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Is the missing "life-ingredient" in today's Earth's existence the reason why we cannot recreate life?
As far as I know, there was no report of "life" popping up in a lab or in nature so far.
Everything that we know is only some copy with similarity to previous life-forms.
We certainly can mix some amino acids and stuff, and even some of the chemicals can retain some structure for a certain time and even form some proto-RNA-like structure (not sure how they called it in one document I have seen), but it's very very far from a living organism.
Does it mean that life cannot be "sparked" in today's Earth like conditions or, was it not even sparked here to begin with? I have read, as many others have done, this article: New research supports an idea that the Red Planet was a better place to kick-start biology billions of years ago than the early Earth was. They argue that you need molybdenum to create life-like structures and that it's not common in the right form on Earth.
What do you as biologists think about the statement that life cannot evolve on Earth because the conditions in the beginning of the Earth were not good for life to develop.

keep in mind todays earth is very different than the early earth, for instance life has drastically changed the atmosphere of the earth.

I have voted to have this question removed as off-topic. Please consult the help to see what questions are unsuitable. A suitable question asks for factual answer to a specific biological problem. "What do you think about the statement..." is not such a question. However interesting it may be it is an attempt to initiate a discussion to which any contributions (answers) are likely to be subjective. That is why it is off-topic.

There is a difderence between "conditions in the beginng of the Earth were not good for life to develop" and "Red Planet was a better place to kick-start biology billions of years ago than the early Earth was". If A is better than B, it doesn't mean (at all) that B is not good enough. Thats also the point people often forget while talking about evolution.

Three important concepts about abiogenesis
Let's start with three important concepts
Definition of life
You'll need to give a good definition of life, because biologists actually don't have one (it is a matter of philosophy to define life, not biology).
Time it took for life to emerge
Life as we know it emerged only after a huge period of time (hundreds of millions of years), which we obviously cannot reproduce in a lab.
Current competition
Even if some kind of protolife would appear at some point, it would still have to face the competition with its veteran partners. Hypothetical protocells would be eaten by some microbe with no doubt.
Panspermia
The idea of panspermia (the hypothesis that the life may have appeard in outer space or in another planets, and then "contaminate" the Earth) has been on the scene in many forms for quite a long time. Regularly we hear of some study which proposes that life, or at least some key biomolecule, may have formed in asteroids, comets, in Mars or somewhere else. They're quite interesting, mainly because they suggest more than one way that life may have appeared.
Molybdenum
While molybdenum is rare in the Earth, it still exists and so the study doesn't deny the posibility that life may have formed in the Earth. Nowadays, molybdenum is used by many organisms as part of the core of some key enzymes, such as nitrogenase (the enzyme complex that catalyzes the conversion of molecular nitrogen into nitrate). Molybdenum has very interesting catalytic qualities and may have been a key factor for the origin of life.
Phosphorus on Mars
However, those studies say that Mars has higher concentration of phosphorus, which is one of the main components of life, and that was pretty rare in the early Earth. The hypothesis is interesting but, without experimental data, it is only that. The authors suggest that nowadays those phenomena may happen in Mars, so the hypothesis may be confirmed in a few years as the exploration of the Red Planet continues.

I modified the format of your answer (I mainly just added names to sections). Please feel free to roll back or re-edit if you don't like my edit.

Note that in addition to "hundreds of millions of years", there's also the fact that primordial life-creating "experiments" where likely taking place over a large part of Earth's surface, not just in a few test tubes in a lab.  So there's extreme parallelism.

This is really quite a question. And many leading biologists have tried (very hard) to answer it.
In my opinion, most of our incapacity to study which conditions can favor some form of "life" is due to a lack of understanding of what is "emergence". And moreover, about or focus on matter over processes, and the reductionist paradigm of modern science.
Life is an emergent, system-level, property of any living system. It is not the material basis of life what is important (for instance, just mixing all the biomolecule precursors in a soup has proven to be a poor attempt to recreate life-like behaviors). What is important is the way this matter is organized. But, again, what we don't understand is what "organization" even means. My intuition says that the answer will come from studying "organization" and not "matter". There is no reason to think that other life-like forms will have the same molecules (CHONPS, and water-based metabolic transformations), out of the astronomically huge universe of possible molecules that can exist by combining the finite number of stable atoms in the universe.
Then, let's understand organization. Let's understand emergence. Better, let's understand "radical emergence". Here I leave a link to some brief thoughts from one of the leading scientists of all of biology, Stu Kauffman.
Here is a more chemically-oriented opinion, by another leading scientist in the field (who recently passed away).


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Which part of the genome are the developmental sequences of embryogenesis located?
Which part or parts of the genome are the sequences located. Are they spread across the chromosomes? If so, how are they accessed sequentially with precision during embryogenesis?

This is a very general question. The "developmental sequences" are just genes like any other. Like all genes, they are semi-randomly distributed through the genome. While there are gene-rich and gene-poor areas in the genome, with some exceptions—notably the homeobox genes—genes are not grouped by function.
As to how they are accessed sequentially, that is a huge question but it is not specific to embryogenesis. Genes will always need to be turned on/off at specific times and in response to specific stimuli. This is particularly obvious during development but is not exclusive to it.
The basic way this happens is through feedback and control loops. Gene A activates the transcription of gene B which activates gene C which then deactivates A. If you manage to turn on A, the rest will follow. One of the ways this can happen in developing embryos is through maternal mRNA. These are mRNA molecules that are present in the fertilized egg and which begin to be translated. This gives us a starting point to activate gene A, which then turns on B etc.
This answer is a huge simplification, but a full answer could take up a couple (or 40) of PhD projects.

Terdon is right on the money when it comes to how is the coordination done, and I know of at least one student working on this for her thesis. However, to answer your other question directly, there was a great review in 2010, which was taught in my genetics class that year.
It is important to note that we still don't know all the genes that are involved with meaningful certainty.  Further, it would be exceedingly difficult to fund and conduct Hong et al's work in the US.
If you read the article you will notice that several genes that are involved are genes that are active through out life at various levels.  Figure 4 gives a good example of how spread out the information.
Notice that the three categories of genes they used were even quite different: Stem Cell Specific Genes, Muscle, fat and connective tissue genes, Significantly Enriched GO term
So when you think about how diverse the genes are, it would be even odder for them to be clustered together.  Again, they are probably not truly random, but they don't seem to have a pattern.
To quote their take home:
Furthermore, by comparing with published data, we identified three groups of maternal genes with distinct regulation profiles during wk 4–9 of development, which provided a molecular basis for the anatomically distinct developmental events that occur between early embryogenesis and subsequent organogenesis and histogenesis.

More important, our genome-wide and detailed developmental profiling
  of the patterns of gene expression has revealed that genes involved in
  the same biological processes are often regulated coordinately. This
  finding has led us to hypothesize that patterns of gene expression, if
  known in sufficient detail as in the present study, might be used to
  predict a role for the gene in a developmental process.

Hong Yi, Lu Xue, and Ming-Xiong Guo, et al. FASEB J. 2010 September; 24(9): 3341–3350.
doi:  10.1096/fj.10-158782 PMCID: PMC2923361

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Genetic Drift: Models, assumptions and empirical observations
There two main mathematical models to describe the process of genetic drift are Moran model and Wright-Fisher model.
My questions concern the assumptions of these models, the existence of other models of genetic drift, explanation of the advantage/disadvantage of these models and the empirical results supporting one or another model.

What are the assumptions of each of these models?

stable population size?
iteroparous/semelparous
what about the probability density function of the fitness?
…?

What advantage/disadvantage do these models have? Or I should say, to which population do these various model applies?
What kind of biological population has been empirically shown to fit better one model rather than another one? What are the key experiments to test the validity of these models?

Please do not hesitate to post even if you answer only partially to the questions! Thank you!

This question has been around for a while, so I'll try to start with a partial answer.
The basic assumptions of the standard Wright-Fisher-Model are:

Constant population size $N$.
Discrete, non-overlapping generations.
Neutrality (e.g. all individuals are equally likely to reproduce)

I prefer looking at the model for haploid/chromosomes. If you bundle up chromosomes to polyploids, then you get the additional assumption of random mating, e.g. all pairs of individuals are equally likely to reproduce.
I might have missed something, but these assumptions should be sufficient to generate the Wright-Fisher-Dynamics: When we build a new generation, we have to fill $N$ spots again (follows from the first two assumptions). As each old individual is equally likely to reproduce (third assumption), e.g. to become parent of a new individual, we get the multinomial offspring distribution.
The main difference in the Moran model is that it assumes overlapping generations. Main assumptions here are:

Again constant population size.
Individuals reproduce at a constant rate.
Neutrality (however the Moran model can relatively easily be adapted to incorporate positive selection).

Every time an individual reproduces, another one instantly dies to maintain the constant population size.
Interestingly, the models have the same diffusion limit, e.g. they behave similarly for large populations (and identically for an 'infinitely large population'). If you trace the ancestry of a sample back in a large population, you will get close to Kingman's Coalescent under both models.
I think the two models exist more because of their distinct mathematical properties, than because one fits better to certain natural populations than the other. I'm not aware of any experiments that have shown how well they fit, maybe someone else can jump in here.

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Identification of this fly?
So I find these flies every year in my mulch, and I've never seen them anywhere else. The mulch becomes full of their larvae, which I feed to my toad and lizards. There are so many that you can hear them moving. The adults are black, look like a wasp or hornet, and have a curious green patch on the underside of their abdomen, which is a clear patch showing some kind of liquid. The larvae are brown and have a little hair on them.

It's about one inch I think maybe a little less. I hope the quality is good enough, because I used my iPod for the picture and you can't do macro with it. Also, I live in Hillsboro Oregon. I am near a small forest and in the suburbs.

A picture (but I think you need more reputation first so I've upvoted) and location would both be very useful for this. also some idea of size.

Hi Keivn, to show us the pictures you have first upload them to a website such as imgur.com and [edit] your post to include the links the site gives you.  Once you have 10 reputation you will be able to this in one step on this site.

You now have more than 10 reputation and can include images in your post.

This should be a comment, but rep is too low. Question: what do you put in your mulch pile? That would help ID the fly.

These links might help: Wasps and BugGuide.

Black soldier fly Hermetia illucens. http://en.wikipedia.org/wiki/Hermetia_illucens
There is a good key to the Dipteran families here. Although it is for British families, it is very thorough.


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What are the characteristic structures of bacillus M. tuberculosis and what they cause?
I answered to this question:

In most forms of the disease, the bacillus M. tuberculosis spreads slowly and widely
  in the lungs, causing the formation of hard nodules (tubercles) in the
  respiratory tissues and form cavities in the lungs.

and got zero points.
What is the correct answer to the question?

Did you read the wikipedia article on this ?

It is not sufficient and very bad. Must be exact in the answer and answer exactly to the question. My answer was apparently too general.


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How do plant cell divide without centrioles?
Most plants do not have centrioles, so what organelle enables them to multiply?

There are many different ways to make a spindle in plant cells:

Mitotic spindles may be organized at centriolar centrosomes (only in final divisions of spermatogenesis), polar organizers (POs), plastid MTOCs, or nuclear envelope MTOCs (NE-MTOCs).

Of these, only the latter has been observed in angiosperms (flowering plants). For more info (and the source of the quote), see Brown & Lemmon, "The Pleiomorphic Plant MTOC: An Evolutionary Perspective"

Plant cells without centrioles build special vesicles from their Golgi apparatus which are important for cell division.
This website has a nice comparison of different modes of cell division. Look for "Cytokinesis by Phragmoplasts" to get to the relevant part. Phragmoplasts are not exactly a replacement for centrioles, but the whole process is a little different.

Spindle formation in plants is very different from most other eukaryotes owing to the fact that plant cells lack centrosomes or spindle pole bodies, which act as the microtubule organizing centers in animal cells. The evolutionary advantage that animal cells gain due to the presence of centrosomes is the ability to direct drastic changes in their shapes during mitosis. On the other hand, plant cells have a rigid cell wall that does not undergo any major changes in shape during mitosis; and the cell wall itself can organize many of the microtubules that form the spindle during mitosis.

Please add some references to your answer.

Animal cells under go cell division in two phases karyo-kinesis and cyto-kinesis.
During cell division (anaphase) the chromosomes are pulled away by structures called microtubule's which are formed by centrioles , just before this the centrioles line up on two opposite sides of the cell . in plant cells microtubules are made by the Golgi bodies. Animal cells are much evolved than plant cells that's why they have centrioles . Spindle formation is very much different in plant cells than in animal cells due to the absence of centrioles .

Welcome to Biology.SE! Please add some references to your answer.

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Why are centrioles aligned at 90 degree with each other?
The centrioles are aligned at 90 degree with each other. What is the function of this?

Do you have any preliminary ideas? Also, if your question is a homework question it should be tagged accordingly.

I have some preliminary idea about cell division but I don't understand the use of centrioles being aligned as such.

As far as I know, the function is not truly known, although there are some seriously interesting guesses.  Part of the problem seems, from scanning the literature, to be that it's not easy or obvious to disrupt centriole orientation.  This paper in PLoS Biology presents some really interesting results, in particular two piece of evidence:

Centriole orientation, to some degree, is dictated by the "mother" centriole during centriole division and is thus passed on from cell to (daughter) cell.
Defects in centriole orientation can result in organelle localization defects in the cell (e.g. nuclear orientation), and at least some of these defects are genetic.

So it seems that orientation is, in some part, a product simply of centriole division, but that there are some gene products that do help determine orientation and localization.  This paper puts forth the hypothesis that centriole orientation determines the axis of cell division which can affect embryo orientation, whereas this suggests that external environmental factors could translate into altered centriole, and therefore cellular, orientation.


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Why are fibroblast used so commonly in cell biology?
Fibroblasts are some of the most commonly used cells in cell biology. What are the properties of those cells which makes them commonly used ?

I'd guess its because the cells are pretty easy to get and they can be preserved and used over time.

agree with @shigeta. Also, they can be differentiated.

@WYSIWYG Why can they be easily differentiated?

This is more a matter of the cells being cooperative and someone getting lucky and finding a protocol to do so.  There could be and probably are cells that differentiate more easily and are easier to maintain, but we haven't really found them yet.  Now we're getting into a real answer - @WYSIWYG do you want to start putting this in an answer?

From the comments by Shigeta and WYSIWYG :-
1.They are easy to get and they can be preserved and used over time.
2.They can be differentiated easily.
3.Due to historic reasons - someone getting lucky and finding a protocol for these cells.


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Function of ER in reviewing mutated proteins
At least in the case of Cystic Fibrosis it happens that a mutant protein (which could actually function!) is held in the ER because the ER detects it as misfolded. Does this happen in every type of mutant protein?
If so, should I conclude that such genetic disorders are caused because of the total absence of a protein rather than because of a misfolded protein? If not, why would the ER or anything else in the cell allow some mutated proteins to do any job (Like in the case of Sickle cell anaemia, where an amino acid substitution happens)?
How do scientists conclude that a misfolded protein could have done a good enough job (Like in the case of cystic fibrosis)?

Membrane proteins have to go to the ER from where they are transported to the Golgi apparatus. Usually these proteins are translocated into the ER while translation is still going on. There are chaperones (such as calbindin) in ER which help in translocation and also catalyze initial steps of folding. ER is also involved in unfolded protein response. Unless the protein is properly folded it is not transported to Golgi. However, this process is regulated at many steps and I wont add a detailed explanation of the mechanism, in this answer.
To conclude ER is involved in this case because the protein considered is a membrane protein.

If we assume that the process which checks whether the protein is properly folded has nothing wrong, then is it safe to assume that all genetic disorders in proteins which are checked by the system happen because of the absence of those proteins (which will be held in ER) rather than because of a misfolded protein allowed to function ?

misfolded proteins can themselves be toxic to the cells and that is why their rapid folding or clearance is important. Sometimes the protein synthesis can overwhelm the folding ability of the cell which may cause the accumulation of the former. Plus, a mutated protein may simply be difficult to fold.
And, ER is not the only site for protein folding. Cytosolic proteins fold with the assistance of cytosolic chaperones (Hsps)


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Why are things conscious?
I've been referred to here from https://philosophy.stackexchange.com/questions/8052/why-are-things-conscious. Could you guys help out? Here's the question:
What is the reason for animals or more general entities being conscious? How did this evolve? What is the advantage?
I'm aware of ideas that consciousness is merely a illusion, however I find them less than convincing. The counter-argument would follow the line "if consciousness is an illusion, who has the illusion and more importantly why?". Additionally I believe that consciousness is a bare empirical fact. Even more, it is the basis for empirical thought. That "consciousness is an illusion" is not a good idea has been discussed by e.g. Searle (a video can be found here http://www.youtube.com/watch?v=yCii726A4Jc)
So what are good explanatory models for consciousness?

What is the operational definition of consciousness you are using? I believe it is a very vague and often ill-defined term that generally leads to unproductive discussions.

Look up Gazzaniga's left brain interpretor idea on google.

There are two very different questions here i) Why are things conscious and ii) What are some good models for consciousness. Could you narrow this down?

Actually, my first urge was to say, things are not conscious, otherwise I would not call them a "thing" anymore. But I guess that's more a question for the SE site this actually came from.

Because man was made in the image of God.

@Memming My working definition for consciousness is that for this question it is related to the experience of qualia, the mental images we form and experience day by day.

@terdon I suppose I'm mostly looking for an answer to the question: What is a good explanatory model for animals being conscious?

The thing is that consciousness is very poorly defined. Are ants conscious? Are amoebas? How about deer?

@terdon we should ask people who know about deer, ants and amoebas. However, I would guess that consciousness is a gradual thing rather than an on/off switch. So the consciousness of ants might be fairly faint compared to the consciousness of deer or you and me. I don't necessarily think that this poses a problem in finding a solution to the question.

Well, that's the thing, "consciousness" is a very vague and human-centric term. How can we know if other animals posses it? How do you define it? Where do you draw the line?

How can you know that I have it? I think that this is something you would assume based on a combination of behavior and similarity. I give somewhat coherent replies to your comments, I am anatomically somewhat similar to you (I have a brain) and so on. The same argument would go for deer and other animals. Having said that, I think that nobody would argue that the actual phenomenon is not real though (forget behaviorism). So it's more about finding a way to tackle the problem.

May I ask the person who downvoted me what the reason was?

Disclaimer: there is a very large amount of literature on the subject and I am in no way expert enough to properly review it here.
In any case, here's a few papers that review the issue and may serve as a basis to look up other references
Evolution of consciousness: phylogeny, ontogeny, and emergence from general anesthesia - Mashour and Alkire, PNAS 2013

We propose that the stepwise emergence from general anesthesia can serve as a reproducible model to study the evolution of consciousness across various species and use current data from anesthesiology to shed light on the phylogeny of consciousness. Ultimately, we conclude that the neurobiological structure of the vertebrate central nervous system is evolutionarily ancient and highly conserved across species and that the basic neurophysiologic mechanisms supporting consciousness in humans are found at the earliest points of vertebrate brain evolution.
  [...]
  The distinction between phenomenal and access consciousness was noted, but phenomenal consciousness itself reflects the dissociable neurobiologica processes of awareness and arousal. Awareness refers to the content of consciousness (red apple vs. blue sky), whereas arousal refers to brain activation and level-of-consciousness (alert vs. drowsy vs. asleep vs. anesthetized). A number of current theories about consciousness propose that the cortex is the primary site containing the neural correlates of awareness, whereas midline subcortical brain structures provide ascending arousal influences to the cortex

This is also reviewed in this paper:
Subjective experience is probably not limited to humans: the evidence from neurobiology and behavior. - Baars, Conscious Cogn., 2005

Thus consciousness is not a metaphysical absolute, but a scientific construct like any other. In humans, the standard behavioral index of conscious cognition is accurate or verifiable report. It has been used scientifically since the beginning of psychophysics in the 1820s. Accurate report is highly reliable, but of course it is subject to limitations like any other empirical measure (Baars, 1988).
  [...]
  In humans the thalamus and cortex are crucial for supporting the contents of consciousness (Edelman & Tononi, 2000). Thalamus is often considered to be an extension of cortex, an added sandwich of interacting layers that controls most traffic to and from cortex. Local damage to cortical sensory regions, like the fusiform gyrus for face perception, results in a loss of conscious knowledge about faces but not about other visual features like color, location, or size. If the intralaminar nuclei of the thalamus are lesioned bilaterally, the conscious state is lost. By comparison, large lesions to cerebellum, basal ganglia, and spinal cord do not impair either conscious contents or state. Cerebellar damage can cause paralysis but not loss of consciousness. Lesion evidence on these points is supported by stimulation experiments using electrodes, transcranial magnetic stimulation (TMS), and microdialysis. It is also reflected in functional brain imaging. The evidence is therefore very strong that the T-C system supports consciousness. That is why many neuroscientists consider the T-C system to be the “seat” of conscious experience, and have done so for at least a century.

Again, citing from the first paper:

The recent experiments with general anesthesia in humans suggest that phylogenetically ancient structures in the brainstem and diencephalon—with only limited neocortical involvement—are sufficient to support primitive consciousness. Where, then, does consciousness arise on the evolutionary timeline? One might be tempted to conclude that consciousness commenced as our mammalian ancestors evolved just beyond reptiles and their predominantly subcortical brains. However, paleontological findings suggest that the synapsid line that gave rise to mammals and the sauropsid line that gave rise to reptiles and birds both diverged from the primitive anapsid line at a single point ~315 million years ago. Furthermore, there is significant evidence that avian species are capable of higher cognition and even consciousness itself. For example, birds demonstrate evidence of explicit episodic recall (i.e., conscious memory of an event) and theory of mind (i.e., attribution of subjective mental events to another being). Thus, it would be misguided to try to identify a single point at which consciousness emerged because evidence suggests that consciousness evolved along two independent lineages.

While it's still a very philosophical question, and neuroscience is not my speciality, I think that selfconscious comes from the integration of several informational sources.
Our brain has maps, that's a fact. We have maps to locate sensorial signals (in fact, all our senses are neural maps representations), to locate our muscles and we even have secondary maps that allow to compare the movements we desire to make and the movements we are actually making. The integration of all of this maps leads to a pretty accurate idea of ourself, and that's critical for selfconciousness.
Furthermore, our brains uses our senses to create images of our immediate sorroundings. They also need to locate other important places (for instance, even if you're at home you would proably have a mental idea of how far your workplace is). Moreover, we have a psicological idea of time wich places ourselfes in a present after a bunch of events that have already happened andd before a set of possible events that we have modelized or predicted with the information from the past. All of this creates an idea of our place in the world.
By combining this two ideas we have a global mental model of our own state, our own desires, our own characteristics, etc... placed in an mental image of the world based in our previous experience. Of course memories and thoughts would have its place, too, but they are more complicated to explain briefly.
Transversely, I don't think that computers would develop selfconciousness by its own even if someday they have more computational power than the brain. First, a computer doesn't need an idea of itself as a phisical being, unless it is programmed to do so (a robot would probably have it, thought). Second, the inner logical architecture of computers and brains is quite different, being maybe the lack of biologycal instincts the most relevant difference. Of course all of this should be programmable. My point is that is quite unlikely that it appears by itself and that a selfconcious computer is a pretty unpractical device.

+1 @Miguel (although I'm not signed up here) for actually posting an answer and a good one too. Besides this, I'm still wondering how neural maps are able to lead to the experiences we have. I simply can't see the mechanism there. That is besides stating that this is what neural maps do. To me this is "spooky action at a distance", i.e. not a real explanation. And I won't believe that a PC will have actual consciousness rather than simulated one until I see very solid proof for it. But an honest thanks still for the answer. There are really good points in there.

Neuroscience is my specialty.  What we call consciousness is thought to be an evolutionary elaboration of a property of cells called "irritability", which is the cell's ability to respond to signals from its environment.  There are many manifestations of this: chemicals binding to protein receptors, light interacting with proteins (as in photosynthesis), mechanical forces causing cell movement, bacterial chemo-taxis, and the list goes on.
The analogy is like this.  What we call eating and elimination are analogous to cell metabolism.  As a whole organism we must eat to replenish the body, and eliminate the waste produced. A single cell must also absorb nutrients to maintain itself and eliminate the waste products.
So, it is like a fractal.  The same functions displayed by individual cells also manifest at the level of the whole organism. So, as the GI tract is the organ analogous to cell metabolism, the nervous system is the organ analogous to cell irritability.  One could imagine that what we experience as our personal consciousness is in fact like taking an integral over the irritability of all the cells in our nervous system.  Many people focus on the neurons, but all the cells in the brain contribute to the brain's function.
Now, this form of explanation is not really an explanation as much as it is a description of our biology.  The obvious question arises: why are cells irritable? Because, irritability is basically the individual consciousness of an individual cell.  Well, one then realizes that the response properties of cells to stimuli come from the action of the molecules and forces that make up the cell. The immediate forces are non-covalent interactions, mainly poorly understood even in terms of physics, such as forms of adhesion (consider Velcro or glue). These are emergent properties that stem from the assemblage of molecules of which cells are composed.
But let us grant that physicists eventually come to understand such "derived" forces in terms of the elementary four forces of the universe: electromagnetism, gravity, strong and weak nuclear.  Then, it is clear that there is a potential contained in these forces to combine in ways that cause complex molecular assemblies that self-organize and display irritability.
Thus, the issue of consciousness presumably links back to somehow being an inherent emergent property of the forces of nature.
Again, this is all relatively uncontroversial, but building such a chain of explanation is not really an explanation as much as just being a description of how things are organized in the world.  And I think it is clear to any thinking person that a description of something is not the same as an explanation of something.
So, if you follow this far, then you can appreciate why the Greeks thought that Atlas, who held up the world, stood on the back of a tortoise, and this tortoise was on top of another tortoise who was on top of another tortoise, all the way to infinity.
We have simply replaced Atlas and the tortoises with language of modern science.  It is still an infinite regress.  The short answer to "why are things conscious" is that it seems to be a property of the universe to display consciousness.
Now, there is one great man who thought about this problem and constructed what I consider the best explanation.  This was Gottfried Leibniz, the man who invented calculus.  Leibniz invented the idea of a "monad", and he considered monads as the basic units, the atoms, in the sense of being the indivisible units of reality.  The monad, as an atom, is pure consciousness.  So, Leibniz came to the conclusion that the reason there is consciousness is because consciousness is the fundamental building block of reality.
Monads are what everything is made of: us, cells, atoms, quarks, electrons, etc.  These are all different forms of monads.  According to Leibniz, they are all different forms of consciousness, and they combine in fractal patterns to make forms of consciousness within forms of consciousness within forms of consciousness.  And this pattern goes in both directions from the infinitely small to the infinitely large.  According to this idea, just because something does not seem to be conscious in the same form we are conscious does not mean it is not conscious.
This is how Leibniz solved what is called the "mind body problem", which is really the heading under which your question falls.
If one wishes merely for intellectual understanding of the nature of our consciousness, it is my opinion that Leibniz' ideas are the best available.
If you wish to go beyond mere intellectual understand to a deeper level of awareness of these issues, then I suggest you look up and study the works of a writer named Patanjali.

Could you please link to some literature at this regard? I never heard about "cell irritability" in the context of the nervous system, or when speaking of multicellular species for that matters. I think that for the scope of this site a proper neuroscience answer would have to be preferred to a phylosophical answer (Leibniz is all nice and good, but he was not what I would call a neuroscientist).


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Could be an union/synergy between Math, Computer Science and Marine Biology?
I'm studing for my bachelor's degree in Natural Science and I have to chose the path for my future life. I have to chose the right kind of graduate studies. Since I love computer science, maths and marine biology more in details I love the tropical ecology especially that of the coral reefs and atols in the pacific ocean, the whales (e.g. the humpback whales and their migrations), the computer simulations and mathematical models. Thus, I want to ask you if is there a branch of marine biology that allow me to study and specialize myself in tropical ecology and in math & computer science too, because in my current course we don't have any exams of computer science and only one of maths, and I'm feeling sad for this. The right path coul be the computational biology? Exist in biology, some field called "Computational Marine Biology" or "Computational Marine Tropical Ecology"? One last thing, what about Ecoinformatics?

You won't find a field as such, but knowing how to do computational biology can be applied to any field. You just need to find a group that works on a subject you like and then offer to do their modelling. That's the great thing about groups, they consist of different people, each of whom has different knowledge and abilities.

This is a very open-ended question, and you could come a long way by just searching Web of Science for the keywords that you have mentioned. I dont know about "Computational Marine Biology" as a defined field, but in population or community models of marine life mathematical models are certainly used and computational skills are clearly useful. To guide on particular topics is almost impossible, and not the subject of this site. GO with what you find interesting and try to find suitable research groups.

I have the intuitive feeling that it may be easier to specialize in computer sciences and then apply this to marine biology than specialize in marine biology and then learn the computational tools. It may be easier to learn the tricky technical aspects with a younger brain, and later acquire the necessary knowledge to apply your technical skills to marine biology. Of course, it would be better if you could study both at the same time, but it may be difficult to arrange this.

This advice is America-centric; graduate programs in other countries may be different, especially in regards to assigned course work, etc. But this should more-or-less be solid. Also, I'm assuming you're interested in a PhD.
I don't know if what you're looking for is a proper field, but that doesn't matter.  Ideally, grad school is where you do research on your own terms, and what lab you join is the single most important consideration. What you want is a competent program that:

gives you the flexibility to create your own subfield
has supportive and knowledgeable faculty that you can work under
has excellent computer science AND marine biology programs (or analogs)

First, find faculty who are doing research you are interested in, and look at the programs available at their schools. Since they're the most important consideration, everything else will fall into place after that.
Next, email 5 of those professors with an introduction of what you're interested in, particularly about their research.  Ask them what programs are most appropriate at their university, and how flexible you can be in taking appropriate coursework.
At some point, you'll probably want to decide if you want to be more of a marine biologist or a computer scientist. Your diploma at the end of the decade is only going to say one of those things.  That shouldn't make a huge difference as to your job outlook, but is worth thinking about.  Practically, the question is whether you want to get your hands dirty, go out on a boat, and collect your own data.  Alternatively, if you join a CS program, you are more likely to be analyzing large datasets collected by other scientists.
At most universities, you'll likely only have the option to join a biology program. But there are certainly excellent CS programs with biology oriented faculty.  Even then, the CS faculty is more likely to be doing genomics and such.
For practical recommendations, the University of Washington in Seattle would probably have something appropriate to your interests. While I was there, my lab was adjacent to an Oceanography lab that had a video wall for visualizing ocean currents and such. Not precisely marine biology, but UW has a very collaborative faculty and I'm sure the two departments work together.
UW also has a strong computational biology program that you can go into either through CS or through one of the many biology programs. You should also check out the Institute for Systems Biology at UW. I saw a presentation there specifically about DNA exchange between marine microorganisms.  I'm not saying UW is your best option, I just know that school because I did my PhD there.
A final word of advice. Once you're in a program, it's very likely your interests will change as you learn about other research going on. And also, it's quite possible you won't get into the lab you want simply because of money or logistics. With both of these in mind, be flexible about where you're willing to go. What you do during your PhD isn't really that important anyway.  If you're going to be research scientist, it's what you do during your Postdoc that will establish your career. Just take the opportunity to learn everything you can and see what's out there.
Hope this helps.  Good luck!

Alexander's advice is excellent in the general case, but since I faced a very similar problem when I applied to grad schools last year, I wanted to offer my perspective on this specific union of fields. Many people (including me) believe that this intersection is about to be a really important field - ecologists are starting to recognize the need for scientists with these skills, but there is not yet a lot of infrastructure in place to train such scientists. This presents a challenge to people like you and me right now. On the other hand, it means that if we can find a way to acquire these skills, we should be pretty well set up to help establish this field (bonus: we should be pretty well set up to get jobs).
I am personally of the opinion that if your interests are truly interdisciplinary, it's a really good idea to go somewhere that has a framework in place to support interdisciplinary work. Otherwise, you can end up in a situation where your adviser doesn't feel equipped to offer guidance on large portions of your projects, which can strain your working relationship and stymie your progress. Despite the lip service paid to the importance of interdisciplinary research, however, programs that are set up to provide interdisciplinary mentoring can be hard to find. The best course of action depends very specifically on how you want to combine these fields.
If you want to stay rooted in biology and use computer science and math as tools without doing research that furthers them as fields, you're in luck. There are a lot of labs with PIs who do this kind of research and many more who are interested in finding people who can, as terdon said, "do their modeling." I would be careful of the latter scenario while you're still in the learning phase of your career, however. As a student, your goal should be to learn how to best do the research that you want to. If you are the lone modeler/math person in a group, you may be in high demand but your rate of learning will probably be a lot slower than if you had an adviser who was actually doing what you are interested in. If these are your interests, your options are pretty varied but take a look at UC Berkley, and UC Davis. Also UW, as Alexander suggested. There are indeed good collaborations between biology and computer science there. I found it helpful to search for people who were studying macroecology, but that might be a label that is used more for terrestrial systems.
However, if you want to do research that actually furthers computer science in addition to biology, things get more complicated (I don't know if there are people who do both math research and biology research so I can't speak to that). Don't constrain your thinking by believing that you have to get a degree in one or the other; dual degree programs exist (and that may sound intimidating, but they aren't necessarily more work, just different work), although they are so few and far between that you might decide that it makes the most sense to just choose one field. If this is what you want to do, take a look at UC Santa Barbara - they do a ton of marine bio research and are home to the National Center for Ecological Analysis and Synthesis. Also, again, UW. I'd recommend my program too, but it's neither marine nor tropical.
In general, if you want to get a feel for how open a lab is to you doing interdisciplinary research, I found that it was best to just ask explicitly. If a place offered joint appointments (i.e. the ability for me to be co-advised by professors in two departments), dual degrees, or even just had research groups that involved people from multiple departments, I took that as a great sign.
In summary, don't start out with low expectations for finding a match for your interests. That said, it will ultimately be valuable to be flexible, as both finding a perfect match and getting accepted to it definitely requires a lot of luck. The considerations that I've brought up here won't make or break your grad school experience or your eventual career. They're just things to keep in mind if you have the option. I also apologize that it's probably a bit late in the application season for this to be useful to you, but I had such a horrible time grappling with these same issues that I just wanted to put what I learned out there in case it can help anyone.
EDIT: I forgot to address ecoinformatics! Ecoinformatics can fall into either the "computer science as a tool" category or the "furthering both computer science and biology" category, although it falls into the latter category much more frequently than modeling does. It still all comes down to what exactly you want to do. Look at research in computer science journals. If doing that sort of thing appeals to you as much as biology research, then you should be thinking about trying to pursue both fields. I found doing some pure computer science research helpful for figuring this out, but you probably don't have time for that.

"Despite the lip service paid to the importance of interdisciplinary research, however, programs that are set up to provide interdisciplinary mentoring can be hard to find." - This is sad, but very true. Even in programs that are set up for this, individual professors may not be comfortable sharing students. It is definitely best to talk directly to faculty that interest you (this applies to any field) and see what kind of mentoring style they're willing to offer.


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What are some possible causes that might explain why the global temperature has remained relatively constant in the last decade?
First - I do not know if this is the best site to pose this question.  However, stack exchange does not appear to have an ecology sub-site. That said, this appears to be the most appropriate place post this question.
Consider this chart:

The chart was retrieved from here here.
I am curious as to whether anyone has any thoughts regarding this trend - note, however, that this is one chart among several that I came across on reputable site. All seem to depict this observed "capping" effect between roughly 2000 and 2010+. Unfortunately, I don't have much to offer right now since I am still looking into it.
Any input is appreciated.

This question appears to be off-topic because it is about meteorology.

Like I mentioned, it does not appear that stackexchange has any sites that may be more appropriate.

There is a Geoscience proposal in Area51 that you might want to follow. Also, your question could maybe find a home at http://skeptics.stackexchange.com/, where there are a couple of climate change topics.

Not my field but I have a couple of thoughts:

According to your link, the blue line represents the change in the trend and the red bars are the temperatures. These have not remained that stable, it is the bar that gives that illusion:

A much more important point are the grey bars extending above and below each year's value. This is the range of uncertainty, the actual values could be anywhere within the range of those bars. Notice how the uncertainty decreases the closer you get to the current date.

I think a lot of the stability you observe is probably due to the line hiding the detail and the far lower precision of the older measurements.

I was thinking the same - and I agree. However, a quick google search reveals many articles published in the last few months about this trend.

@Mlagma in that case I refer you to my first sentence, not my field :). That was my 2 cents. You might have better luck over at Physics.SE.

I do not mean to criticize - I simply wanted to bring out what I recently found.

@Mlagma This question is on hold so I won't put this in a true answer, but basically it's because El Nino peaked right before 2000, the Sun was at a lower point in its cycle and, because China is using lots of coal.  http://www.newscientist.com/blogs/shortsharpscience/2011/07/why-global-temperatures-held-s.html


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I think evolution has goal
Richard Dawkins says evolution doesn't have any goal. But I think evolution has one. At the end evolution creates intelligent being. If we find another earth like planet evolution sould have the same pattern. Evolution is not a chaotic event. Am I wrong?

This is not much of a questions, but only an empty proposition which is not supported by any logical arguments or empirical proofs.

What do you mean at the end? What makes you think we are at the "end" of evolution? If anything can be said to be the "most evolved", that would be viruses, not humans.

Yes you are wrong I am afraid. Evolution is the process of change through time of species by inherited changes. Heritable differences mainly come about from random mutation in the genome. These genetic differences between individuals lead to fitness differences between individuals, ie one individual is better able to produce offspring, thus spreading more of its genes in to the following generation, than another individual. For example, environmental change causes selection for a dark body morph in moths, stabding genetic variation and new mutations affecting body colour is then more favored by selection, and those with the dark body genes survive and reproduce better.
There is no end or goal to evolution. It is often mistakenly said that humans have stopped evolving. This is wrong and to suggest we have is to suggest that evolution is directed and has an ultimate goal. As long as genetic fitness variation exists there will always be some level of evolution because there is a difference between individuals in selection coefficient. Selection is also very unstable, it can change drastically an rapidly, evolution could only then stop if selection was constant and favored one "ultimate genotype" over all others in which case all genetic variation would cease to exist.
If we found another planet which had the exact same conditions and time as earth we may find the same species, but it is not likely. It requires the same mutations and selection processes occurring. Analogous to this is the observation of "many solutions to one problem" where different species use different adaptations to deal with a common problem. For example, geting oxygen is difficult for water deelling species. Sea mammals like whales gather oxygen by going to the surface and breathing and then holding their breath. Fish have evolved gills, a different solution to the same problem, to harvest oxygen from the water. These solutions evolve from random changes with selection acting only on the results (those that could filter oxygen from the water or hold their breath the best survived and reproduce best).

I'm writing this on my iPhone in an airport - if people have some references for examples and reading please feel free to add them.

What do you think what is the next evolutionary step for mankind?
I didn't said we would find same species in another planet. I said we may find same pattern. I think evolution has a pattern and there for it can be said as a goal. You put the initial value you will find the final value. I think it is not a chaotic process.

Just remember that every species is undergoing evolution and few, if any, have evolved intelligence...

@KarziArafatAhmed Just as evolution can lead to different solutions to one problem, as above, it can also lead to similar ones between species. This is called convergent evolution, given the same selection as on our planet, another planet could host similar species as ours. It is not moving towards a goal. How would it know where to go? What is controlling it?

@KaziarafatAhmed On the inherently tricky and mostly unanswerable topic of future human evolution you can look at these earlier posts: Scientifically based theories of future human evolution?, Is evolution possible in contemporary humans?, ...

[cnd]: ...also Medical progress and human evolution? @KaziarafatAhmed


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What is 'calcium conductance'?
What is the meaning of calcium conductance in ion channels. I encountered this in the following text:

It was established that the µ and δ opioid receptors open potassium
  channels, which results in reduction of calcium conductance (Simon, 2005).

Also why should opening a potassium channel reduce calcium conductance. How are they related ?
Reference:
Simon, E. J. (2005). Opiates: Neurobiology. In J. H. Lowinson, P. Ruiz, R. B. Millman & J. G. Langrod (Eds.), Substance abuse : a comprehensive textbook (4th ed., pp. xxiv, 1421 p.). Philadelphia: Lippincott Williams & Wilkins.

This might be a mistake in the text you read or the referenced book. Opioid receptors can regulate calcium channels as well as potassium channels.

@MadScientist you're right that opioid receptors regulate both calcium and potassium channels but the snippet is about mu and delta receptor types. The text also says:
The activation of κ receptors was found to reduce calcium conductance by closing calcium channels. It was recently found that all three types of opioid receptors can act by both mechanisms; i.e., they can open potassium channels or close calcium channels

Conductance is the inverse of resistance, and measures how much of a given substance flows throught a channel. In this context, it means how many calcium ions enter the cell in a period of time.
There are at least two ways potassium channels may prevent the calcium to enter in the cell.
1) Potassium intake by ion channels decrease the membrane potential, restoring it to its rest state. Since many calcium channels are voltage-dependent, a reduction of the membrane potential would close them, effectively decreasing the calcium conductance.
2) Potassium channels may be coupled to different signaling pathways (i.e. G proteins), wich may affect indirectly other calcium channels.
In the case of opioid receptors it seems to be the first mechanism. With potassium channels open, the neuron is less likely to be activated, because it needs higher stimulation to reach the action potential. Calcium channels open in neurons mainly during action potential events (althought they may exist other calcium channels that open in other conditions, i. e in response to hormones or neuromodulators).


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Domains in cell membrane
How is movement of proteins and lipids between different domains of cell membrane prevented?
Why is the noncytosolic layer not able to do lateral movements between domains but cytosolic layer is able to do so?

First of all, often it is not. Many receptors for example move around the membrane. You might want to have a look at wikipedia's entry on lipid rafts though.

There are various mechanisms through which membrane proteins can remain localized in the membrane. See the below figure from MBOTC (book):

(A) They can aggregate together so that their relative positions are constant.
(B) They can be anchored to the Extracellular Matrix
(C) They can be anchored to the cytoskeleton
(D) They can be anchored via cell-cell interactions (adherens junctions, hemidesmosomes etc)
(E) Not mentioned in the figure; mentioned in the comments. Lipid rafts are membrane regions which are composed of rigid lipids like cholesterol and sphingolipids. Lipid rafts are thicker than regular membrane and do not diffuse into the latter. Some proteins are specifically anchored to/incorporated into the lipid rafts (T-Cell receptor, IgE receptor) and their relative position with adjacent proteins (co-receptors) remains constant.

Why is the noncytosolic layer not able to do lateral movements between
  domains but cytosolic layer is able to do so?

Where did you read this. Both layers can do lateral movements; if proteins are specifically "anchored" to one side of the membrane then the concept of domain applies to that side only.


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How is the mRNA transported out of the endoplasmic reticulum?
In eukaryotes the nuclear envelope is continuous with the ER, so what helps it out of that?

Have you read the pages on Messenger RNA and Nuclear pores?

Yes but I still did not get any information about what exactly guides it through ER.

What exactly are you looking for? The name of the protein channel(s) through which it will pass? The sequence signals that target it for export? It is hard to know at what level to answer your questions, your profile states you are 15 years old so I assume that giving you references to published reviews describing the process in detail is not what you're after since (very reasonably) you won't have the necessary background to absorb that level of detail. However simplifying it while giving more information that what wikipedia does is kinda hard. This is not a simple question.

I'm with @terdon - a few more specifics would be nice.

@terdon  I am actually after what mechanisms guides it through the "maze" of ER.Does it move through lumen? Does it pass straight out,piercing the membrane ?I don't want to know what guides it out of nuclear pores .

Don't hesitate in including any published reviews. If not now,it will be useful in future ! It will also be useful for anyone else having the same question. :)

I'd make a comment if I could, but I don't think mRNA ever enters the ER. When a ribosome is building a protein destined for export or for being inserted into the membrane, it travels to the ER membrane and binds to a protein in that membrane called Sec61, which guides the new peptide sequence through the membrane. However the portion of the ribosome that reads the mRNA is always in the cytoplasm. So the mRNA never enters the ER, it just gets close the cytoplasmic side of the ER membrane.
Have an image from a German website.

I understand that mRNA never enters in the ER for protein synthesis. My question actually is whether it has to pass through the ER when it is exiting the nucleus. Isn't ER membrane continuous with the nuclear envelope ?

The ER is continuous with the nuclear envelope, but the nuclear envelope isn't a solid wall. It is perforated with nuclear pore complexes that form tunnels through the envelope and allow proteins, RNAs, and charged small molecules to pass. Take a look at http://en.wikipedia.org/wiki/Nuclear_pores

The proteins mediating the transport of mRNA out of the nucleus (nucleoplasm/karyoplasm) are called "karyopherins" and belong to the nuclear pore complex family.
Prior the creation of the final form of mRNA, various proteins are attached to the so called pre-mRNA and a mRNA-protein-complex is built (co-transcriptional). Some of these proteins carry factors for splicing and processing, later RNA-binding proteins are added. (RNA binding proteins such as $Npl3p$, $Gbp2p$ and $Hrb1p$ (serine/arginine-rich proteins) accompany mRNA out of the nucleus. )
After mRNA processing mRNA export is initiated by dephosphorylation of $Npl3p$, leading to binding of $Mex67$ (Saccharomyces c.), forming a complex that interacts with the nuclear pore complex.
That is the way mRNA is able to leave the nucleus.

Translation can occur either in the cytoplasm or in the ER. At one point it was believed that all mRNA begin being translated in the cytoplasm. However, if the protein the mRNA codes for happened to be a secretory protein or a membrane protein, it would have a certain sequence near the start of it (N-terminal sequence). This sequence binds to something called the Signal Recognition Particle (SRP). And once the SRP binds to the mRNA/ribosome/partially-synthesized peptide, it would help it locate to the ER.
So to summarize: Many proteins that need to be synthesized at the ER have a certain sequence that binds to SRP. The mRNA begins being translated in the cytoplasm, but once SRP binds it is moved to the ER.
Of course people now are starting to think this is wrong or at least not the whole story. You can read about the SRP and why some people think its wrong in the intro of this paper


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Why to choose a grammar from a lot of grammars that can describe structure of proteins?
Why do we choose a grammar from a lot of grammars that can describe structure of proteins? Usually, there are a lot of (maybe infinite) grammars that can describe one language. Why do we choose a specific one? Especially the language of proteins of gene just has finite sentences or words.

Are you talking about protein nomenclature or what?

@MiguelÁngelNaranjoOrtiz,no,what I am talking about is the description of the protein structure by formal language,it is research that tries  to predict the structure by DNA or RNA

Actually when describing the 3D structure of a protein you only need the angles formed by the peptidic bond of every aminoacid, and the aminoacidic sequence. This is the kind of data yyou obtain when proteins are resolved by X-ray diffraction. Those are raw data thought, and they usually describe protein structure by different nomenclatures, such as domain organization or secondary structure prediction. In this case, you describe regions of the protein with a particular structure, often related with its function.

@MiguelÁngelNaranjoOrtiz You also need the sidechain orientations for a complete structure. The raw data for X-ray is the electron density, though in NMR torsion-angle space is often used for structure calculation.

I did not understand your question completely but this is what I guess you want to know:

Why genetic code evolved to be what it is ?
How the sequence of the protein coded by a mRNA give rise to a particular structure ?

Answer to first question cant be definitive. The textbook explanation for why a 3-letter code exists is because a 2-letter code cannot describe all the 22 amino acids, with all its permutations. But then comes another question: why only 22 amino acids. I can't even speculate the answer to this question; the simple amino acids are fine but for an example why lysine and not a similar amino acid with a shorter side chain - no idea.
So, given 22 amino acids, a 3-letter code and 4 nucleotides, the multiple codons for an amino acid are similar in sequence (usually the first two bases are conserved in accordance with the wobble hypothesis. The last base usually doesnt base pair strongly with the tRNA and is of minimal importance).

The answer to second question is somewhat straightforward. The sequence can give rise to infinitely many structures but in a given environment (consisting of the solvent, other solutes etc), the sequence adopts a particular structure in accordance with the free energy minimization principle. There is a possibility that given an environment a protein can have two different optimal structures and can switch between these two structures.

Good,thank you for your answer,but I don't know why somebody voted down my question.

,thank you,I know you did not.To tell the truth,I am not a biologist,and I am not familiar with bioinformation.

perhaps you can restate your question based on the comments and the answer. even if your query is answered it will be better for someone who looks up an existing answer.


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Amount of Heterozygosity
How many loci in the human genome are heterozygous? How about other species?
EDIT:
I was wondering, considering for example the whole world population, how many of the human genes actually have two or more different alleles, or, vice versa, which genes everybody shares because there are no different versions of them. Since this seems not to be clear, I don't consider a mutation in a single individual an allele, maybe take 1% occurrence amongst all individuals as a start? I'm no biologist though...
By loci I mean whatever you think makes sense. Again, I don't mean single bases, preferably something like the classic idea of a gene. But I'm happy for whatever you can tell me.

Please elaborate on you question. Do you consider heterozygosity as the presence of two contrasting alleles in a diploid individual or the presence of two different alleles for a trait in the species genome?

in diploid organism, theoretically every locus can be heterozygous.

Please don't add words just to make your post long enough to get past the quality filter - if the site isn't accepting your question it's usually an indicator that you're not including enough information.

I was wondering, considering for example the whole world population, how many of the human genes actually have two or more different alleles, or, vice versa, which genes everybody shares because there are no different versions of them. Since this seems not to be clear, I don't consider a mutation in a single individium an allele, maybe take 1% occurence amongst all individuals as a start? I'm no biologist though...

If you want an actual number, well, it depends (of course).  First off, what is your definition of loci?  That term is broad, and can be construed to mean everything from large, megabase-length genes to every individual base.
That being said, it turns out there are some serious runs of homozygosity (ROH, meaning long regions of the genome that are homozygous) in human populations.  This of course will vary widely from population to population, and amongst outbred individuals.  This paper has some AMAZING figures that are worth checking out but are a little more involved.  Here is a table from this paper which is likewise quite excellent; also, check out figure 3.

EDIT
Your new/edited question is actually very difficult to answer.  For an extreme example, look at the Human leukocyte antigen; some have hundreds or thousands of alleles, but if you were homozygous for each it would be bad (disease susceptibility) but you'd be fine otherwise.
Again, it depends on what you consider an allele or locus.  Most studies look at single base changes (SNPs) because they are 1. easy and 2. useful.  It turns out that there are a lot of these single changes.  The Human HapMap project is hard at work on this and recently published a data set with 3.1 million of these SNPs, among 270 individuals from different populations, roughly one every kilobase.  In a similar vein, the 1000 genomes project recently published an enormous catalog of variation from almost 1,110 individuals in 14 populations.  Both projects focused on major variants.
The best answer I can give you from these studies is that, within a given population, any two DNA strands are around 80% identical, of which around 0.5% is by direct relation (table 5.  Those numbers vary hugely between populations, with Yoruba Nigerians being the most diverse, followed by Utah Whites and then Han Chinese and Tokyo Japanese.  This is just an average across the entire genome, as purported functional differences are comparably rare, with over 85% of protein-altering changes being very rare (<0.5% frequency).
In summary, almost every single site we know of has more than one version somewhere.  Most traits are very complex and are affected by many genes, so even similar appearances can come from very different genetics.  Individuals tend to be highly heterozygous, even if populations on a whole have limited heterozygosity.  A single pair of siblings mating can produce massive defects, showing just how necessary our heterozygosity is.  We each have dozens of large, lethal mutations (deletions, mostly) that don't usually matter thanks to heterozygosity.

Thanks for your answer. I'm no biologist though, and I have no idea what these papers are talking about, or what a run of homozygosity is, or how to find an answer to my question from your data. Would you mind reading my edited question, and elaborate a little bit? I'm wondering how many of the human genes are so important that having a different version than everybody else is fatal; roughly speaking, how much of what we are is actually our parents and how much is merely human

@Bananach I tried to match that a little better, it's a complex question.  My summary at the end tries to be a short answer for you.

Thanks again. My interest comes from statements like "The genome of humans and chimpanzees is to 98% the same" and what they actually mean.

@Bananach: Perhaps you should have a look at this question: Do apes and humans share 99% of DNA or 99% of genes? What is the difference?. If that isn't adequate, you might ask another question getting at the issue.

actually this just raises more questions. like, what do you mean by sharing a locus? what do you do if one bases is deleted in humans? (then all the following bases differ in direct comparison with the chimp bases). do you allow the same genes to be on different loci in the different species? how do you compare the different frequencies of alleles on one locus? (maybe humans have 99% allele A and 1% allele B and chimps the other way round. does it still count as the same?) summing it all up, a percentage just doesn't seem to make sense to me at all

and by 'you' I don't mean you, but the general biologist who compares DNA :)

@Bananach You're absolutely right, percentage really doesn't make sense.  It's convenient and popular in the press, but alignments are more complex than a simple fraction.  To your point, I saw a fantastic presentation once trying to show that what separated humans from chimps wasn't mutations but deletions.

Ok, thanks. I think this is what made me dislike biology in school. The more you learn about a thing the less you understand it :)

The number of possible genotypes from only a few loci is great, and can be calculated using the formula
k(k+1)/2
where k is the number of alleles at a particular locus.
The parameter k also represents the expected number of homozygous genotypes, and k[(k-1)/2] represents the expected number of heterozygous genotypes. The observed heterozygosity can be compared to the expected heterozygosity, and the deviations between these values can indicate important population dynamics.


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How long can C. Tetani survive in soil?
Clostridium tetani (C. tetani) is a bacterium commonly found in soil and is excreted in the faeces of many animals (both mammals and birds) and serves, by means of the exotoxin, tetanospasmin, causes the life-threatening condition tetanus.

Soon after asking this question I found a reliable source, the National Institutes of Health. It can survive for over 40 years.

Clostridia form endospores and can survive for years as a dormant spore. You can check this article about viability of clostridial endospores but it doesn't really talk about how long it can survive.

The paper however includes a general passage on endospores saying that: Once they are formed, endospores can stay dormant for extended periods of time, from thousands (8, 13, 20, 25, 33) to millions (3, 35) of years, although for the more extreme claims of longevity it is difficult to rule out modern contamination (37). So apparently the potentially survial is extremely long.

yeah.. i did read that statement but thought that it is too hyperbolic :P


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Strongest muscle of Human Body
Which is the strongest muscle of human body ?
Confusion b/w Masseter muscle (Muscle of Jaw) and Tongue and Muscle of Heart and Muscle of Uterus.

What do you mean by strongest? The one that can apply the highest force or the one that has the greatest endurance?

First internet search result gives you everything you may be interested in, and looks reasonably reliable: http://www.loc.gov/rr/scitech/mysteries/muscles.html

You'll be interested in THIS Wikipedia article. It really depends on how you define "strongest" (Newtons, Wattage, Newtons per Kilogram, etc.). Here are a few relevant excerpts from the article:

In ordinary parlance, muscular "strength" usually refers to the ability to exert a force on an external object—for example, lifting a weight. By this definition, the masseter or jaw muscle is the strongest. The 1992 Guinness Book of Records records the achievement of a bite strength of 4,337 N (975 lbf) for 2 seconds. What distinguishes the masseter is not anything special about the muscle itself, but its advantage in working against a much shorter lever arm than other muscles.
If "strength" refers to the force exerted by the muscle itself, e.g., on the place where it inserts into a bone, then the strongest muscles are those with the largest cross-sectional area. This is because the tension exerted by an individual skeletal muscle fiber does not vary much. Each fiber can exert a force on the order of 0.3 micronewton. By this definition, the strongest muscle of the body is usually said to be the quadriceps femoris or the gluteus maximus.
The heart has a claim to being the muscle that performs the largest quantity of physical work in the course of a lifetime. Estimates of the power output of the human heart range from 1 to 5 watts.[14] This is much less than the maximum power output of other muscles; for example, the quadriceps can produce over 100 watts, but only for a few minutes. The heart does its work continuously over an entire lifetime without pause, and thus does "outwork" other muscles. An output of one watt continuously for eighty years yields a total work output of two and a half gigajoules.


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Where can I find an at least Semi-Comprehensive list of what biochemical reactions Acetyl-CoA participates in?
Acetyl-CoA has a number of biochemical roles in the body and I'm curious as to whether anybody knows where I can find at least a semi-comprehensive list (i.e. comprising all the major roles in the human body it serves) of the biochemical reactions in which acetyl-CoA partakes in the human body.

Have you tried wikipedia? All the major ones should be there.

I may be missing some fantastic resource, but my first thought is to send you to KEGG.  Is that crazy?  Maybe, but a simple search for Acetyl-CoA in humans can give you tons of useful information, including GO terms, enzymes, genes, and, yes, biochemical reactions; just use the KEGG Pathways tool and specify humans (hsa).  You can click on each individual pathway for more information, such as the cholinergic synapse.

Are these reactions solely those that occur in the human body?

@BrentonHorne Wow sorry, I TOTALLY missed that!  It's now updated to be homo sapiens only.

Metacyc is an excelent methabolic pathways database that includes all kind of organisms. Of course you can search for methabolic compound.

You should look at Lehninger's Principles of Biochemistry. Just search for Acetyl-coa in the index, and you will find it's roles in different aspects of the metabolism.


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How to calculate virus titre from qPCR
I harvested some lentivirus from 293T cells and want to titre the result. I infected 293T cells on a well plate with 400,000 cells per well which I infected with virus stock, and 1 in 10, 100 and 1000 dilutions (as well as a few uninfected wells). After 72h incubation I trypsinised the cells and used FACS to titre first, but 293T do not express the promoter under which GFP is located in some samples and hence these do not appear on FACS. As an alternative, I extracted the genomic DNA from all samples using a QIAGEN DNeasy kit (also the samples which I was able to titre by FACS already) and then performed qPCR on them.
I used the ABI PRISM 7000 SDS: http://www.cgenetool.com/products/abi_prism_7000.shtml
Included on the PCR plate were:

Number standards: 1000, 10k, 100k, 1m copies
Samples in triplicate
No-template controls as well as untransduced controls

Each of those was doubled, once with primers and probe for WPRE (an element specific for the lentivirus) and once with primers and probe for beta-actin (a housekeeping gene present in all cells).
The results returned by the machine include for each well the cycle at which the threshold fluorescence was crossed - along with the automatically calculated quantity of copies (which the software calculates from the standards I assume).
Since I named the triplicate samples identically, it also automatically calculated the mean quantitiy among each triplicate (practical, eh?). I checked if there were any outliers which should have been excluded from the means but everything was fine.
So now for example I have a result of 700k for the quantity of WPRE in sample A. The quantity of beta-actin in sample A was 6.82 x 106. The transfection was 400,000 cells per well, sample A was transfected with 10uL of viral stock diluted 1:100.
How do I calculate the virus titre per mL from this?
I have been given the formula: WPRE Qty / (b-act Qty*0.5) * cells in well (400k) * dilution factor (100), but am struggling to figure out a) why b-act Qty is divided by 2, b) whether the result would be virus titre per uL or per 10uL (transfection volume) and c) how beta-actin can have almost 107 copy numbers consistently across all samples when there were only supposed to be about 105 cells...

Having gained a lot more experience with how research works, I can actually answer myself now:
a) beta-actin quantity is divided by 2 because it is a human gene and hence present twice in mammalian cells, dividing it by 2 gives an estimate of the number of cells present.
b) The result gives an estimate of how many viral copies will end up in cells from the amount of virus solution used - thus if it was 10 uL of a 1:100 dilution this represents 0.1uL of neat virus solution. So the result's unit in this case would be "viral infections per 0.1uL".
c) The number of beta-actin copies doesn't correspond to the number of cells initially seeded. 400k cells which double once per roughly 24h would make 3.2m cells after 72h (3.2x106) so that's not all too far off the copy number.

I have 2 doubts here.

You obtain your viruses from the media whereas Actb measurements can be performed only in the cell lysates.
Actb is just a reference to normalize for the cell count: higher the cell count higher will be the viral titre because of higher number of infected cells. But that is immaterial if your aim is lentiviral transduction where you are only interested in obtaining titre values and not measuring the efficiency of its formation.

You can simply do qPCR with the media sample and the standards and regress the measured Ct values of the samples to obtain titres.

Thanks for the reply. I see that I left out relevant information so I added that - have a read of the first paragraph again and let me know if that makes more sense now :)

I think it makes more sense to qPCR the lysates for copies, with all virions removed, as that should give me an idea of how many cells a mL of virus stock can transfect, which I believe is actually the important factor - I don't think I really need to know exactly how many viral particles that mL contains in order to transfect that many cells. Does that make sense?

I think it is the media that will contain the viruses and that's what you are going to use for transfection post concentrating the virions to whatever concentration you want. So you ought to do the qPCR with the media right? I might be mistaken so please let me know if that is so.

The initial prep is 293Ts in a medium with the viral plasmid as well as packaging and envelope plasmids; cells are perforated (but not killed) by adding PEI which leads to production of functional virus. That's then harvested, aliquoted out into stock vials and frozen. I was told it's not possible to just directly qPCR the aliquots - I assume the viral proteins are the problem. I used one of the vials to infect cells with decreasing concentrations of it, extracted their DNA after three days and qPCR'd that in order to analyse how many viruses actually integrated into the cellular genome.

Your method seems overly complicated to me. Surely you have a control virus? I would recommend a constitutively expressed GFP construct to make it compatible with FACS analysis. Use the GFP virus to directly calculate viral titre by FACS, then verify your other viruses by plaque assay.

Yes, one of them was a constitutively GFP expressing control, and plaque assay would have probably been a lot easier but wouldn't have been possible due to various practical issues (ironic really considering how complex qPCR is...)

I'm still not clear why you are trying to titre viral pfu using the manufacturing system (HEK293T cells) rather than your intended experimental system? Infectivity is certainly a function of host cell, but only makes sense in your experimental system. I guess my question is, why is a plaque assay system that difficult to use? Perhaps I have not understood some nuance of your particular system.

Haha, don't worry, there's nothing like a particular nuance about the system that would have been a problem; the issues were on a much higher level of practicality :)


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Why do we have no enzyme to digest cellulose?
As we know, cellulose is the most abundant polysaccharide in nature. Why don't we have an enzyme to digest cellulose?

Evolution doesn't make everything perfect.

I removed the line about evolution making things perfect. It is obviously wrong. Try watching an albatross land for example and tell me that they're perfect.

@terdon or take off for that matter ...

Bcoz human body doesn't have appropriate enzymes to breakdown beta acetal linkages.

If we were able to digest cellulose which is the fibre which protects us from colon cancer, don't you think many of us would die of colon cancer? Probably we lost the gene for producing cellulase, the enzyme that digests cellulose, during evolution to our advantage.

The question is really: "Why can't humans OR bacteria easily digest cellulose". It's very hard! Ruminants need a large, specialized bioreactor and to chew food for hours, "ordinary" gut-and-microbes won't do. If a bacterium found a quick, efficient way to digest cellulose it and it's animal host(s) would mow down forests (until trees evolve another defense that is).

While it's true that cellulose is full of calories, it's very difficult to get the calories out.
Symbiotic bacteria take ages to digest cellulose, and as a result animals that digest cellulose with specialized symbiotic bacteria have a huge gut to house them in.
It's likely that the reason humans can't digest cellulose is because mammals generally can't. And mammals generally can't because it's way too much work, and we don't need to.

"mammals generally can't"?

Even ruminants that eat grass and so on mostly just let bacteria eat the cellulose then digest the bacteria.

Are there animals who can digest cellulose without the help of bacteria?

Some termites, but I think that's it.

@Resonating imho your answer would improve, if you incorporated your comments.

This seems one form of a common question about evolution.
That being: "Trait X would seem to be an advantage, so why can't organisms adapt to X?
That is, why don't we have all traits that are advantageous at all?  Why not just digest cellulose, but maybe why not lignin as well?  Why shouldn't we photosynthesize our own food?  What about sonar as well as eyes?  We know that some living thing can do all these things.
The answer, somewhat mentioned elsewhere here, is that some advantages are not enough for the adaptation to take hold.  You have to consider that there is a cost to each such ability as well.
Cellulose is energy poor and any animal which relied on cellulose would have to specialize in cellulose metabolism to the point that they might not compete against fellow animals that got their food from other sources like meat or vegetables.
thanks for the comment below:  addendum:
energy poor in this case is a combination of how common the material is, how advantageous it is to digest (woody plants don't grow back very quickly once you eat them up).  i don't know why i wrote that there are not cellulases.  there are plenty of them and we use them a lot but they tend to be from slow growing fungi...
if you want to follow your question to the conclusion : "celluose digestion is a huge advantage in all respects" then the question is why aren't they in every bacteria that grows around plants?  because evolution is not how cellulases are created?
in fact woody plants include other materials supporting their structure to prevent this eventuality.  lignin is a non carbohydrate semirandom fiber based on phenols that is indeed very slow to digest and difficult to get at with an enzyme... at the moment it does seem to be enough to prevent plants and paper celluose from dissolving and being eaten...

You make a good point. I think these questions also come from the wrong perception (which was evident in the original version of the question) that evolution is finalistic towards making a species "perfect".

we make the same mistake when we buy cars too - a V8 2 ton pickup with back seats and i'll have the perfect car - it can do anything! But in biology a tiny fly is perfect and so is a rock clinging piece of lichen...they just do what they need to do well enough

shigeta, I agree with nico, evolution does not make things "perfect". Not by a long shot. Living organisms are a mess, riddled with hopelessly inefficient mechanisms. Think Rube Goldberg machines. It's nowhere close to what a decent designer would have come up with, but it's what you get from random mutation + selection. This more general question probably deserves an answer in itself ...

there's lots of shades of meaning here, which is definitely interesting to talk about.  Organisms are so optimal for selected traits that they amaze and astound us - better than we can design ourselves in many cases.  Where selection has not had as much pressure (e.g. long life, resistance to damage and disease, empathy, speed, intelligence) it can seem that they are strangely vulnerable.

"Cellulose is energy poor" Excuse me? You're basically saying glucose is energy poor. You should specify that it's "energy poor" in the sense that it's resistant to enzymatic breakdown or something (I don't know if that's the actual reason, it's just what I'm assuming based on other answers in this thread.)

energy poor in this case is a combination of how common the material is, how advantageous it is to digest (woody plants don't grow back very quickly once you eat them up).  i don't know why i wrote that there are not cellulases.  there are plenty of them and we use them a lot but they tend to be from slow growing fungi...

Why don't we have any enzyme to digest cellulose?

Why should we?  We don't use it as a source of energy so why bother?  Even animals that do "digest" cellulose, like ruminants, only do so because of symbiotic bacteria; it would be a poor system indeed in which every organism utilized the same resource.  We occupy enough of the food chain as it is.

The question forgets that organisms consume materials for two reasons: To capture chemical energy (which it focuses on) and to gain molecules that the organism cannot otherwise produce. Cellulose effectively serves only one purpose in organisms that digest it: energy production. Eventually, it is broken down into H2O and CO2, both of which are excreted.
Throughout the millennia, getting calories was not that difficult, but getting enough essential micronutrients (vitamins, minerals and amino acids) as humans moved into different environments has been where there was selective pressure. Selective pressure for other calorie sources, such as cellulose, has never really happened. Beyond this, there is a ratio of optimal caloric intake to optimal nutrition intake a human should get from his diet for that human and humanity in general. A mutation or sudden symbiosis with gut bacteria  that allowed for cellulose digestion would make it even more difficult to keep that ratio, but it is non-optimal situations where selective pressure occurs. The issue here, in my opinion, is that that would be too great a selective pressure on decreasing the micronutritional requirements. The human would far too easily get calories and need to eat many times more in calories what he needed to get the necessary nutrition. So actually, there is selective pressure against cellulose digestion. Further, because of the way humans are built and the other great primates, this sudden mutation or symbiosis seems very unlikely.
Also, cellulose already serves a vital purpose in the gut. It is commonly called fiber, and allows the feces in the colon to remain moist enough to be passed. Some mammals have adapted colons that can pass very dry feces (the Camel's feces is so dry that you can start a fire with it), but they are typically arid climate species, where water is by far the most precious resource. So the selective pressure was on water intake, not calorie intake.
So there has been no selective pressures on humans to digest cellulose, nor will there ever be, so long as there is such a high need for vitamins, minerals and essential amino acids. Such selective pressure would take the form of there first being super nutrient rich foods (relative to humans), then that same food becoming calorie poor. Basically, humans would have to start replacing a meal or two per day with only vitamin supplements. Even with that, the only mammals I know of that digest cellulose are actually utilizing symbiotic gut bacteria to do so. I can't imagine the clever way humans might get that bacteria into their own guts. Actually, I can.

I don't want to bump with an edit, but I recall a criticism of this answer that accused the line about nutrition to calorie intake ratio hinging on that common error that evolution makes perfect. I want to clarify that's not what I mean. I mean to point out that currently, because of known evolutionary pressures, there is an optimal ratio and an adaptation to digest cellulose would gravely affect that, therefore that would have to adapt as well.


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How to secrete a recombinant protein from E. coli?
What are some secretory pathways that can be used to secrete a recombinant bacterial enzyme from E. coli?
I have a recombinant protein (29kDa) that I will express in E. coli BL21 cells.  For now I have been sonicating E. coli to extract the enzyme, but in the future I would like E. coli to secrete the enzyme.

I think E.coli doesnt have secretory system. You might have to use Bacillus spp. which have a secretory system. Also, you need to add a secretory signal sequence at the N-terminal of the protein.

According to the 2012 iGEM Kyoto team:

The Twin Arginate Translocation pathway(TAT) is [an endogenous] secretion system in E.coli. This system can carry proteins that have torA signal amino acid sequences at N terminal. TatA, TatB, TatC and TatD compose Tat complex on inner membrane. Tat complex recognizes torA signal peptide and then it transports protein (with torA) from cytoplasm to periplasm. In addition, protein that has passed through TAT pathway cut off the torA signal. Proteins which are secreted by this system have no tag that obstruct the activation of the protein.

The team created a cassette with the TAT genes to increase the expression of the pathway and also included the Kil gene, which perforates the outer membrane, possibly aiding the external diffusion of the secreted protein. They noted, rather tongue-in-cheek, that

Needless to say, function of outer membrane as membrane is essential for E.coli to survive. In other words, overexpression of Kil causes cell death. In this reason, we must find suitable amount of expression.

Note: according to their lab notebook, the team never observed extracellular GFP via confocal microscope (search that page for 'confocal'). So. Beware :)
Their project page also includes some references to the following literature:

Tracy Palmer and Ben C. Berks "The twin-arginine translocation (Tat) protein export pathway"
J. H. Choi. S. Y. Lee "Secretory and extracellular production of recombinant proteins using Escherichia coli"
G. Miksch · E. Fiedler · P. Dobrowolski · K. Friehs "The kil gene of the ColE1 plasmid of Escherichia coli controlled by a growth-phase-dependent promoter mediates the secretion of a heterologous periplasmic protein during the stationary phase"
Brad A. Seibel* and Patrick J. Walsh "Trimethylamine oxide accumulation in marine animals: relationship to acylglycerol storage"


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observed luminescence in a piece of plaice
A plaice fish bought for human feed has been cleaned and cooked.
Some parts of the raw body have been left out of the fridge at about 22°C for about 15 hours.
During the following night a luminescence phenomenon has been observed on the meat of the fish.
The second shot has been taken in a dark environment with a professional camera using a high sensitivity and long-time exposure.

What could it be?

It's probably bacteria.
Here's a pdf describing the phenomenon, along with an in-depth history of the reported occurrence, which should tell you everything you might want to know.

These seafood products exhibited luminescence due to the presence of certain bacteria that are capable of emitting light.  Luminescence by bacteria is due to a chemical reaction catalyzed by luciferase, a protein similar to that found in fireflies... Most of these species require salt except for the two nonmarine luminescent bacteria.

There is some link to potential pathogenicity, so I'd recommend not eating it.  That document also requests that you contact the researcher, so why not?  Here is a potentially-relevant paper but 1. is very old, 2. is in Russian, and 3. I have no access to it.  And this supposedly tells you how to isolate them.

thanks, very useful, we find ourselfs in one of the cases that the FDA document describes (the one of the cat). we are not sure about emailing the researcher because we live in europe so probably the fda is not the 'right' authority to report to. i will wait few days then mark your answer as accepted.

I can only second this. There are bacteria growing on the fish. Interesting example though.