are not).

The function of a lysosome is to essentially digest and break down molecules (often compared to the stomach of the cell).
For example, a cell with high proportions of lysosomes would be a macrophage, as its function is to neutralize pathogens. After the pathogen is engulfed by the macrophage, the vesicle formed, called a phagosome, fuses with a lysosome, and the lysosome's digestive enzymes work on breaking down the pathogen into harmless bits and pieces.
In most cells, however, lysosomes also function to recycle the cell's own components, called autophagy. Damaged organelles are broken down by the lysosome and recycled.
So, yes, there are many cells that do have lysosomes.
The importance of the lysosome is shown when there is a malfunction in the lysosome. These diseases, called lysosomal storage diseases, occur when the lysosome does not function properly and the cell eventually is impaired by the buildup of a molecule that should have been broken down by the lysosome (e.g. Tay-Sachs disease).
References
The AP Biology textbook

Campbell Biology 7th Edition, Chapter 6 - "Lysosomes: Digestive Compartments", although this is pretty much the same in any edition of this textbook
Campbell Biology in Focus, Chapter 4 - "Lysosomes: Digestive Compartments"

Welcome, and thank you for your answer. You may want to consider an edit to provide some references to the information in your answer. It can help to provide the person who asked the question or others reading your answer who would like to research further a starting point.


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What type of creature makes those mounds?
Location: South Ireland,
Appeared: 2020
Nearest river: 500 meter down hill south
Water is running down the hill also but there’s drainage to not flood the grass
Seen before: potted plant
I  used earth like this from a different location to plant a potted plant into a plant pot and those type of mounds happened afterwards in there also. Just on a smaller scale.
Never seen anything move though. Probably night active.

What size are the mounds? How close are you to a body of water (river, lake, etc)?

Added measurements and water proximity

do you know what worm mounds are like? if it's in a lawn then it's probably a worm cast, worms dig by passing soil through them and travel to the surface to place blobs there like black spagettis, when it rains they can lose their spagetti shape, so you only have 20% of your ones, the most recent that are still spagetti shaped.

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Could a normative population ever be non-heterosexual?
In the modern documentary called "Bi the way", one American geneticist said that if modern American youngsters may as well be functionally bisexual, then some generations ahead Americans could be possibly born with a strong inclination towards the bisexual lifestyle. If we let aside the futuristic theory according which bisexuality should become an evolutionary norm concerning the human species in the long run, then is there a strong bio-sociological possibility that modern societies could transform normally to sexually fluid homogeneous spaces?
So the problem is if humans will naturally evolve to a species which is homogeneous in terms of dynamic bisexual differentiation, while in the meantime producing stable behavioral norms.
Then it has to be decided if society will integrate this procedure naturally or through competition.

I doubt it's a biological question in this formulation. And I personally have no idea, what "normative population", "functionally bisexual", "evolutionary norm by necessity", "bio-sociological possibility" or "sexually fluid homogeneous spaces" mean.

@mad-scientist - I accept that Valintine Wiggin's wording was a bit incoherent, particularly the infusion of terms which I'm pretty sure were coined on the fly. However, I think the academic scenario and theoretical implications were quite clear.  Hence why I took the time to reply!

Evolution does not think. It does not have a goal or aim in that sense. It just is, because some individuals within a population manage to reproduce. What it comes to bisexualism, who says that it is a new phenomena among American teenagers? An American geneticist. There are indications of bisexualism in the history from the Ancient Greek and beyond. Maybe bisexual individuals have a higher fitness? Men/women are attracted to individuals who show an interest to their own sex and these individuals get to reproduce. In that case bisexual life-style would likely remain in the population.

First, your question makes a few assumptions. We can totally run with those assumptions, but I thought two needed to be noted:

There is a genetic predisposition to bisexuality.
This genetic predisposition does not already dominate the population. (Perhaps suppressed by social pressure)

A genetic predisposition in a small minority, in order to infiltrate and achieve dominance, would need to either:

Directly possess advantages over the absence of said predisposition
Be "luckily" carried by hosts which maintain some other advantage in order to infiltrate the population.

Off the top of my head, some direct advantages of bisexuality could be:

Arousal of opposite gender with homo/bisexual acts or displays
Maintenance of psychological and physical fitness during short term gender imbalance
Self advancement socially regardless of audience's gender
Frequent physical activity (exercise) in a sedentary culture.

I'm sure the list could go on. Specifically with this sample of potential advantages, a cultural stigma would likely both :

Suppress the fulfillment of this predisposition, thus leaving it unhindered in their offspring
Produce reproductive hostility toward those who exhibit signs of this predisposition

Lifting such stigma, and assuming the advantages somehow outweighed the innumerable disadvantages, I would conclude "yes", it is possible for a society to be birthed where sexual exclusion by gender was not even considered.  That is, there would be no such thing as "sexual orientation" in the populace's mind share.

"one American geneticist"?  You realize that that's how you would describe a crackpot, right?  It's not clear to me at all the American youth are "functionally" bisexual.  For one thing, I don't think American high school culture is all that encouraging of boys experimenting with each other, though I can easily imagine straight girls being under pressure to titillate the boys in their group with lesbian displays.


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What is a mechanical cue?
I was attending a talk related to neurogenesis. So one professor was asking a question related to biochemical cues and mechanical cues (related to signaling pathways I believe). Cue as far as I understand is a signal, right? Biochemical cue is understandable for me.
But what does mechanical cue mean?

Mechanical pressure, stress, strain or distortion are mechanical cues. In general, cues sensed by mechanoreceptors are mechanical cues!

It is not necessary that mechanical cues are sensed by mechanoreceptors. These cues can also be relayed via the cytoskeleton and the adhesion proteins.

I doubt adhesion proteins can transduce mechanical signal. They can only recognize specific molecule or protein on opposite cell (or ECM). They are sending chemical signals not mechanical.

Adhesion proteins relay the mechanical stress as they are directly connected to the cytoskeleton. They are not really like signalling receptors. See this abstract:  "Experimental evidence confirms that cell differentiation or proliferation can be regulated according to the extracellular matrix stiffness...". So adhesion proteins are involved in relaying these signals.

In given paper, there is no clear indication of any adhesion protein. Given study is mathematical model with correlations. However I found this line in that paper's conclusion, "α5β1-integrin could switch between relaxed and tensioned states in response to traction forces generated by a cell.". This gave me this reference. Which suggest that 'a5b1' is 'most likely' candidate who changes confirmation by mechanical stress. In that case 'a5b1' will be mechanoreceptor by definition :P

Well they are not classified as mechanoreceptors, if you are getting what I am trying to say. I am not refuting what you are saying, but you cannot call integrins as mechanoreceptors. This is just like the equilibrium- steady state argument. It is a matter of classification and not an all pervasive superlogic :P


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Doubt on genomic code for nucleosome positioning?
I was reading "A genomic code for nucleosome positioning" (by Eran Segal et al). And I am having 2 doubts.

The figure(b) in this image from the paper shows the graph of fraction (3-bp moving average) of AA/TA/TT dinucleotides of nucleosome dna sequence they analysed statistically as far as I understand.
What is 3-bp moving average here?
I also don't understand how they chose 0th position (the so called dyad).
Also what does it mean to have oscillations (correlation?) in this graph?

UPDATE : I am adding some supplementary information related to finding the dinucleotide fractions. Still I don't understand why is the fraction found so?

Your image is a little blurry. Can you upload a higher resolution image?

@WYSIWYG : done

Okay I edited the answer. Let me know if that is clear.

Dyad is the centre of the DNA that is wrapped around the nucleosome core (It basically is the centre of symmetry of the nucleosome). It is a common practice to set it at 0 thereby making incoming DNA half, negative and outgoing DNA half, positive.
By oscillations the authors mean that there is a periodic repeat of A/T dinucleotide. IMO it is actually not correct to call it oscillation which is mostly used in a time course dynamical sense.
I guess this is what is meant by the 3-nt moving average:
You have conditional dinucleotide probabilities for each position (As shown in the figure). Now you calculate the A/T dinucleotide probability which is:  P[A/T] = PAA + PAT + PTT + PTA
Now you find the moving average for 3 steps:
MA(n) = (1/3)×(P[A/T](n) + P[A/T](n-1) + P[A/T](n-2))

where n is the nth position of the DNA

The term "oscillations" is my word, not authors'.

I did not understood the 3-bp moving average filter argument, but now I have access to ~70 page supplementary data of the paper. I am updating my question.

In the graph (b) of first image but "AT" is not mentioned? only AA/TA/TT is mentioned.

@dexterdev I think TA and AT are grouped together as TA (combination of T and A); there is no rationale for not including AT.

AT and TA in this paper are different. AT is T after A and TA is A after T. The supplementary data shows a different separate plot for this. Should I update the question with those plots. I am still in confusion?

@dexterdev Unless I read the entire paper I wont know what they have done. I know that AT is different from TA but all I am saying is that when TA is counted then it makes no sense to exclude AT. You need not modify your question because this doubt is just about what have they counted and for that you just need to look at the paper. The answer will still remain the same.

Any way thanks for the effort, but they are counting both the AT and TA differently.

@dexterdev they must have mentioned why they are doing so. You just need to read the paper carefully. You must exempt me from that effort :)

I agree to that. :)


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What is meant by "genes involved in the stress response"?
I would like to know about the term stress response. For example "some genes of a species under study is involved in stress response". What does that mean? I got this as a part of my assignment question.

In which context did you find this phrase?

Sounds like genes that are activated during stress, e.g. during the pathway of cortisol synthesis.

heat shock proteins are the first thing that came to my mind! could you elaborate on the type or the context of stress?

@Chris : Please see the edit.

The comment by @fileunderwater is apt: stress-response-related genes are genes that are activated during stress, such as exposure to heat. In bacteria, for example, there are heat-shock proteins that are involved in keeping the tertiary structure of proteins (folding/3D shape) intact during periods of heat exposure. Genes encoding these heat shock proteins are then called to be upregulated, and you would find them back in a typical micro array experiment. Hope this helps.


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Is the fin of ray-finned fish live tissue or more similar to scales?
In ray-finned fishes, are what exactly are the fins made of? Is it modified skin, dead tissue like scale or nail on humans, or something completely different? Can the fin heal?

In teleosts, the fin skeleton is made of structures called lepidotrichia and actinotrichia, whereas homologue structures called ceratotrichia are found in the fins of the chondrichties. These are covered by living skin.
Lepidotrichia are calcified, segmented and branched bone-like rays that extend along the whole length of the fin, shaping it. Actinotrichia are mostly made of collagen and are found at the distal end of the ray, where they provide flexible support to the fin edge1.
Fins are able to regenerate, and this capability has been studied in a few different teleosts2,3,4.
References:

I. Durán, M. Marí-Beffa, J.A. Santamaría, J. Becerra, L. Santos-Ruiz,
Actinotrichia collagens and their role in fin formation, Developmental Biology, Volume 354, Issue 1, 2011, DOI: 10.1016/j.ydbio.2011.03.014.
J. BECERRA, L. C. U. JUNQUEIRA, I. J. BECHARA, G. S. MONTES, Regeneration of Fin Rays in Teleosts: A Histochemical, Radioautographic, and Ultrastructural Study, Archives of Histology and Cytology, 1996, Volume 59, Issue 1, DOI: 10.1679/aohc.59.15
Norman E. Kemp, Jae Ho Park, Regeneration of lepidotrichia and actinotrichia in the tailfin of the teleost Tilapia mossambica,
Developmental Biology, Volume 22, Issue 2, 1970, DOI: 10.1016/0012-1606(70)90157-0.
Uemoto, T., Abe, G. & Tamura, K. Regrowth of zebrafish caudal fin regeneration is determined by the amputated length. Sci Rep 10, 649 (2020). DOI: 10.1038/s41598-020-57533-6


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Why do cows (and other hooved animals) need a hierarchy?
Clearly numerous animals have a hierarchy - hereditary one.  For example, I understand zebras have a pecking order, and must map this hierarchy from highest to first in line and lowest to last in line when traveling, and they can be brutalized for breaking this hierarchy.  (Interestingly, they allow looser rules for their young.)  (Reference.)
Cows apparently spend inordinate amounts of time with certain other animals, and avoid others still. (Reference.)
My question is: why do animals need the hierarchies and alliances?  Because human adults tend to make friends with people based on the kind of people they are.
I would imagine that they may have signals that indicate competing survival strategies (for example, a man with thick, tattoo covered arms vs a man in a tie) and that these likenesses try to propagate at the expense of others by forming alliances using organisms that possess these attributes (very vaguely akin to "the selfish gene.")
Or does it have something to do with advertised fitness?  I just have to wonder how grazing animals manage to compete over food.  Does it control access to reproduction?

Practically all social groups have hierarchies. Why shouldn't cows?

Why is this closed? The question is super clear and well bound.

@bobthejoe Why is this closed? I explained my reasons in a "comment-answer" below. I still don't think it is clear. But if you understand the question, you can maybe address my misunderstanding below to help others. Or you could eventually directly try to answer the question.

I think this is too broad an unclear. There are many types of herds and social groups in different species, some loose, relatively  unstructured groups used e.g. during migration and others based on territorial males, with intermediate stages in between these extremes. Some might also be based on relatedness between individuals in the group (so aspects of inclusive fitness might apply). I therefore think this currently is too broad to answer in a Q/A format, and it is also unclear exactly why you are asking and what species you are interested in.

@fileunderwater, I frankly disagree. Meaning that a question covers a large amount of space should not rule out its answer-ability. If the question contained multiple questions, then I would agree. However, this is directly asking for the social hierarchies of herd animals which I think is a well bound question.

Could not fit in a comment...
There are several issues with your question.

The correct question is not why such species need something but rather why it occurs in this species. In other words, why did a hierarchy evolved in a given species?
It is unclear to me why your are interest in cows (or other grazing animals) rather than any other species that has some kind of hierarchy and therefore your question is a bit unclear.
There are several questions in your post. A post should always be limited to one question.
I personally have never heard of the concept of "advertised fitness". How do you define it?
I am not sure how much you are interested in the evolution of social traits and especially about reputation and how much you are interested in Machiavellian intelligence. In any case, you may probably want to read about the evolution of social traits (kin selection, it may take you some time) and about the social selection pressures for the evolution of cognition, such as Machiavelian intelligence.

For all those reasons I vote to close. But I hoped that those comments can help you to clarify your post and to seek for more information.


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SNPs mapping into protein
Starting a new project on protein-protein interactions and SNP analysis tool development. I would like to ask how does SNPs is mapped into protein? What does mapping means?

I assume SNP means Single-Nucleotide Polymorphism? I'm confused exactly what your question is - how does one take a SNP and see what effect it has on the protein sequence? Is that it?

Well SNPs are single nucleotide polymorphisms. Some SNPs are in the coding regions of genes and they can result in changes in the resulting protein. For example, the SNP rs1801131 is a human variation where some individuals have a G instead of an A at position 1515 of the gene MTHFR. When the gene is transcribed and then translated into protein, this variation (the presence of the G nucleotide) causes a Glutamate residue at position 429 of the protein to be a Glycine instead.
So, SNP rs1801131 maps to position 429 of the protein MTHFR.

@MattDMo you've got a dirty mind... :)


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Why only female mammals have well developed mammary glands?
In course of evolution (possibly), mammary glands became vestigial in male mammals, but became fully developed in females. Is there any plausible explanation for this characteristic?

what exactly do you mean by plausible explanation?

Male mammary glands aren't vestigial, they're embryologically related to female mammary glands. So the question is "why are mammals sexually dimorphic" which gets tautological because the clade is defined in terms of mammary glands in the first place.

@Ryan Don't provide answer in comments. You can post it as another answer (saying "addition") if you provide some extra points that are not mentioned in previous answers. Use comments only for requesting clarification or providing suggestion related to post (not content).

Perhaps due to the close hormonal interplay between pregnancy and lactation it is more efficient to have the females generate milk. To let a male start to lactate a new mechanism needs to be developed in evolution, because a continuous 'just-in-case' lactation is energetically cumbersome. Developing new characteristics is not favored in evolution. Rather, coupling of a lactating mechanism to pregnancy (breast tissue growth) and labor (start of lactation) seems an evolutionary more parsimonious way of regulating lactation.

Just a note - they're not fully vestigial. Male lactation occurs in some species, including humans (the same mechanism that starts lactation in females still works for males). The Dayak fruit bat in particular has full blown lactating males. But yeah, taking mammals as a whole, these are relatively tiny exceptions. If you care about humans, though, yup, males can lactate just fine (though I have no idea about the amount or quality of milk so produced).

It comes down to investment in offspring. Males invest little in offspring only a little sperm whilst females have to develop the more expensive egg and the energy used through its development. In the mammalian line, this investment has increased in amount, initially through viviparity and then through the secretion of feeding fluids.
In species, such as humans, where there is a lasting pair bond and both male and female invest in rearing the young then I suppose there could be a situation where it makes equal sense for both males and females to nurse - although the cost of mammaries on other functions may favour specialisation anyway - but remember that, in many mammals, it is the mother alone that rears the offspring.
You may also find the answer to this question useful: Do any birds beside the family Columbidae (or any reptile or mammal) feed their young “Crop Milk”. What I hadn't realised is that there actually two species of bats where the male lactates.

It is not generally so that males invest little in offspring, especially not in humans. In fact, it is hypothesized that the rapid growth in brain volume in homo was made possible, at least in part, through the contribution of males in rearing the offspring (by gathering food etc.). Moreover, the 'more expensive egg' can be debated, as the vast amount of sperm cells generated during a male's lifetime vastly outnumbers the resources needed to ripen  the relatively small amount of eggs during a female's life.

I addressed your first point in the second paragraph. Male investment is high in humans, it is not in mammals in general and the dimorphism in mammaries did not evolve in humans. As to your second point, it's certainly true that males invest in reproduction to similar levels to females but in the individual offspring the investment is higher in the female.

The mammary glands in human males is not vestigial but rudimentary.
Human females have XX chromosomes and males have XY chromosome,here the "Y" chromosome is provided by father and "X" by the mother. At the time of fertilization, the father can provide either X or Y chromosome. If he provides Y chromosome the child will be male and if he provides X then child will be female. The mother always provides X chromosome. So the Y chromosome in the male child is responsible for the development of male sex organs and due to the presence of X chromosome the female sex organs are suppressed. Note that the female organs are suppressed but they are not eliminated. At the time of puberty males don't receive hormones which initiate the development of female sex organs. As a result the mammary glands stay in males as nipples but the hormone effects are only present in females and cause the formation of large amounts of fatty tissue near the nipples and develop as breasts.

A distinguishing characteristic of the class Mammalia is the presence of mammary glands. The mammary glands are modified sweat glands that produce milk, which is used to feed the young for some time after birth. Only mammals produce milk. Mammary glands are most obvious in humans, as the female human body stores large amounts of fatty tissue near the nipples, resulting in prominent breasts.
  http://en.wikipedia.org/wiki/Female

.

While estrogens are present in both men and women, they are usually present at significantly higher levels in women of reproductive age. They promote the development of female secondary sexual characteristics, such as breasts.
  http://en.wikipedia.org/wiki/Estrogen

The last sentence in your wikipedia quote is contradicting the first sentence in your answer.

@fileunderwater: I saw it but it may be because they just used "vestigial" as an inappropriate organ(literal sense)they may not be thinking the controversy in using "vestigial" and "rudimentary".

I rather see it as a reason to have healthy scepticism towards unreferenced statements in Wikipedia. But the reason is probably, as you say, how they define 'vestigial' (I don't think human nipples should be labelled 'vestigial' using normal definitions of the word though). It makes for a contradiction in your answer though.

@fileunderwater:I just edited the answer and removed the portion, but I think its unfair to remove that portion, but it is for a good reason.Also you are thinking that it shouldn't be labelled as "vestigial". I have learned many things from your past comments and I am hoping your assistance will improve my knowledge and my approach towards SE.Thank you !!

I just added [citation needed] to the WP article's sentence in question.

I think this answer, while of decent quality, does not actually address the question the OP is asking. This is the mechanics of how there is a difference not the reasons why there is a difference.

Incidentally, the XY system is not used in all mammals so there is a slight lack of generality here.

@JackAidley:From my narrow knowledge in the field I tried to give an answer, do science know the reason why there is a difference ?


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Proteins with alpha helices alone and beta sheets alone?
I would like to see some examples of proteins with PDB ID so that I can download and see them in VMD software. I need some proteins with alpha helix only and proteins with beta sheets alone.

You may consider taking a look at the SCOP structural classification of proteins to check all beta proteins and all alpha proteins. As per specific examples and though not belonging to the SCOP classes mentioned above, Porin for a beta protein (PDB:1A0S), and Rhodopsin for an alpha protein (PDB:1F88) are two nice structures to look at.

Very helpful answer.

You can find examples by using the "drilldown" function at the RCSB PDB homepage:
Click on the number 103921 at the top of the page at http://www.rcsb.org then find the "SCOP Classification" section and then e.g. select "All alpha proteins".


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Neural coupling between Pinsky-Rinzel (reduced Traub) neuron with a Wang-Buzsaki neuron?
I have read two papers related to modeling neurons. The first one is the paper by Pinsky and Rinzel and the second one by Wang and Buzsaki. The first mentioned neuron model is a excitatory neuron based on NMDA and AMPA neurotransmitters. The second one is inhibitory neuron model based on GABA. So I modeled them individually. Now trying to couple such that pre synaptic PR neuron will connect to post synaptic WB neuron which also connects to PR neuron. That is in effect an excitatory-inhibitory coupling with feedback.

Now how would the action potentials of both neuron look like?
Will both oscillate, or only WB neuron alone oscillate?
Is there any specific conditions for the oscillations to occur?

Any speculations, ideas, references (like books, related papers) would be helpful.

NOTE : By action potentials, I mean the neuronal membrane voltage signal which varies with time.

your first link to Pinsky and Rinzel is invalid. Try linking DOI or the abstract page.

@Memming : corrected the link.

By "action potentials" you mean the pattern of firing, not the shape of the action potential itself? Also, what's driving these neurons?

@Memming : I have explained "action potential" too.

are you asking what will happen when these two systems are coupled??

@WYSIWYG : Yes. At least in the simple case considering an excitatory neuronand inhibitory neuron. It can be suggestions, references and so on.

@dexterdev you need to simulate the coupled system for that. For non-linear systems the input-output relationship is not that straightforward (hence non-linear :P). Can you paste both the equations here.

There is no straightforward answer to this.
It completely depends on the properties of the neurons and the network they are in.
I would recommend you to study Central pattern generators. Those are usually small networks that can create a repetitive pattern of action potentials. However, the exact pattern they generate depends on how they are connected (number and type of synapses, network structure,...) and a presumably large number of neuronal properties (like the conductance, the shape of their dendrites, the expression level of various ion channels and all kinds of intracellular messengers/peptides/proteins/molecules). For example, there are "leaky" ion channels that can cause a neuron to spontaneously depolarize (and fire action potentials) regularly without requiring any synaptic input. This means that you can have a regularly firing neuron even without network feedback mechanisms. example
There are many different rhythms in the brain and they are all generated by smaller and/or larger networks of neurons with different properties. Neurons can even participate in multiple different rhythms, depending on the situation (e.g. theta rhythm vs. SPWs in the hippocampus). Thus, even the same neurons in the same network can generate different rhythms.
So, the rhythms that you can build depend on how you tune the neurons' properties and the way they are connected. With just the information you provided (simulated excitatory and inhibitory neurons, but no info on their excitability, network,...) I can't tell you what the resulting rhythm will look like.
I'm afraid I didn't really answer your question, but I hope this was still helpful.


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When and How do pacemaker cells develop during the cell aggregation process of Dictyostelium discoideum?
I was reading a paper by Tang & Othmer about oscillations and waves in Dictyostelium discoideum. Under certain condition like starvation period in the life cycle of a Dictyostelium discoideum community, they evolve itself into a multicellular organism in a process of cellular aggregation. I have read about Pacemaker cells among these individuals which transmits periodic cAMP and attracts other cells towards them.
So I was wondering: When and How do these Pacemaker cells develop from a "normal" cell into a pacemaker cell excreting cAMP?
References, links or answers would be very helpful for me.

What exactly do you mean: 1) How are they are evolving (into the next coming million years?); 2) How did they evolve (in the last couple of million years?) or 3) How they come into being in a micro environment like an erlenmeyer flask with cAMP floating around (wax and waning effect in a few hours time)?

AliceD : By evolving, I mean how do some cells "become" Pacemakers.

Thanks. I have linked that same article again you linked before, as it is the same literature you are referring to am I right?

@AliceD : Done. I have attached the paper.

We were working on it simultaneously: all good :) Thanks! +1

Yes, this happened twice now.


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Is there a genomic code for nucleosome positioning?
What does a genomic code for nucleosome positioning in eukaryotes actually mean? By the code is it right to think that specific DNA sequences favour nucleosomes and others don't? I see that there for and against arguments on this topic. What is the current view on this topic?

Yes and no. Part of the issue is that there are different definitions for what a "genomic code" is and there are different definitions for what "nucleosome positioning" is. You may be interested in this review written by the two leading researchers involved in this debate: http://www.ncbi.nlm.nih.gov/pubmed/23463311

The genome is the complete set of DNA in an organism, including genes and non-gene sequences of base pairs (bp).1 Each codon of three base pairs in a DNA sequence specifies one of twenty different amino acids. There are four available bases in DNA; Adenine (A), Thymine (T), Guanine (G), and Cytosine (C).  Four letters taken three at a time (where order matters and repetition of a letter is permitted) gives 64 possible codes. There are only 20 amino acids necessary in most life on earth, so only 20 codes are needed from the 64 possible. One codon is also used as a start codon (start translation) and three codons are used as stop codons (stop translation). So there are 41 extra codons available. As it turns out, for most of the 20 amino acids several different codons can specify the same amino acid, but each codon only specifies a single, unique amino acid, so there is no ambiguity. The code is therefore said to be redundant or degenerate. This degeneracy allows the same protein (composed of amino acids) to be coded with different base pair sequences, which is important if one base pair sequence is better than another in its mechanical properties of bending DNA around a histone octamer to form a nucleosome.
If the DNA molecules in a typical human cell were lined up head to tail, they would form a string about 2 meters long. The diameter of a cell nucleus is only 5 μm (0.000005 meter), so the DNA really must be packaged or organized to fit. The packing solution eukaryotes developed is to coil DNA around histone proteins to form beadlike units called nucleosomes (packing the DNA also has implications for gene expression, but we will ignore that here).
Each nucleosome constains a 147 bp (base pair) stretch of DNA, which is sharply bent and tightly wrapped in a 1 and 3/4 turn (a left-handed superhelical turn to be exact) around the histone protein octamer. There are many of these nucleosome beads on each strand of DNA. Human chromosome 19, for example, has 58.6 million base pairs, so that makes for a lot of 147 base pair beads, even with streches of unwrapped linker DNA between the beads--about 75 – 90% of the base pairs end up wrapped in nucleosomes.
The bending of the DNA around the histone is made easier or more difficult depending on the geometrical and mechanical properties of the specific two base pairs or dinucleotides at the bend. This is not a trivial mechanical property: Some sequences may have a more than 1000 fold capacity to bend around the histone octamer compared with other sequences; we will say these sequences have an affinity for nucleosome positioning since they make it easy for the DNA to wrap. Conversely, some sequences are very "stiff" and are much more difficult to bend, e.g. poly dA:dT sequences. On average, high affinity sequences have more AA, TT and TA steps at positions where the minor groove faces inward towards the histone octamer, i.e., when more bendable di-nucleotides like AT and TA occur on the face of the helical repeat where it can directly interact with the histones (the helical repeat is about every 10 bp; see below).
What do we mean by "grooves?" Remember that DNA is a double stranded helix (as if you were twisting a flexible ladder) coiling two chains of sugar-phosphate "backbones" around the outside of the helix with the nitrogenous base pairs that connect the strands (with hydrogen bonds between base pairs) pointing toward the center of the helix (if you were twisting a flexible ladder into a helix the rungs would be the connected base pairs beween the two backbones). If you held up a screw you would see the threads as "grooves" in this similar helical structure. The backbones of the two strands are closer together on one side ("minor groove") of the double helix than the other ("major groove"). In undeformed β-DNA, the complementary base pairs of the "rungs" rise about 0.34 nm and twist ~36 degrees around the center axis of the "ladder" from each base pair rung to the next. A "helical repeat" will therefore occur every 10 bp's (10 x 36 = 360 degrees) as the helix completes a full turn around its axis. Don't confuse this helix with the wrapping of the DNA around a histone core; the DNA is a double stranded helix and that is in turn wound around the histone in a nucleosome.
But do nucleosomes in actual living organisms ("in vivo") actually tend to position themselves on sequences of DNA that wrap more easily around the histone core of the nucleosome, i.e., do nucleosomes in vivo actually show an affinity for specific DNA sequences?  If they do, then that could be considered to be a "genomic code  for nucleosome positioning." There are other factors (e.g., remodelling complexes which can move nucleosome positions) and related questions, e.g., do stiff sequences like poly dA:dT inhibit the formation of nucleosomes (and are nucleosome inhibitory sequences more common in DNA sequences like transcription start sites that should be exposed to facilitate interaction with trans proteins), but we will just consider simply the basic question.
By analogy, suppose I had a printer that could only print strips of paper a sentence high (vertical height of the strip sufficient to contain a 10 pitch character, say 0.1 inch high) but of arbitrary length. Imagine the printer is fed with a spool of this strip paper, like an old time printing calculator (or ATM receipt printer). If I printed this answer text page, out would come English sentences (at least I intend this to be recognizable English) on a long, thin strip. This sounds rather like a phylactery (tefillin) printer, now that I think of it, but that is a topic for comparative religion. If there are 66 lines of 7 inch long sentences on my page, then that is 38 feet of 0.1 inch paper strip to carry around for every page of text. I might find it more convenient to wind up portions of that long strip on little wooden dowels (like empty sewing thread spools for example) and then unwind them only when I wanted to read my article again (which I can never do enough). If DNA is kind of like this analogy (it is far more complex actually), then the spools are "histones" and when wrapped with paper strip become "nucleosomes." Does it makes sense that the letters I chose to construct the words in the sentences of my article were chosen to some extent based on some hypothetical capacity for some sequences of alphabetic characters to bend and coil around a spool (say some sequences had less cumulative stiff ink drying on the paper strip)? That gives you one angle on the controversy involving the idea of nucleosome positioning by genomic code. However, consider that, as in the case with degenerate DNA codons, I can choose different sequences of characters, i.e., words, to mean the same thing, so possibly I could still choose my words for meaning, but select synonyms that hypothetically bend easier, making it easier on average to coil my sentence strip up on spools.
A recent study, Multiplexing Genetic and Nucleosome Positioning Codes: A Computational Approach, demonstrated that the local minima (the easy bending sequences) of a real gene could be repositioned (in computer simulation), that is, the nucleosome moved to another place in a real DNA gene sequence, by substituting equivalent base pairs (remember that a single amino acid can typically be defined by several different codons) to preserve the same protein encoding (a protein being a specific sequence of amino acids). This suggests that nucleosomes can at least theoretically be positioned anywhere on top of a gene, multiplexing the genetic information with the mechanical information as it were.
But do real genomes show any evidence of multiplexing genetic and mechanical information as described above? Experimentally mapped nucleosomes on top of genes do show strong signals in the probability for occurrence of mechanically favorable dinucleotides, but that does not prove the case (since shifting nucleosomes on random sequences may also demonstrate similar signals). The researchers in the study just cited then reasoned that if multiplexing is actually occuring, that is, if actual genomes have to balance the energy benefit of placing nucleosomes on DNA sequences where it is easier to bend the DNA into a coil around the histone, then it must be easier (and a more frequent occurrence therefore) to do that in non-coding sequences of DNA where only the "mechanical preference of the amino acids" need be considered (and not the necessity to maintain a specific sequence of amino acids to encode a particular protein).
Accordingly, they looked at the probability distribution for the amino acid threonine codons along nucleosomes on top of coding and non-coding regions of the S. cerevisiae and S. pombe genomes (high resolution nucleosome maps exist for both organisms). Both spectra showed a peak at the 10 bp (remember our earlier discussion of helical repeat), indicating that the codons for threonine display an overall rotational preference with respect to DNA bending within nucleosomes, but the non-coding peak was significantly higher for both organisms. When the 10 bp periodicity was plotted for all 20 amino acids for coding vs non-coding regions in both organisms the majority of points exhibited higher amplitude outside of genes, i.e., in non-coding regions where only the position preferences were a factor.
These findings (that the local minima, the easy bending sequences, of a real gene could be repositioned using degeneracy; that strong signals in the probability for occurrence of mechanically favorable dinucleotides are found in real genomes; and that the amplitude of 10 bp periodicity is higher in non-coding regions of actual genomes) at least suggest the possibility that nucleosome positions are the product of a mechanical evolution of DNA molecules, i.e., that there is a genomic code for nucleosome positioning in eukaryotes.

Welcome to BiologySE! Very comprehensive answer... If you are so inclined, you could add some links to terminology or other helpful resources to support individuals trying to follow your answer that aren't quite familiar with all the terms. It would only make your answer even better. Thanks for your effort on this answer.

Thanks, @VanceLAlbaugh. I had just worked through that paper and thought I would share what I learned. I really relied only on that paper, the link given by Bitwise in his answer earlier and an excellent Biology textbook at link for terminology and relevant concepts/context.

This is an outstanding answer

@Luigi Thanks for the tip of the hat (and Vance also). I hope this answer makes this topic more accessible to many. The OP question was in fact my own question, so I worked hard to understand.

There are definitely genomic DNA sequences that nucleosomes preferentially package in vitro. They are A/T rich and have a periodic structure that facilitates bending.  However such sequences would typically not be found on exons in vivo (because their protein-coding potential is reduced). Based on the accumulating literature, active promoters (and regions that will soon be activated) are usually Nucleosome-free, but I have yet to see evidence that this correlates with sequences that do not favour nucleosomes binding. These open areas are sensitive to DNase I, and the first nucleosomes downstream are phased.
For Epigenetic codes, people focus on the many post-translational modifications on the Histone tails.


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What does the term "relay competent" mean?
I was reading the article of Dallon & Othmer (2010) which deals with cell aggregation in Dictyostelium discoideum. In the introduction of the paper it is said that cells becomes "relay competent". I googled for the term but could not find a good explanation for it.

After a period of starvation they become chemotactically sensitive to cyclic adenosine 3 , 5- monophosphate (cAMP), as well as relay competent.

Can someone help me understand this term?

If you read the lines immediately following your quoted line (on p.391, left column, last paragraph in the linked article) it becomes clear what relay competent means (and I quote):

As a result, the cells sense and move toward a source of cAMP, and they relay the signal as well by secreting cAMP. [..] After about 8 h of starvation randomly located cells, called pacemakers, begin to emit cAMP periodically (Raman et al. 1976), the chemotactically competent cells move toward these pacemakers, and eventually the entire population forms a mound-shaped aggregate of up to 105 cells.

In other words, starvation makes cells move toward cAMP by chemotaxis, and  makes them secrete cAMP as well, which factually relays the cAMP signal back to other cells that are also attracted to cAMP due to starvation.


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will an earthworm survive after covering its skin with a wet cloth
I am very curious about this question. I got this doubt when I was studying anatomy and physiology of the earthworm Lampito mauritii. It breathes through its skin (cutaneous respiration) and if we cover its body with a wet cloth and all the necessary external openings are left uncovered (such as nephridia and other genital pores) then will the earthworm survive?

Assuming it still has access to oxygen through the wet cloth, and the moisture content remains constant, I don't see any reason why it wouldn't survive...

i can't get your point do you mean that earthworm will survive that situation

sorry, it was a double negative. Yes, given sufficient oxygen and a steady supply of moisture, the worm should be able to survive quite happily for some time.

but how would it respire in such watery environment ?

If it's submerged, it won't be able to. But, if the environment is just damp, it will be fine. It's the difference between covering it with a soaking-wet paper towel, and one that has been dampened, then squeezed out some.

yes they do.. they survive on damp tissue papers.. I've tried it..

This is one of those speculative questions where you don't have a definite answer unless you specifically experiment and find out for yourself.
It is a known fact that earthworms breathe through diffusion. It has a thin cuticle over its body and requires moist skin which is achieved by a slimy mucous (reference). It is interesting to note that earthworms are also capable of going into a state of hibernation called estivation (in American english) (reference) which helps them maintain a low metabolic state.
Since you are planning to cover it with a cloth, the material of the cloth also matters. It has to be a material with low breathability. For eg: the survivability of the worm would depend on if you were using a wool or a silk cloth to cover it. Here is an article on the breathability of different fabrics (reference).
In conclusion, I would take a guess that it should survive if the material let air pass through and would go into a state of estivation on low availability of oxygen but maybe not die. After all, they are said to be able to survive even in water  if it contains enough available oxygen. (reference).

this might be a different question but what would happen to the earthworm if you dry it using a wet cloth and then at the same instant make its skin wet by applying water ?

@agharehanabbas It would survive again. There should be  a little bit of time and direct exposure to sunlight to get it sun-dried.

but i think that would effect its repiratory rate and doing so continuously would kill him

@agharehanabbas It has the ability to produce slime to stay wet on its own and moreover, you make it wet by applying water as soon as it dries which is hardly enough time to effect its respiration. In my answer I have already mentioned that it is able to survive underwater and also go into hibernation.


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why didn't natives of south america evolve darker skin?
I understand that darker skin tone is caused by melanin which helps to protect against the extra UV radiation that comes from more direct sunlight. It evolved in Africa before we migrated away from Africa and as I understand it was later evolved away from in areas further from the equator, where less sun meant less need for UV protection, because less sun also made it harder to get sufficient Vitamin D. Thus those near the equator tend to have darker skin and the further from the equator one goes the lighter the skin.
There are parts of South America which reside right on the equator, where melanin would provide important UV protection and where vitamin D deficiency was not a concern. I would expect them to have black skin, as dark as someone from Northern Africa or the Indonesians has, due to the extra UV exposure associated with the equator.
However, natives of Brazil and other equatorial parts of South America don't seem to have the same skin pigmentation as I see in the other equatorial areas.  They have skin darker then Europeans and other northern natives sure, but not to nearly the degree of other equatorial natives.  They clearly have the mutation for melanin, since that existed before we left Africa and they do have partial dark skin, which suggests that for some reason there was an evolutionary advantage to having skin as dark as theirs, but not darker.
Can anyone explain to me why South Americans wouldn't have evolved (or not evolved away from, depending on what part of the world they originated from) the almost-black level of dark skin the other equatorial natives possess?

This question really needs to be pruned down a lot. Focus on the core question (Why are indigenous people in South America not as dark as sub-Saharan Africans living at the same latitude, with the same intensity of sun exposure?) and get rid of all the fluff, background, and other unnecessary material.

The current prevailing wisdom on human migration holds that the Americas were populated last and from groups that migrated from Northeastern Asia. Evolutionary time was likely not long enough and difference in environment, Rainforest or high mountains versus savanna could have contributed. Also it has been shown genetically that H.sapiens that migrated out of Africa came in contact with and integrated with other Homo species that left Africa several hundred thousand years before who had the traits of lighter skin, straighter hair etc associated with Europeans and Asians....

That these genes survived in H.sapien today likely has to do with environmental selection that you mention.

@AMR Your answer is the correct one. Why don't you post it as an answer instead of a comment?

@LeonardoCastro because my comment is inferred from information that does not directly relate to the question. As I cannot cite actual research that tests the idea, this is more my opinion, which is more correctly placed in the comments than a researched answer that has factual evidence to support the answer. Even if I was to write an answer that cited the sources that that led to my "hypothesis," none of the research that I was aware of at the time directly tested the question.

There hasn't been that much time for it to happen, and it may not be that much of a strong selective force. The main Amerindian peoples apparently arrived 14-15 thousand years ago, at the height of the ice age. They were from cold climates, Siberians, travelling a bit like Eskimos in the snows of Alaska. Indeed, they may have not evolved light skin after coming out of Africa 50mn years ago, but they may have acquired light skin from Neanderthals and Denisovans who had lived in cold climates for over 1/2 a million years.

Could not fit in a comment....
Northern Africans and Indonesians have pretty much the same skin color (to my first impression). Sub-Saharan African (that you don't talk about) are darker. And Northern Africa in not an equatorial region (not more than Los Angeles) as it is right under the tropic of cancer.
Also I am a little confused about who you call "we" and who call "they". I think that by "we", you mean any non-sub-Saharan African human but I am not sure. If this is the case just naming sounds more appropriate that to make a big category that you call "we" to exclude some ethnic groups :)
I think that when you are talking about Brazilians (and other people in South America living close to the equator such as Ecuadorians), you are mostly talking about people from Spanish and Portuguese descent. So let's talk about the great migrations
The Indonesians arrived in their lands about 70,000 years ago. The indigenous South-Americans arrived in South America about 10,000 years ago. The Spanish and Portuguese arrived in South America about 500 years ago.
I think you might want to read a bit more about the geography of those big migrations.

Your paragraph about time of arrival should be expanded into a "real" answer (and the numbers verified), as this is most likely the exact reason that indigenous South Americans (and North Americans as well, really) are not darker than they are - they didn't arrive that long ago. Here is a good place to start.

They have been pushing back the dates of the migrations into the Americas with new archeological findings... They are looking at closer to 15k years now. Also with the work of Svante Paabo and others, it may very well be that the mutations that we associate with Europeans and Asians arose in non Sapien humans and that modern humans inherited those traits from breeding between the groups.


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Does the genetic material the sperm carries affect its physical properties
Basically, what I'm asking is, is the actual sperm cell built from the blueprint in the DNA of the man or is it itself also a consequence of the DNA it carries?
I'd like to know a few more things related to this. For example, which DNA is in the nucleus of a sperm? Is it the same as the DNA of other bodily cells in the man's body, or is it just the DNA it's delivering? Can the sperm's performance be affected by any specific genetic traits that can be observed in a potential human the sperm could make? For example, a sperm swims faster if it's carrying the genetic material that would result in a tall person (probably a silly question).
The original question I had is if the statement that female sperm live longer is true. If it turns out that the man's body makes all the sperm more or less the same and they're just boxes that can swim, then I would guess the answer is no.

Does not answer your question but is related: (inter-males) Sperm competition

Sperm Biology: An evolutionary perspective might help here - I'll take a look this week at work. There is also a group in my department looking at selection in the haploid/gametic phase so I'll chat to them.

I think there is a strong driving force for sperm to be free living haploid versions of human beings.  Since they are a product of meiosis sperm are the product of recombination of both the male chromosome sets.
While I'm sure that if we look closely enough, the germline cells that produce the sperm are contributing some protein and structure to the sperm, the life cycle of the sperm is mostly the result of the genome that it contains within itself.  Sperm are prone to defects.  On the average in human beings about half of sperm are non-motile: simply unable to form the flagellum or power its motion adequately for motility. That's a pretty strong selective force in the life of our other, 'half genome' selves.
Sperm selection - the sorting of which sperm from a single male achieves fertilization is pretty rigorous.  It can take 30 minutes to days.  Once in contact with the ovum, the sperm executes a critical set of transformations and biochemical activations to get past the various layers of the cell.
Sperm are from the man, but they are each living creatures on their own which we hope will deliver themselves up to the ovum to create another human being.  They vary in their genetic quality and effectiveness and this is highly related to their genetic make up.
Because each sperm is the product of two stages of Meiosis, they can be full of genetic defects, most of which would be fatal in a diploid human being.  The functions of the sperm as it goes through its short but competitive life weed out genetic abberations and help assure that the next generation of diploid human beings is as healthy as they can.
So they are not DNA boxes that swim.  I'd be hard pressed to think of a passive role for a cell in biology - they are all working pretty hard... I'd be interested in a comment with suggestions of something that is not under selective pressure in biology.
It sort of reminds me of the old argument about passive mating in females. Behavioral biologists used to think that female animals had little or no active role in mating.   That myth was retired about 30 years ago now.  That link points to an introduction to an entire volume reviewing that whole discussion of active female roles in reproduction in case anyone reading is interested.
BTW I'm not an expert on gametes, but I'd be surprised if the ova also didn't have a complimentary but quite different selective process they had to get through to become a fully presented candidate for fertilization.
Just to add a note about how the functioning sperm genes affect the diploid organism: This is one of the most important things that sperm does.  The genes that function in the living spermatazoan are the same genes the diploid organism uses, or at least a substantial number of them.  Further, these genes are scattered across all the chromosomes and so major chromosomal defects and important genes are functional if fertilization is completed.  As an example here's a cool blog post about how mosquito sperm have been shown to use odorant receptors to orient themselves in the fertilziation process. Those same receptors and the signalling genes that link that signal to the sperm behavior are probably quite useful to the adult mosquito.  I'd be surprised if human sperm also did not use similar pathways to function.
Not to beat a dead horse, but the recent nature has a report of small RNAs in mouse sperm as being an epigenetic carrier for stress.

Thanks for the answer. What's still confusing to me is the connection between a sperm not functioning properly and a potential human not functioning properly. For example, humans with mental retardation often have above average strength. Does that mean the sperm they used to be was defected or above average? It seems to me that there would have to be some defined standard of a normal DNA that the sperm would check against to determine how "broken" it is, and I doubt there's something like that.

Hey Darwin - I've added a note above.  you have to remember that a substantial of human genes are found in yeast.  Those core functions are absolutely necessary for viability. Our lives as single celled organisms use most of the same genes.  neat, eh?

Meiotic drive would be a cool example of a sperm cell's genotype affecting it's phenotype

@GriffinEvo are you thinking of selfishness, sometimes referred to as Drive?  If so you have brought up one of the most famous examples of sperm activity - a locus which causes a sperm that contains it to actually inhibit other sperm even if they come from the same male.  A classic example of sperm genes in action and evolutionary biology.

yes, SD in Drosophila and T-haplotype in mice are the two main examples if i remember correctly

That is indeed the classic example of active sperm selection isn't it? There are books about it now. @Darwin if you want you can search at bn.com/amazon for 'sperm competition'.  its a big world out there. As an equal opporunity presentation, here's a picture of a team of sperm using hooks on their heads to cooperate and swim together.  http://www.nature.com/news/2010/100120/full/news.2010.22.html

Apropos of nothing... giant fossil sperm longer than the male animal itself. http://www.nature.com/nature/journal/v509/n7501/full/509402c.html

Shigeta, you have some good points there.  I wanted to clarify some things.
Sperm and ova are considered tissues, not individual living creatures.  They are not individually capable of cell division nor production of offspring.  They are specialized cells with specific functions that are created by a multicellular organism as a means of transferring DNA.
The sperm carries 1/2 of a chromosome set from the male's own DNA, after cross-overs during meiosis (meaning that the DNA in a sperm has some different combinations than the parent DNA).
Metabolism primarily occurs at the mitochondria.  Protein synthesis does occur in the sperm, using nucleus-encoded mRNA.  What I was unable to find an answer to was whether this mRNA was transcribed from the nucleus of that same sperm, or whether it was from the primary spermatocyte DNA (diploid) or from the sperm nucleus (haploid).  The chromatin in the sperm nucleus is several times more tightly wound than in a somatic cell, so I am not sure how it would be accessible to transcription, nor am I sure that the full set of enzymes required for transcription, modification, and translation is present in the spermatozoa.  I'll be very interested in hearing if anyone is able to find this information!

what does a sperm do besides reproduce?  The haploid phase of some animals like coral can be weeks long.  Yeast haploid genetics are a big topic in research and the halpoid phase can be maintained for quite a while.  Here's a reference for sperm mitochrodrial transcription. Sperm are not the main system for research of hapoid life cycle though http://humrep.oxfordjournals.org/content/22/6/1585.short

I really don't know who makes these decisions, but I'm not sure this is an unanimous opinion nor one that is necessary to hold in all circumstances.  you are of course free to have whatever opinion you like.

For example, a sperm swims faster if it's carrying the genetic
  material that would result in a tall person

and in the comments

It seems to me that there would have to be some defined standard of a
  normal DNA that the sperm would check against to determine how
  "broken" it is, and I doubt there's something like that

If some aspects of sperm cells indirectly connected with some parts of phenotype, so we can expect that result, but not because of sperm cell carries that noble phenotype gene.
DNA in sperm cell is packed and not expressing (not transcribed).
Because DNA is packed and because test checks consuming energy, which sperm needs for another tasks - pretty wise to shut down checks, repairs.
Also DNA is not like ZIP archive, where cell can check the check sum, to make shure it works witch good DNA. Cell have difficulties working with information, if it needs to connect information results from distance sources. (Let say as example: if gene A have mutation A* and gene B have mutation B* then do X).
Also there is big big difficulties with that mater: some defined standard of a normal DNA - all DNA that leads to organism which is able to procreate, to survive - is good enough for nature. Thats Evolution spirit). And who can, who not - will be sorted out, later and with 100% accuracy.

For example, humans with mental retardation often have above average strength.

Our DNA actually consists from imperfections, which showed up long ago and became standard de facto, some are compensated at the moment and are RFC(Request for Comments). This or another set of genes is a balanced system. Balance can be shifted and that will have some consequences, actually thats how another system is prepared for testing by Evolution factors. By shifting balance far enough, for making some things at extreme, we may expect that another things have to break. But strength is not because of mental retardation, or vice verse. (It may be connected, may be not; also I would not trow away, some ontogenesis matter in that case) They both are results, not cause. But there are some reasons to be connected, if you take look on apes behavior as example.

just boxes that can swim

Man it's a Rocket


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Is it reasonable to assume that RNA polymerase would bind preferentially to the promoter of the long allele of the SERT gene?
I'm trying to come up with an idea for a school project (a hypothetical research study).
I'm looking at depression and the serotonin transporter gene, which is highly expressed in the human cerebellum. There are 2 common alleles of this gene, a "long" and "short" version. The difference is that the long version has 16 repeats of a certain sequence in the promoter, and the short has only 14 repeats. Though there have been some controversial findings, the short genotype has been linked to patients with depression, suicide, less serotonin uptake, and less localization of the serotonin transporter at the cell membrane (synapse).
My hypothesis is that RNA polymerase binds preferentially/more strongly to the long allele's promoter over the short allele's promoter in human cerebellum neurons.
This would explain higher levels of transcription of the serotonin transporter gene (though this hasn't actually been shown) and increased serotonin uptake (has been shown), resulting in lowered susceptibility to depression.
I was thinking I would do this using ChIP. I would get cerebellum tissue from deceased patients of each genotype (long/long, long/short, short/short) and compare bound RNA-pol in the different genotypes.
My two questions are:

Is this a reasonable hypothesis (does it make sense based on what I have described)?
Hypothetically, is it possible to do ChIP on dead brain tissue?

I don't know anything about SERT, but your hypothesis sounds plausible to me. However, if you want to determine relative transcription levels, RNA-seq may be more appropriate. I believe ChIP would tell you whether or not RNAP binds the promoter and where, not necessarily how well it binds. Furthermore, I feel that addressing whether or not the transcription level is actually affected may be the step to take before determining why its affected.


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Help reading chromatogram
A genetic variation is found in this chromatogram:

It says that the "reference sequence" is the top line and that I can use the general genetic code to find the reading frame.
I can see that there are two N's instead of a G and a C. However I don't know what this means. I'm also not sure how I'd find the reading frame? I suppose I could look for a start and stop codon but I could read them both ways?
Last question: Is this change likely pathogenic? I'm not sure how to classify a variation as pathogenic or not.

So the two Ns that you see are not necessarily variants, but rather likely just poor quality reads. Essentially when you sequence DNA and the sequencer can't make a call as to what the base is, it will just designate it N meaning that the base could be any of the four DNA bases.
As for finding the reading from, if you know this sequence contains a stop codon, that helps, and just look for any of the stop sequences. If not, look for bases that match codon sequences and if you get a full strand of sequence that codes for amino acids you will likely be correct.
For reference here is a link to a codon chart that will help you decipher the reading frame.
Does that help?

Yes absolutely, could you tell me if you can, whether the mutation is likely to be pathogenic, though? And if so, why?

So as cagliari says above it does not look like you have any mutations. You cannot call N a mutation because this could be any base including the one from the reference genome.

The traces you have come from Sanger sequencing. N in genetics means nucleotide (surprising right?). N is used when the base at a given location is unknown (or could be any base pairs).
In your case you have Ns because the base-calling software is unable to determine the nucleotide. The first N is due to two peaks overlapping (G and A signals) and the second one should be a C rather than a N.
From what I can see, you have no apparent mutations so no those changes are unlikely to be pathogenic. A mutation can be called when you know a base in the reference is modified in your sample, which is not the case here (simply N -> G and a N -> C). The signals for your Ns look very similar between your reference and your sample therefore not suggesting a mutation.
For the reading frame, you have to look for a start (ATG) and a stop codon (TAG,TAA or TGA) to identify the open reading frame (ORF). Multiple software do that and here a link to an online NCBI tool called ORF Finder.
As you pointed out the ORF can also be in the reverse strand. You don't want to look at the reverse sequence but at the reverse complementary sequence. Usually tools to detect ORFs have the option to look at both strands.


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"CO2 is plant food" - What is the actual effect of increased CO2 on plant growth?
A frequent talking point by global warming deniers is that CO2 in the atmosphere is actually beneficial because "CO2 is plant food". I'm a non biologist trying to figure out under what circumstances this is actually true.
Here are my thoughts so far:

Plant growth is more or less governed by Liebig's law of the minimum - the plant needs sunlight, CO2, water, nutrients in a certain composition, whatever is lacking limits growth
In addition to it's role in photosynthesis, water is needed to transport nutrients from the soil, so dry conditions can limit effective nutrient availability
The energy needed to assimilate CO2-carbon is independent of the CO2 concentration
The rate of photosynthesis is (within the limits given by energy etc.) governed by CO2 concentration and active plant matter
photosynthesis only works in a more or less narrow temperature band

From this, it follows that a higher CO2 concentration in air will boost plant growth only if everything else (light, water, nutrients) is abundant.
So I have two interconnecteed questions:

How wrong is my simplistic view, does my conclusion hold?
What do we actually observe in the wild or in experiments?

Possible duplicate of http://biology.stackexchange.com/q/681/3340

Definitly helpful. Need some time to read linked papers in the answers over there.


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How plasma cells switches secreting different Ig classes?
In Type 1 hypersensitivity how do B lymphocytes switch Ig classes, from synthesizing IgG to IgE? What is the mechanism? I studied multiple pathology books, it says the same as for IgG secreting pathway. So how does the body know how to change the Ig secretions in response to allergens?

The mechanism is called Class Switch Recombination and it is a form of error free NHEJ. Appropriate signals activate the recombinases.

In T-dependent antigen recognition, the B cell can switch the isotype by first altering the heavy chain gene. This is driven by Tfh cells. The specific cytokine stimulating the class switch determines the isotype of the heavy chain to be synthesized. For your example, interleukin 4 (IL-4) drives the class switch to IgE. You also need a costimulatory signal from the CD40/CD40L interaction between the B cell and the Tfh cell. This induces activation-induced deaminase (AID), see bottom paragraph on this.
There are switch regions (denoted S) in the introns between J and C segments at the 5' end of each CH locus, and upstream of that is an I exon (region denoted I) w/ it's own promoter. Induction by CD40 and whatever cytokine is present starts transcription of the I exon, switch region and CH chain of the H-chain the B cell is meant to switch to. This germline transcript facilitates dsDNA breaks at the switch regions Sµ for the IgM (switch region mu) and the switch region for the class to be switched to, Sε in our case for IgE. The intervening DNA is deleted and the coding region Cµ is replaced by Cε coding for the IgE heavy chain BUT, it ends up with the same V domain as the B cell originally had!
Some enzymes involved are AID, which deaminates cytosines and allows the germline transcript to hybridize in the switch region, Uracil N glycoylase UNG which removes uracils from the DNA, and APE I endonuclease that generates a nick at the abasic sites generated. These nicks lead to dsDNA breakages in the switch regions. Text shows that the switch region DNA is G-C rich and can form stable RNA:DNA hybrids with the coding strand of the switch region and the germline transcript. This is what frees up the noncoding strand for alteration by UNG and cutting by APE. The result is that the V region becomes associated w/ a new constant region.
I'd also be careful with the terminology plasma cell as used in the title because we aren't yet at the high-affinity secreting stage when we're talking about class switching. This is mediated at the activation of the actual B cell by Tfh cells.

All information above is summarized from Cellular and Molecular Immunology, 8th ED


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Is it possible to print humans?
According to this news, scientists can use stem cells to print objects. So say theoretically, is there any possibility to print human beings?

This question has been migrated from scifi.stackexchange as it is not a good fit for our stackexchange site. However I believe it is answerable on this site, biology.se.

When a generic-press article about science says "XXX could be used to do YYY" it generally has to be read as "in at least 15-20 years, an extremely improved version of XXX, that will probably not even resemble to XXX anymore, will be able to be used to do a proof-of-concept YYY." :)

The easiest answer to this question is NO. We will not be able to print humans any time soon, if ever. Despite the potential of the technology, it will likely still make more sense to use stem cells to fight genetic diseases, create limited cellular masses such as hearts and other organs, and to do reconstructive surgeries such as skeletal repairs.
The reasons vary but will include:

The human being is not just a single series of cells, we are a complex melange of integrated systems connected together in a predetermined manner by our genetic code.
The standard 3D printing process might be most effective for producing a single type of cells or a simple organ whose structure is simple and whose configuration could be managed with computer aided design to produce the cells needed at the time of the organ's creation. Even an organ such as a liver will need connective tissues, for blood to be provided for the organ and those cells would need to be integrated as well.
Brain tissue would be the most difficult part of this process. Even having the tissue matrix derived from stem cells would not give us the understanding of how to create an actual brain from a printing process, which uses a layering method to deliver the material into a 3D structure.

It is certain that some things we may do in the future may be done by printing output that resembles cellular matter, i.e. bone repair and restructuring.

In the case of fixed materials such as bone, a 3D model could be taken and then replicated on a printer. The replicated material is then integrated into an area of the body and allowed to either grow in place or artificially stimulated to grow to replace the damaged area.
I use bones as an example since they have very limited purposes and once replicated artificially, would be relatively easy to put in place. This would certainly transform the dental industry, perhaps hip replacement surgeries.
If the technology could be applied internally to damaged tissues, perhaps spinal injuries could be repaired and with proper rehabilitation, a person who may have lost mobility due to an injury could have nervous tissue regrown and learn to walk again.

The potential for specific cellular development is outstanding but the method for growing complete humans has had millions of years evolution and not likely to be surpassed by Humanity in the next thirty to one hundred years unless we come to a far greater understanding of the human genome and the genetic/cellular relationships between systems in the human body as a collective whole.

Any biomaterial scientist working on bone will read this and just think "I wish..." :)

No.
The reason is that development is extremely important for getting tissue organized on the appropriate scale.  We can place groups of cells or a scaffold somewhere, but we can't assemble a working cell from component bits, much less make one that has one end in one's toe and the other in the spine (as is the case with sensory neurons for our legs).
So 3d printing of tissue is limited to tissues that have very simple or robustly automatic developmental processes.  This includes things like skin, liver, and bone; it does not include things like muscle, neurons, joints, or blood vessels.
As technology and knowledge of developmental processes advances, we will be able to print more complex things, but it's not clear to me when or if we'll start running into physical limitations that mean that we basically just have to let things grow and develop the way they normally do.


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How difficult is to renature a protein?
I know of Anfinsen's experiments and I'm aware that some denatured enzymes may regain their lost activity through the removal of the denaturant agent. What I'm unaware of is how rare is it for a protein to be able to renature? Can all proteins do that? If not all of them can do it then how rare or common is it to find a protein which can be renatured?
P.S. To avoid answers like "depend on your denaturation process" let us assume that a protein can be renatured if it has been shown to renature in at least one experimental setup.

This is a very difficult question, and I doubt the answer is known to any satisfying degree of certainty.  The best suggestion I have is to look at proteins requiring chaperones to fold.  Even that I couldn't find any numbers on, but there might be some papers out there addressing it.

The answer is more like "It depends on the protein, and the renaturation (or refolding) process." There are a lot of factors that contribute to an individual protein's ability to refold, including size, sequence, secondary structure, amount and type of inter-amino acid links like disulfide bonds, number of subunits, the presence of chaperones/heat shock proteins, and, yes, how it was denatured in the first place (sorry, I couldn't resist). Smaller proteins will refold more easily than larger ones. Hydrophilic proteins tend to refold better than more hydrophobic ones, especially membrane-bound proteins. Multi-subunit proteins/complexes tend to need some help to properly reassemble. Adding in chaperones/heat shock proteins will almost certainly help the process along for all but the smallest and hardiest samples, and will give you better results than just dialyzing all the salts/detergents/chaotropic agents away into PBS. Finally, if you denature by boiling in Laemmli buffer, you're going to have a very difficult time refolding most things, while going from Guanidine HCl to PBS isn't always that bad, depending on what you're looking at.
So, unfortunately the answer is "it depends." You have to remember that the intracellular environment is very complex, and is designed to correctly fold proteins after they're made, and break down misfolded proteins before they can aggregate or cause other damage. There are hundreds of thousands of proteins just in humans, so it is rather difficult to make blanket statements, but for the sake of resistance to damage, many smaller, single-subunit proteins can likely be at least partly to mostly refolded and regain some or all of their original activity. As complexity grows, however, the likelihood of successfully regaining function decreases.

my impression has been that only relatively small proteins (~10kDa) are readily renatured and used in protein folding kinetics experiments.  Its pretty unlikely that anything larger will be useful.  Do you have any specific examples of a larger protein that has been refolded by any means, and if so do you think this is a typical result?

@shigeta - I was specifically thinking of antibodies (150 kDa, 4 subunits disulfide-bonded to each other). At my previous job we experimented with purifying antibodies by eluting them from an antigen column with varying concentrations of guanidine, then dialyzing directly into PBS. We didn't do any biophysical characterization to look at the extent of denaturation, but in our functional assays they performed similarly to those eluted by the standard (pH-dependent) method.

those antibodies would not be fully denatured. just enough chaotropic agent probably to disrupt protein-protein interactions to get the antibodies off the column.  Antibodies have one of the more stable folds and will not usually denature under such conditions.  if you did I would be surprised if you could reconstitute a functionally folded protein... imho


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How and why did mouth and nasal cavity evolve separate?
My initial objection is that nose filters air, mouth is for eating but is used for breathing also, plus they both are used to create sounds. What is the cause and reason in this case, why do we need two "holes" and one is not good enough?

Neither the nostrils nor the mouth originally evolved for breathing.  Fish have (two pairs of) nostrils which they use to smell and mouths which they use to eat, but they breathe through their gills.  Some lobe-finned fishes (the ancestors to tetrapods) evolved a connection between the posterior nostrils and the oral cavity called choanae.  A fossil called Kenichthys is a transitional form in this development.  The evolutionary reasons behind this development are not particularly well understood.  (This should not be surprising when discussing something that happened in the Devonian.  It's only recently that the discovery of Kenichthys ended the controversy of whether chonae in tetrapods are homologous to posterior nostrils in fish.)
Basal reptiles have nostrils and mouths and can breathe through both of them, but do not have a separation between the oral and nasal cavities.  The next important development is a secondary palate (which separates the nasal and oral cavities).  This allows animals to continue breathing while swallowing food.  Animals without such a separation must hold their breath while swallowing.  This ability is certainly useful in many situations, and unsurprisingly several solutions to this problem have evolved in different lineages.

I'm not sure if other can do that, but I cannot breath when I start swallowing, there is a break on breathing even via nose. But I can keep chewing food in mouth and breath at the same time with nose. What are the other "several solutions"?

Snakes have an extended trachea "straw" called a glottis, that allows them to breathe while swallowing.  See http://www.youtube.com/watch?v=Pq18vg6vBGA

Adult humans can't breath while swallowing, but infants can. That we can't breath and swallow as adults is related to the facts that we are upright and have throats highly modified for speaking.

Yes, I remember reading, that part of the throat called larynx shifts at some age to get on more proper position for speaking. I could accept this answer, but waiting if there comes other views and especially explanations how this happened in evolutionary terms.

@PHPGAE  Added some more info.

In general, only mammals (animals like humans, dogs, cats, mice and cows) have an epiglottis. Some reptiles have an extra flap of skin that does pretty much the same thing as the epiglottis, but it does not have cartilage in it. This is an example of what scientists call an analogous structure (same job, but made in a different way) instead of a homologous structure (made in the same way – although sometimes it has a different job). ref


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Difference vector target and genomic target
In Pfu turbo DNA Polymerase AD information sheet (and possibly in many other) different amplification targets are divided in Genomic DNA targets, Vector DNA targets and cDNAs.
What is the difference between the first two?

Genomic DNA is a DNA that has whole set of genetic data of an organism. You usually extract it with a whole DNA extraction kit.
Vector DNA is a vector (usually a plasmid, it can also be artificial chromosome,...the type of vector depends on the species and strategy you are using) that has you desired string of DNA in it (for example a gene you want to insert in to a organism) and you are using it to get your recombinant DNA to the organism.
I hope it helps!

Genomic DNA is usually bigger and more complex than plasmid DNA which is a relatively simple DNA ring of limited size.


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Databases for metabolic pathways of human disease
Which databases contain the metabolic pathway of human diseases?
I have searched Metacyc and KEGG but didn't find the appropriate metabolic pathway.

What exactly are you searching for, and how specifically did KEGG and Metacyc fail to meet your requirements? Please [edit] your question with additional details so we can provide focused answers.

nearly any pathway can exhibit a disease if its damaged in the right way - disease is a dysfunction.  this is pretty difficult to answer in a way that makes sense.

NCBI BioSystems help file contains a list of their sources:
http://www.ncbi.nlm.nih.gov/Structure/biosystems/docs/biosystems_help.html#SourceDatabases
Please specify what you need as stated in the comments as it is almost impossible to give you more (relevant) information then this.

I need the details of Ubiquitin/proteasome pathways which is responsible for cervical cancer from E6 and E7 oncoproteins?

I've been doing some research but I couldn't find exactly what you're looking for. I'm not a cancer research expert but you might find what you are looking for from this page: http://www.ncbi.nlm.nih.gov/biosystems/?term=DNA+repair+Ubiquitin
I'll let you know if I know more.

I need the step wise rections of ubiquitin/proteasome pathway. I have to calculate its parameters for COPASI.