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How did the cardiovascular system evolve?
How has evolution created our blood, lungs and the heart?
We can't exist without blood, which transports the oxygen to all areas of our body. However, the blood needs a lung, which gives it the oxygen to transport. The blood also needs something which lets it flow through the whole body, which are our veins. And in order to allow the blood to flow through our veins, an organ is needed to pump the blood, which is our heart. We also need a brain which controls all that, and the brain in turn needs the blood in order to function right.
Evolution makes very slow steps....."it just doesn't jump". So, How did evolution manage to create all that?

The systems you mention, the blood, heart, vessels, and lungs exist in partial forms in other organisms. For example, insects have open circulatory systems with primitive blood vessels and a simple heart. Instead of lungs, air is moved through a system of tubes. Earthworms are even simpler, they get their oxygen by diffusion across their skin, but they still have a simple heart and blood vessels. The systems did not simply appear fully formed, but evolved one piece at a time over many millions of years.

But even for those little creatures, with less organs and simpler structure, applies the same thing.
For example the earthworms: in order to allow blood flowing, a heart  and a oxygen input (by diffusion across their skin) is needed. But how did that evolve by one piece after another, when no piece can exist without the other.

this is a complex/broad question... basically asking how did evolution lead to the body as well know it... do you think you could narrow down your question a bit?

Of course: There had to be a jump in the evolution, because, as written above, there are many functions, which can't exist without other functions. So, evolution is taught, that this isn't possible, because the steps are made very slowly.
So my question: how is this possible, or is it even possible if laws or rules of the evolution are considered?

In case of interest: Understanding Evolution by UC Berkeley is a short and free online very introductory course to evolutionary biology.

Aspagus, you contradict yourself: you say that all these systems are interdependent, then you gloss over the fact that worms don't have lungs, and continue to claim that all these systems are interdependent and can't exist without each other. The fact that worms don't have lungs is evidence that the circulatory system does not exhibit irreducible complexity.

user151841, concerning lungs you are right, but I didn't just mean the organ, but the process or the function, which makes all that interdependent.
Because, the system of the earthform still can't be without getting oxygen through the skin.
So, the earthworm can only live, when the blood is flowing.
In order to allow bloodflowing, there have to be a heart, vessels, and, to let the blood carry the oxygen, a function of getting in oxygen.
But now I know a little bit about how this has happened, and that this is clearly possible.

So: All that didn't come at once, there just have been other organs or other "ways in order to bring the body to life" which replaced these functions.
For example: There wasn't always blood which was transported through the body, but other ways in order to maintain the body, which didn't need organs we have today.
I really don't understand everything about it, but all answers gave me "a picture" of it.

@asparagus A good course in comparative anatomy will show you all the intermediate forms you are looking for. Try Kardong's Vertebrates.

@asparagus A closed circuit (blood vessels) is not essential to a circulatory system (see open circulatory systems). Nor does a pump require a circulatory system to work effectively (see flatworms), but it does need one to work efficiently. The circulatory system isn't even IC...its just that each part works so much more efficiently with the other parts...

Makes me want to create a breadboard-type kit that allows for incrementally adding, and later obsoleting, components so that there is continually increasing complexity and capability. It could help illustrate things in a very testable, repeatable manner. New components would have only incremental improvements.

@asparagus "Because, the system of the earthform still can't be without getting oxygen through the skin." The key to a surprising amount of what our bodies do is diffusion. I.e. molecules just... moving around like they do. That's how oxygen gets through the earthworm's skin, and it's also how oxygen gets from our lungs into our blood. Most of our super-complex organs are, when all is said and done, about making diffusion more efficient. Understand that it's all diffusion and you go a ways to understanding how the cardiovascular and digestive systems could have evolved.

While others have addressed the big picture aspects of your question, I think it would be useful to look at the specifics.
Have a look at the heart (or more accurately, the hearts) of the earthworm:
They're nothing more than veins with some pumping muscles wrapped around them. It seems almost a stretch to call them hearts, they are shaped so different from what we think of as a heart proper.
Also, note the earthworm's lungs, or rather, lack of them. It doesn't have any! Why not? It doesn't need them. It gets enough oxygen through its skin via osmosis. It's only larger organisms that need dedicated systems to concentrate oxygen from the surrounding environment.
So, the worm has a simpler system (no chambered heart, no lungs) that works.
All vertebrates descended from a common ancestor that was very similar to this earthworm. It had simple hearts, and no lungs. You can follow the evolution of the human heart through fish heart:
which is a more sophisticated pumping vessel with two chambers.
Amphibians evolved from fish, reptiles from amphibians, and mammals from reptiles. In this diagram, you will find that the heart becomes more sophisticated and efficient in each:

So, this should give you a good idea of the evolution of the human heart from simpler, working system. I won't take the time to draw out the evolution of blood vessels or lungs; maybe someone else will, or you can google them yourself, the information is readily out there. But they all follow the same pattern: gradual, incremental improvements on working, simpler systems.

the evolution of the human heart from simpler, working system How did this simpler system appeared? the information is readily out there Can you please share some links to that pages?

@A.L Sure! Here is a graphic of the evolution of lungs: http://images.slideplayer.com/13/4156687/slides/slide_2.jpg To get this, I just did a google image search for "evolution of the lungs".  For the evolution of actual bloodtubes from non-tube systems, it's a little more tricky. You could start at this page: https://en.wikipedia.org/wiki/Flatworm#Distinguishing_features see the "more advanced bilaterans" column

This kind of question was raised in a book called "Darwin's Black Box" by Michael Behe, who is a biochemistry professor in the U.S. - he calls this 'irreducible complexity' (IC). For example, the blood clotting cascade system where you have a large number of components that are all apparently essential for the process.
Now I have to say I find the idea that this is a problem very unconvincing, to say the least. However, it's a reasonable question to ask; how does a system of interdependent elements evolve, if we assume that no part can change gradually without the whole system breaking?
There are - at least - two major problems with this. Firstly, the assumption that you can't change any part of such a system has mostly turned out to be false. Secondly, systems would obviously evolve from other, simpler systems which are just as effective.
Say I start out with three elements in my system (three proteins, for example). They are all essential as each requires the other to function properly. Now I introduce another protein to the system and make it dependent on only one of the existing proteins. Is this system IC? No, we can remove the new protein and the whole thing still works. Gradually, we make the other parts of the system dependent on the new protein and suddenly we have an 'IC' system.
In other words, the 'problem' lies in imagining that you have to go from nothing to a complete working mousetrap. What seems more likely is that elements of a system are changed one by one, and that the system evolves through a series of states where you could point to some element and claim that it is essential.
One final point to note is that no multicellular organism is born whole in one step. The processes that an embryo goes through are conceptually similar (though not exactly ) to evolution in that you can have different organs developing at different times, or simpler versions of them that can work together as a simpler system.

To make this a little less abstract, consider the earthworm example given in the top answer. It has just a simple heart(s) and blood vessels - it doesn't seem that difficult, therefore to add in some lungs. Here's a trivial diagram:

The lines here are interactions between the organs - the heart pumps blood through the vessels, and the lungs (if any) oxygenate the blood. We evolve from the simpler system (1) to the more complex system (2) just by adding another element.
However, the difficulty with some systems is that the interactions between the parts are dependencies. A very simple example could be proteins that activate/deactivate other proteins (by phosphorylation, say). Then we could theoretically get a situation like this:

Here, the final system (4) looks like it is 'irreducibly' complex because you can't remove any of (A, B, C, D) without breaking the cycle. However, at each step, we only added or removed one dependency. This also shows the importance of redundancy in biological systems. If you knock out either C or D from system (3) then it still works.

This nearly makes the point of the most convincing argument I've ever heard for evolution. That is, the intermediate steps for the "mousetrap" were simply to make a better paperweight, and the resulting random configuration accidentally worked as a mousetrap. But it still ignores the "required functionality" aspect of the original question. Each of the functions in an IC system is separately required, but each structure is collectively interdependent.

@JedSchaaf Yeah, the mousetrap is a pretty standard metaphor. It may even have been used in Behe's book. I think the key idea is that elements of the system and dependencies within the system can be introduced independently. I see it like a network or graph, where elements are vertices (eg: proteins) and dependencies are edges. I can add a new vertex, then add a new edge, then another edge, and suddenly I have an 'irreducible' system where I can't delete that vertex! Perhaps I should add this to the answer...

If we have a system where A depends on B and C, B depends on A and C, and C depends on A and B, then we could add D that depends on A, but we cannot then make A also depend on D. A might incorporate D into its functionality, but it doesn't depend on it. D could be removed and A would still work.

@JedSchaaf Hmmm. Unfortunately my model is too simple to say what 'depend' really means. I just have some association between two elements (say protein-protein binding) like an undirected edge.

This doesn't answer the question except in the most general, abstracted sense. To someone who doesn't "get it", a mousetrap probably doesn't seem all that complex, compared to the vertebrate cardiovascular system.

@user151841 Fair enough. That's why your answer is much the better one. I still think it is worth addressing the general, abstract sense if only because it's a problem that potentially affects biology at all levels of organisation - including organs. I was going to add a diagram, but maybe I'll save it for when (if) there is the more general question.

This is a good question, but it has a vast scope, as you're talking about the progression of millions of different living animals over hundreds of millions of years, none of which are still alive, so we have to make inferences based on what we observe in their surviving offspring.
That means if you want to learn how 'intermediate' (say, not-quite-lungs, not-quite-heart, not-quite-brain) body systems could function, you'd first need to learn about the biology of lots of other animals.  Not all animals have lungs or hearts or nervous systems.  Not all animals have blood.
More to the point, though, the key factor is that several hundred million years is a really, really, really long time.  It's such a long time that it's well outside any typical human scale of comprehension.  Consider the entirety of your life experience thus far and everything you've seen change.  In comparison to how long the evolutionary process has been operating, your life's span has been on the order of a millisecond out of a day.

Thank you for your great answer!
What I don't understand is, how the evolution managed it to create that all.
Because, the evolution makes very slow steps, so "it just doesn't jump".

The amount of time is irrelevant if there is no method that can show how the changes would have occurred. The fact that other organisms exist with structures that could be called 'intermediate' is also irrelevant for the same reason. Remember, these other organisms also need to have evolved through other 'pre-intermediate' "stages".

I would argue that this is a poor answer for someone who lacks a fundamental understanding of biology and evolution. Truthfully, one can talk about how the cardiovascular system at a simplified, generalized level without learning the biology of lots of other animals.

Simpler forms developed to handle simpler requirements. Take planarians, for instance, which are thin and small enough that they can receive their oxygen supply by diffusion straight through their surface. Now imagine a slightly bigger animal that needs a slightly more sophisticated system to oxygenate their internal regions well. A muscle with an aberrant, autonomous twitch would be enough to stir/circulate more oxygenated fluids through the body. Past that, any little accident that facilitates this (e.g. some cells bind to oxygen a little better, the muscle twitches a little stronger or more regularly, etc.) is another form closer to what we see today.

A good question, indeed, and not easy to answer (or grasp). I'll give a very simplified answer. Bear in mind that the processess I'll describe are REALLY complex.
You have to think way before blood, brains, etc. Billions of years ago, organic molecules were formed in the planet. These organic molecules started to """join""". Millions of years latter, simple cells which didn't even have a nucleus were formed. Some millions of years latter, cells with nucleus started to form. Latter, these cells started to agreggate, turning into colonies of unicellular individuals. In time, these colonies turned into multicellular individuals, but with all cells being equal to one another. After that, cells in one organism started to differentiate into some functions (digestive and neural, for example). Slowly, more complex organisms were formed, as the cells which formed these organisms started to differentiate and form various kinds of tissues, which, through millions of years, developed into more and more complex organisms. Think of Cnidarians, for example. They are very "simple" (I use "simple" as a proxy for "not complex") beings. They have no circulatory system. A circulatory system developed in latter groups: the first, "simple" circulatory system appeared in Nematodeans (if I'm not mistaken). But it was really "simple". With time, other, more complex, circulatory systems started to originate due to various evolutionary pressures. The same applies to every type of cell, tissue or organ you can think about in any organism: complex organisms are the result of millions of years of simpler organisms which generated more complex organisms, by really little steps.
I hope you get the idea of what I'm trying to say. For really grasping all this, you have to study a lot of evolution, because it is a hard concept for us to deeply understand.

you have to study a lot of evolution That's a strange answer, like this is a secret kept by biologists. Can someone that studied evolution write explanations of this concept for everyone?

Well, I didn't express myself correctly. When I said "a lot" I didn't mean that one must have a major in biology. What I think is something like this: suppose one has a class about this topic ("How does evolution creates complexity"). When the class is finished, one might think "Ok, I get the idea", and maybe that person gets the idea, but to really grasp the concept of how evolution creates complexity from simplicity is harder to understand than just by watching a couple of classes. It takes reading and critically thinking. I just wanted to emphasize that.


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What is the source of the electrons generated in the Krebs cycle?
In the Krebs cycle, where do the hydrogens and electrons that NAD+ and FAD accept come from? It seems that citric acid only loses two hydrogens because it starts out with eight hydrogens and then becomes oxaloacetic acid, which has four hydrogens.

where have you looked for answers? have you tried google - this is a relatively straightforward question that should be easily found... try googling "where do electrons from krebs cycle come from"

Yes, I have googled this, discussed the question with friends, and thought about it myself and I have not found an answer. That's why I'm asking on stack exchange.

Nice, so electrons are coming from carbon and hydrogen bonds, and great information btw. But how is this happening. Is carbon double bonding where it wasn't previously, so that it can give up some electrons?

Very interesting question. Clearly this is far from obvious, with conflicting statements in the literature. I don't know if one should call it "splitting water", but the TCA cycle does take up 3 oxygen atoms from H2O (one via phosphate) which end up in CO2. Given that, it's not clear to me where the electrons of H2O end up, especially considering that electrons in the carboxyl groups are delocalized ... @TomD, were you able to find the missing references you mention in your other answer?

@TomD  Completely agree. Thanks for the reference! I think the summary equation of Herreos and Garcia-Sancho settles this question nicely, maybe you should turn that into an answer.

@user3163829 Citric acid has 8 Hs and not 6 Hs. If you consider the anion of this acid, the state usually found in body fluids then Citrate has 5 Hydrogens and Oxaloacetate 2 Hydrogens.

@TomD — I've thrashed out an answer from the references you gave. I felt the question was too interesting to be left without that in a formal answer. Do feel free to suggest changes.

The two electrons and a proton of NADH comes from a H$^-$ ion of a Krebs cycle intermediate during Isocitrate dehydrogenase reaction and Malate dehydrogenase reaction.
In the following reaction, Isocitrate is oxidised to Oxalosuccinate and in the process two Hydrogens are lost one as H$^-$ and the other as H+. This H$^-$ is accepted by NAD+ to form NADH.
Note: Oxalosuccinate is an intermediate formed during oxidative decarboxylation of Isocitrate.

Now coming to FADH$_2$ $-$
During oxidation of Succinate to Fumarate, Succinate looses a H$^-$ and a H+ ion which constitute the two protons and electrons of FADH$_2$  . Here's an image that illustrate the mechanism:

The alpha-ketoglutarate dehydrogenase complex reaction is similar to pyruvate dehydrogenase complex reaction(PDC).
PDC reaction is an oxidative decarboxylation reaction of Pyruvate in which the 2e$^-$ of NADH are derived from the electron shared between COO$^2-$ and C=O groups of Pyruvate.

The Hygrogen (H+) of NADH is either derived from the H+ of CoA-SH or from the medium. There's a series of complex reactions which need to be studied to fully understand the source of H of this NADH.
So you can understand that the 2 e$^-$ of NADH produced in Alpha-ketoglutarate dehydrogenase complex reaction are the electrons between COO$^2-$ and C=O groups of Alpha-ketoglutarate and the H is either from the medium or the H+ of CoA-SH.
Reference: Biochemistry by Berg

The malate dehydrogenase step is similar to ICD? Whats the intermediate there? But isn't the other reaction, the a-ketoglutarate step similar to pyruvate dehydrogenase? The former is a C-H bond, while the latter is a C-C bond. Correct me if wrong! Sanjukta Ghosh @TomD ?

H- ions? Do you have a real source for that?

@Chis I have deduced it from the diagram that I have shared from Biochemistry by Berg. They haven't mentioned H- ion, but that it what the picture says. Referring to the first diagram, H- and H+ must leave the Isocitrate to form Alpha-keto acid, oxalosuccinate.

@David I'd like to hear your views on the concept behind my answer. Do you find it correct?

@Polisetty Yes you are right MD step is similar to ICD step. Thanks for pointing out, I was in a hurry so I had messed up, but now I've corrected it. The PD step is also similar to AKD step.

@Chris This wiki page talks of the proton, hydride thing in NAD redox reactions https://en.wikipedia.org/wiki/Nicotinamide_adenine_dinucleotide#Physical_and_chemical_properties

This is a question that has been a source of disagreement between some quite senior biochemists, so, although I am no angel, I waited a little to find an elusive volume of a journal before rushing in. At the outset it seemed to me that:

What was important in the oxidation of acetyl-CoA in the tricarboxylic acid (TCA) cycle was the source of electrons, not the
  source of hydrogen atoms. Oxidation is the removal of electrons.
The source of the electrons must be the carbohydrate being oxidized. It could not come from anywhere else (such as water).

This point was made in a comment (not an answer) by TomD, who pointed to his answer to a different but related SE Biology question. In that answer he refers to two ‘letters to the editor’ on the subject in TIBS vol.6, p.6 (1981), which unfortunately are not available in the online version of the journal. I recalled them from my own university library’s archives and have made them available here as a text pdf, although in the meantime TomD posted a scan himself. I recommend reading the letters carefully to consider their arguments, but quote extracts from each here to show why I personally tend towards their view.
D.E. Atkinson
Atkinson’s key point, as I understand it, is that although the H may come from water, this is only as a result of ionization — the water is not oxidized, so cannot provide electrons:

“Electrons cannot be tagged and traced, but the stoichiometry is clear:
  in the oxidation of an acetyl group to 2CO2, eight electrons are lost.
  Of these, six are used in the reduction of NAD+ to NADH and two in the
  reduction of the flavin of succinate dehydrogenase. Water is not
  oxidized; thus no electrons are supplied from water to be: ‘raised to
  the level of NADH2’ or for any other role. When water ionizes, the
  electrons all remain associated with the OH– ion; whatever the proton
  may do, it cannot reduce anything.”

B. Herreros  and J. Garcia-Sancho
These authors emphasize that it is the C–C and C–H bonds that are providing the electrons:

“As pointed out by Losada the carbon compounds themselves are the only
  source of reducing power in the TCA cycle, not water. The difficulty
  in realizing it arises from the contabilization of the reducing
  equivalents as pairs of H rather than as electron pairs. It is true
  that one molecule of glucose can not supply 12 pairs of H, but it can
  certainly supply 12 pairs of electrons…
… In the TCA cycle, the electrons shared in the C–C and the C–H bonds
  are the source of reducing power; they are transfered first to
  pyridine nucleotide (and flavin nucleotide) and then to the vicinity
  of oxygen through the respiratory chain.”

Towards the end of his letter, Atkinson writes “I have found it a useful pedagogical device to ask students to work through respiration (glycolysis plus the citrate cycle), keeping careful account of water and proton so that their equations will sum to the proper balanced overall equation.” I am afraid I haven’t provided that in this answer, limiting myself to surveying the wood rather than examining each tree.

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Would short term increases in oxygen lead to beneficial effects?
After some thinking, I am wondering if having a 30% atmospheric oxygen concentration (or some other concentration) for a short time would increase the regeneration of energy in a body? It seems like it does have some mental effects, but I haven't found any other positive effects on the body.

what positive effects have you found? can you add those sources to the question?

Giving someone oxygen, who has had COPD for a while, could be fatal.

You can't really go by simple percentages.  It's generally the partial pressure that matters, so for instance the FAA requires pilots of non-pressurized aircraft to use supplemental oxygen above IIRC 14,000 ft.  (And no whining about non-metric: the FAA regulation says feet :-))  OTOH, using normal air for deep diving can cause oxygen toxicity - though nitrogen narcosis generally happens before that's a problem.

Humans are pretty well suited to a 21% oxygen atmosphere (at STP). It's what our lungs are used to dealing with, and it's what brings the appropriate amount of oxygen to our brain (in particular, most organs are more forgiving, although not a lot more).
A lower concentration grows quickly and strictly deleterious, leading in short order to hypoxia, subsequently death. A higher concentration is also deleterious, leading initially to an oxygen high (as seen with Oxygen Bars), but also causing vision problems, seizures and death.
Oxygen is also highly reactive, and increased concentrations for even short bursts could, if frequent, lead to cancers, especially lung cancer. (The primary cause of lung cancer prior to asbestos and smoking? Breathing.).
There are cases in which increased oxygen concentration can be beneficial, but they are rare and specialised.

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What spider is this? Is it dangerous to humans?
What is the species? Is it dangerous to humans?
I chanced upon this beautiful one near our water well. It stood at a height where an adult could accidentally walk through the web and the spider would land on one's face.
As a test, I dropped a piece of leaf onto its web, and the spider jumped to action, checking what it was and it took out the leaf from its web.
Size: Web, almost circular 50 cm diameter. Spider, about 8cm.
Location: Malabar region, Kerala state, south of India

Most spiders are harmless (unless you're a bug). Here are the medically significant ones.

Im in Kochi (same state in India) and I was told it would sting, so stay away. I also remember them as they appear to have only four legs (with claws) and jokes that they defy their very name, which means 8-legs in Malayalam.

This is most likely a spider from the genus Argiope, which has a few members native to India. See here for a list, I think this is most likely
Argiope pulchella, see the image from the Wikipedia:

Wikipedia also says that these spiders hunt insects, but are not dangerous for humans.

What are your thoughts about @Thomo's answer?

Its definitely an Argiope pulchella - Native to India, rather than an Argiope keyrselingii (Australian species). Either way, its completely harmless to humans, as are most spiders...

It's a St. Andrews Cross Spider (Argiope keyrselingi), and quite common in Australia too.

Thankfully, one of the non-toxic non aggressive spiders. Here are some good sites for further information on them:
A Spider Identification site:
http://www.spiders.com.au/st-andrews-spider.html
And the Australian Museum site:
http://australianmuseum.net.au/st-andrews-cross-spider


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Genome and Proteome
Due to the dynamism of protein expression, a genome can give rise to different proteomes, but could we say that a proteome comes from different genomes?

Do you mean this in a hypothetical sense, or if it has been observed?

Related: Why is there more variation in proteins than genes?

Yes, different genomes can produce the same proteome.
Imagine a genome that only has a single protein-coding sequence (without splicing isoforms), the rest of the genome is simply regulatory sequences. Whatever those regulatory sequences may be, as long as that single protein is expressed, it'll be the same proteome.
If you consider a single nucleotide difference enough to say two genomes are different, then there are probably quite a lot of different genomes on earth that produce proteomes identical with at least one other genome.

In my opinion a proteome doesn't just which sequences are present, but also how much of each sequence. And you also overlooked the modifications to the proteome which might not be of biological origin but could have biological consequences.

Would you say that affects whether or not different genomes can (theoretically) produce the same proteome?

No, if you want to have a generally valid statement. You can not say: "that a proteome comes form different genomes".
The official (MeSH) definition of the term "proteome" is:
The protein complement of an organism coded for by its genome.
https://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?mode=&term=Proteome&field=entry

Correct answer according to the phrasing of the question, which aims for "is it generally true" rather than "is it possible" (which I assumed was the question in my answer).

Taking the first two answers into context, you cannot say given two proteomes that they came from different genomes, but as stated above in the first answer, if you consider a single base change to constitute what is a different genome then yes you probably have a lot of different genomes producing the same proteome.
There are a few fallacies here.
Firstly you cannot say based on a single base change that they are different genomes, Consider this, if your body is constituted by 10^13 cells, then from the time you were a zygote, with each turn in replication the replisome constituted by the DNA polymerase, introduced a few mutations in the genome.
Why you ask?
Because the fidelity of polymerase delta is 10^6 meaning that every one million bases it will introduce a mutation (link explaining differences between different types of mutation). But hold on, there are a few repair machanisms involved, this raises the aggregated fidelity to 10^9. Which means that every 1 billion bases you can expect to find a mutation in the sequence.
Are these all different genomes? No, of course not.
These are  somatic mutations which are aggregated over the course of a lifetime. This is why we age, why we get cancer, and why we ultimately die.
Now consider this, your body is constituted by cells which are somehow different from each other based on their DNA sequence, they are also differently specialised to perform different tasks. These specialised subsets among those 10^13 cells produce different subsets of the entire proteome which as a cumulative whole represents the entire proteome of the organism.
Are they producing different proteomes? No, they are producing a subset of a larger whole superset, but the proteins produced are at different levels by all these cells. If you are interested, you can take a look at single cell sequencing
So I hope you understand that the question you asked has few underlying considerations which must be accounted for.
Next coming to the question at hand? Can we start from two proteomes which are the same and say they came from two different genomes even if you ignore the second answer above? Nope.
This is because of how proteins are translated. You can check out the  reference translation here. Translation, the process which converts RNA to protein exhibits codon degeneracy a feature where amino acids are coded by two or more three letter combinations called codons, making the process of translation very robust to DNA mutations.
So finally, to make a very long answer short. Can we start from a proteome and say they came from different genomes? No


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Blocking buffer for actin and fetuin-b in western blot
I have been working on western blots for about a month now using actin and fetuin-b primary antibodies to no avail. My background is always high and I only had one good result. I want to know if there is a certain blocking buffer I should use instead of 5% milk with my membranes to get a better result.

There are commercial ones available (usually pretty expensive, but work ok), you could also use BSA for blocking instead.

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I have only used milk for blocking a couple of times but it was always beaten by bovine serum albumin (BSA), casein, or BSA/casein.
My standard blocking buffer is 1 - 5% BSA in tris-buffered saline with 0.1% tween20. I have also used the Western Breeze kits from Invitrogen and in my hands their blocks and alkaline phosphatase detection reagents were very reliable. The preservatives that they include in the stock reagents also allow the block to be reused for up to a week if handled and stored appropriately; keep everything clean, use up to 4 times, and store @ 4 degrees when not in use.
Some antibodies will require specific blocking buffers to perform well.
Background can come from many sources so if you have background with both primary antibodies you should check for other issues as well. Background is a very general term and can be caused by many things, a few I can think of are;

Overheating during transfer
Primary/secondary antibodies binding to the membrane.
Primary/secondary antibodies binding non-specifically to the proteins.
The interaction of detection reagents with buffer components (phosphate and alkaline phosphatase, tween)

When I was working with actin antibodies I used 2% horse serum in PBST to block and to incubate with antibodies. Or just washed membrane really good from 5% milk in TBST(like 5 times 5 minutes in TBST) because goat antibodies doesn't like milk. But I incubate with milk for 45 min-1h. You can also wash 3 times 5 minutes with TBST after secondary antibodies and then 2 times 5 minutes with TBS. It really helps.


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Are wasps attracted to a sting
A little backstory, I was trying to get something that was in a little wooded bit at the back of my garden and stepped on a swarm of wasps was stung 3 times and got out of there but I brought 8 wasps inside and was wondering if they know if you've been stung and are attracted to it and also out of curiosity what would happen to a wasp if it was stung by another wasp

Tackling the second part of the question first: If a wasp is stung by another wasp, that's usually super bad for the wasp in question. Wasps are pretty good about not stinging one another, but occasionally wasps from other communities come in and cause a ruckus, or even predate on other communities of wasp specifically. If a wasp gets stung by one of these, it's about to die horribly, then get eaten.
On the other hand, if it's stung by 'friendly fire', it'll just die horribly. The venoms wasp stingers carry, while merely irritating and only occasionally fatal due to allergies on our scale, are generally pretty lethal to insects, arachnids, and other tiny critters; also, having a huge hole in your exoskeleton doesn't help.
As for the attraction question, the answer is a solid and absolute 'Eh, probably not.'.
Wasps, like a lot of insects, communicate on pheromones and dancing, but on the whole their 'deal' when not hunting is to repel, not kill. They don't care if what they sting gets killed or not; so long as it gets out of their zone of control. While they do issue alarm pheromones and other calls to action, these are not associated with stings in particular, which mostly deliver poison and sharp force trauma, not orders to the swarm.
You'll probably want to clean out the stings in any case, but it's unlikely that your new house guests want anything so much as just going home. Usher them out the door, and they'll be happy as clams.

I thought Wasps don't eat other insects, they do feed them to their larvae.

@RHA That seems like a petty distinction. Are wasp larvae not wasps?

Well, they have a different diet. Wasps eat sweet stuff (either excreted by the larvae or from your soft drink).

@RHA I think that varies by species. Wasps are freaks like that.

Well, all species of Vespoidae work like that. These are the colonybuilding, stinging creatures that most people call wasps. There are off course many solitary wasps, but these hardly ever sting people.

@RHA True enough. But if we're not rigorous in what constitutes a wasp, then why are we here?

I was stung this afternoon. I drove home, washed the site with vinegar and was icing it, when out of nowhere a wasp came in through the open window and began to buzz around the part of my arm where I was icing. It landed, walked around for a few seconds, as if it was investigating. It was the oddest thing!

Hi. This is not an answer, but rather a comment about something that happened to you. Please delete this as an answer and move it to be a comment instead.


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Why do we need to replicate incomplete DNA fragments by PCR from a crime scene?
If the DNA from a crime scene is damaged, why would it be helpful to replicate it by PCR (polymerase  chain reaction)? Even if we get billions of those copies, it is still incomplete, isn't it? How can the PCR make the forensic process easier?

As far as I know (and I know little in this domain), there are statistical to deal with damaged sequences. Typically, different nucleotides have different probabilities of being altered with time and this can be taken into account. However, on a crime scene, there is no reason for DNA to be damaged in any. The main issue is probably a potential problem of contamination.

This process helps with the signal to noise ratio.  In theory, you could use the fingerprinting techniques to dice up the few billion copies of the DNA and carefully measure them.  However, it is far easier to replicate the DNA to increase the number of molecules of DNA available to the process.
Remember, fingerprinting for crime investigations doesn't involve reading the DNA, but merely uniquely identifying it.

does that mean we need about billion of  that same copies to show on the result of gel electrophoresis. so we need to replicate it by PCR

Yeah.  If you think about it, the final step of the process is to stain the DNA fragments after they have been separated by weight.  You need enough material at each position along the gel to make a noticeable stain.  You also need enough of them to be able to use statistics to account for any random variation in your gel.

sorry,could you explain what you mean by "any random variation"? and why the process need to be helped with "signal to noise ratio"

Electrophoresis is dependent on diffusion, which is a rather inexact process.  If a single molecule of your source material finds an easier path than average, it will move further than it should have.  However, if you have billions of said molecules, it is far less likely that all of them will find the easy paths.


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Reconstituting genomes of archaic tribes of humans
Will it be logically possible for genome studies to reconstitute the genomes of our local human populations as they were 2000 and 4000 years ago? What is the mathematical precision and science for that kind of thing?
I am fascinated by human facial features and i wonder what our archaic tribes looked like regionally when they were isolated, a few thousand years ago, before mixing into the melting pot that they are today.
If we can one day image facial construction from DNA using some thousands of facial genes, it will be cool if we can also find what local dna pools were like precisely a few hundred generations ago. Is it possible?

Thrilling thought. May already possible. 4000 year old specimen can still be fine for sequencing.  https://en.m.wikipedia.org/wiki/Ancient_DNA   and faces can already be partially reconstructed from DNA sequences https://www.newscientist.com/article/mg22129613-600-genetic-mugshot-recreates-faces-from-nothing-but-dna/

Are you asking about genomes from individual people 2000-4000 years ago, or population structures? Full genomes have been sequenced from a number of individuals in that time range, but understanding population-level genomic information is a very different task

You should not believe that many human populations lived in isolation for long times. Almost all human populations had massive gene flow with many other human populations. Human history basically is a history of migration after migration after migration. Humans have always been genetically heterogeneous (rather than previously homogeneous and then faced a 'melting pot' that caused heterogeneity).

You should not believe that many human populations lived in isolation for long times An Aboriginal Australian Genome Reveals Separate Human Dispersals into Asia says "We show that Aboriginal Australians are descendants of an early human dispersal into eastern Asia, possibly 62,000 to 75,000 years ago.  ... Our findings support the hypothesis that present-day Aboriginal Australians descend from the earliest humans to occupy Australia, likely representing one of the oldest continuous populations outside Africa."

The answer is basically 'No.'.
Too much mixing has happened since then. Fortunately, in most of the world we had scientists 2000 years ago describing facial features, and in part of the world (i.e. China) we had scientists describing facial features 4000 years ago.
We do occasionally recover viable DNA samples from both 2000 and 4000 year old corpses, also actual corpses that still retain significant vestiges of their facial features, but expecting to recover even general facial features over hundreds of generations from present DNA is quite frankly unrealistic.
The good news is that human facial features aren't actually super variable; humans are just super good at spotting small differences (which comes with the territory as social animals). The bad news is that as a modern reader of latin or chinese texts on phylogeny (if you can find them, which I won't guarantee) the subtle differences in what they mean when they describe a nose as, let's say hooked, will probably be lost on you, or me, or any of us.
Your best chance is probably sequencing corpses from the relevant era and matching them up with phylogenisists' descriptions to form an idea of what they were talking about; and you might end up with a general sense of what people looked like.
I expect it will lead to severely underwhelming results, but I suppose it's worth a shot.


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Are there proteins with multiple motifs?
Does each protein adopt a single specific structural motif (zinc finger for example) or are there any proteins with multiple motifs along the chain?

Your question is very unclear. Please [edit] your post to add context and explain exactly what you're asking.

@MattDMo I think some of the confusion is my fault. I suggested some of the wording, here : http://biology.stackexchange.com/questions/49168/does-protein-structure-depend-on-phylogeny but didn't quite get what the real question was. I'll make an edit, and Muna Ar can revert if it's not right

You are right @gilleain still waiting for answers though :D

Most large proteins contain multiple motifs; if you search online for pictures of protein structures, this should be immediately evident. Here's an example from something I was working on the other day: the WD40 repeat motif. It appears in many proteins, but those proteins are certainly much more than a bunch of WD40 units. If you investigate some of the proteins listed at the bottom of that Wikipedia page, you should be able to confirm that they are complex and made of many different sorts of domains, shapes, and parts.
You also mention zinc fingers; those are a DNA-binding motif that show up in many, many different DNA-binding proteins. Those different DNA-binding proteins have many different functions, and their specificity is handled by a vast array of different sorts of motifs and domains that sit on top of/outside of the zinc finger itself. The Wikipedia article on zinc fingers shows many different structures in which zinc fingers can be embedded, and even those structures are only small parts of the actual functional proteins that perform work in a cell.


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Does sodium lower the harmful effect of potassium on kidneys?
As far as I have read so far, it seems that potassium and sodium are trying to expel each other from the human body. A lot of documents on the web say too much sodium pressures the kidneys could cause a kidney failure. The same is also said for potassium.
If a person eats a lot of potassium-rich foods, does increasing sodium intake cancel out the harmful effect of potassium on the kidneys, or just double the harmful effect (he/she gets the harmful effect from both potassium AND sodium)?

Chemically speaking, sodium and potassium are very, very similar, and also pretty common, and our body needs both.
Due to their similar electrical properties in particular, they are used as kinds of 'counters' in some processes in the human body, as they can be distinguished to some extent by other processes, and the balance of the two is important.
What it is important to note, however, is that more potassium than sodium is needed, so an overly-high-potassium diet is rarely considered a health risk, even if only due to it being infrequent. People tend to be potassium-deficient rather than sodium-deficient.
Generally speaking, unless you are consuming way too much of both, having a potassium surplus is less problematic than a sodium surplus, and harmful effects certainly don't "stack", at least not trivially. Rather, extra potassium will tend to offset extra sodium, ameliorating rather than aggravating health effects.
Even so: All of this can vary wildly with general diet and other factors, so the prudent thing to do regarding ones sodium/potassium balance is to see one's doctor and have blood work done.


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Interspecies competition and pathogen
Following my answer to this question, a debate ensued on whether the loss in population of one species (namely red squirrels) due to its lesser resistance to a pathogen brought by a competing species (namely squirrel parapoxvirus and grey squirrel) should be labelled as a result of interspecies competition or not. Here I will try to state it as a question with in a more general setting. I'll give my own answer to it, and would welcome other views on the issue.
Assume the following: Species $A$ lives in a closed ecosytem and has reached carrying capacity $A=M_A$. At time $0$, a new species $B$ is introduced which is in competition with $A$, and additionally bears a pathogen to which it is resistant but which causes a high lethality rate in $A$.
It is observed that $A$ dimishes while $B$ thrives. Can we necessarily ascribe it to interspecific competition?

If you are specifically thinking about longer-term, evolutionary effects (see tag) I think that you should make that more clear in the actual question. As it is written now, I don't really see why [tag:evolution] is relevant.

No, you cannot for certain ascribe it to competition, without further information. The mediation by a pathogen is similar to the effects on prey species that are indirectly caused by shared predators (e.g. Prey B increase -> Predator X increase -> more predation on Prey A). Such effects, which can be tricky to separate from direct competition, are usually called apparent competition (see e.g. the classic paper Holt. 1977. Predation, apparent competition, and the structure of prey communities. Theor Popul Biol 12).
However, to some extent, the terminology used may depend on what you view as "the environmental background". All species have lots of adaptations to certain aspects of their living environment, and these naturally differ between species. Some might be more resistant to a certain pathogen (of to drought or other abiotic factors), but this might trade-off against other traits. I that respect, you might view species B as outcompeting species A in a certain environment (e.g. in the presence of the pathogen). However, since you specifically know about the pathogen (which is the focal point of the question), and that species B will probably function as a host/source population of the pathogen, I think it is more useful and informative to label the effect as apparent competition. To partition the direct and indirect effects you will however need moe information.

There are two possible effects on the evolution of A:
(i) interspecies competition with B which effectively reduces the carrying capacity, which can be modelled by writing $M_A^{\textrm{i}}(B)=M_A \frac{A}{A-\alpha B}$ (Lotka-Volterra model), and
(ii) infectivity with an infection rate $k_I A B$ which can be treated as direct mortality if pathogen is 100% lethal for A (which is a good approximation for red squirrels it seems, here we've even supposed A once infected didn't live long enough to pass disease).
The question is: can we have a population reduction even if there is no interspecies competition, i.e. $\alpha=0$? The answer is yes, since as long as $B>0$, there'll be a decay of $A$ to a fraction of $M$ (with a simple logistic model, this would be $\frac{r}{r+k_I M B} M$ where $r$ is the rate of natural increase)
This matches with the interpretations of Tompkins et al transcribed in National Geographic

You should give your suggested answer with the question. I edited your question accordingly, feel free to edit further. I also tried to make it a bit clearer as I did not understand some of your phrases. Please also check for misconceptions I introduced. I will try to suggest an answer to your question in the following days (little time these days ...).

I'm not sure why I should put the answer in the question-- it's a possibility offered by SE to provide your own answer to your questions, and allow SE process to discuss and improve them independently of question. Thanks for your other edits anyway, I'm incorporating them.

@AlexDeLarge self-answering questions is not only allowed, it's encouraged.

@MattDMo I know. But I just felt it would fit the question better than as a self-standing answer and therefore suggested an alternative. I have no problems with it being the way it is, though. :)


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Rate of production of enzymes in human
In the metabolic pathways, each of the reaction needs an enzyme(protein) in order to occur successfully. Is there any quantitative measure that can be associated to this enzyme? Like synthesis rate of enzyme, degradation rate, mRNA transcription rate, enzyme activity, amount of enzyme present per unit measure of protein in the cell and if there is rate of generation of the enzyme's product, the rate of production of this enzyme in the human body, etc? I wanted to know the list of features that can quantify enzyme activity in the cell.

Your question is very unclear. There are plenty of quantitative measures when looking at a particular protein - synthesis rate vs. degradation rate, mRNA transcription rate, enzyme activity, amount of enzyme present per unit measure of protein in the cell, rate of generation of the enzyme's product, and on and on and on. Please [edit] your question and explain exactly what you're doing and what kind of data you're looking for. This is definitely an XY problem.

@MattDMo edited the question. Is it clearer now?

This is very broad. Measures of abundance and synthesis rate of enzymes (and other proteins) can be found in proteomics work such as the paper mentioned by @tsttst below. Measurement of enzyme activity is completely different, and is often studied using isotope-labeled metabolites in a technique known as metabolic flux analysis, see for example http://msb.embopress.org/content/2/1/62.abstract  Both are large, active research fields.

Your question already answers a fundamental point: namely that there are several distinct quantitative measures that can be associated with enzymes (the list could also be extended, and you will discover more in biochemical textbooks...).
If experimentally or theoretically accessible, one additional important quantity is the formation of product over time divided by biomass ( e.g.: Jacob et Monod 1961)

I wanted to know all those points and how they are calculated...

Note that the more direct quantitative measures usually require enzyme-specific experimental assays (and measuring the activity within cells usually is even one step up - and something that has only been achieved for very few enzymes). If you want to look at quantitative measures, which can be measured well for most enzymes (and quantities that can be estimated reasonably well by models based on those measures), you could find them (for some cell lines and growth conditions) in Schwannäusser et al. 2011 http://www.nature.com/nature/journal/v473/n7347/full/nature10098.html


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Method of figuring out how much of a certain mRNA is present in a bacterium
I am trying to develop a method for figuring out how much of a certain mRNA is present in a bacterium. This is what I have so far:

Perform a mRNA extraction
Using Electrophoresis, to isolate the wanted mRNA strain (based off of size)

Now, I am not sure how I would quantify the amount of mRNA. I was thinking of using nano drop to test concentration, but I am not sure if that will give a good enough answer. What other methods could I use to quantify the amount of mRNA in my sample?

You should be running qPCR to quantitate how much of a certain mRNA sequence is present in a sample. Remember that there are thousands to tens of thousands of different mRNA sequences present in an RNA prep, not to mention ribosomal RNAs, transfer RNAs, etc. If you then run your RNA prep out on a gel, you're just going to get a smear. Even if you cut out a portion of the gel that corresponds to the expected size of your mRNA of interest, there are going to be lots of other sequences present in that portion as well, so doing a gel purification step then measuring concentration with Nanodrop (which is quite accurate within its working range) won't tell you anything.
Quantitative real-time PCR (qPCR), on the other hand, when run with appropriate controls and standards, can give you a very good idea of approximately how many copies of your sequence of interest there are per nanogram of total RNA.

So I can run qPCR with the standard curve ect... to find the number of mRNA. But how would I isolate the fragment of mRNA I want to test if a gel will not give me good results?


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Why and where do red blood cells die?
Textbooks commonly state that red blood cells are removed by the liver and spleen. Do those organs destroy the red blood cells within capillaries that course through those organs or are they transported into the liver/spleen cells to be broken down into their constituents? What causes them to be destroyed/removed from the circulation?

RBC's lifespan is about 120 days. RBC's don't have a nucleus or endoplasmic reticulum, but they do have enzymes in the cytoplasm, capable of producing ATP from glucose. This energy is used mostly to maintain the structure and flexibility of the cell. The erythrocyte is a biconcave disc, that is ~7 micrometers in diameter, but the cell is pliable and it should be able to squeeze trough narrow spaces without breaking the cell membrane. Over time these metabolic systems become less effective and damaged, and the cell slowly becomes more fragile and prone to rupture. Spleen has special trabeculae (bands of connective tissue) in its red pulp, that the blood passes trough. The spaces between them are narrow and "old" RBC's tend to rupture while trying to squeeze trough. Then macrophages "catch" any cell fragments down the stream. This can happen anywhere in the body, but spleen and liver are kind of filters for blood contents.

References
Guytons physiology textbook
Ross histology textbook

To take the easiest bit first: Red blood cells are destroyed because lacking a nucleus, they aren't quite as powerful as other cells when it comes to self-repair and longevity.
As for where; it really is all over the body. They are swallowed up (literally) by macrophages lining the blood vessels, which are particularly concentrated in the liver, spleen and bone marrow, but present everywhere.
As they age, they deform, and the macrophages are capable of recognising this deformation and reacting to it (by eating the red blood cells).
When the macrophages have eaten and destroyed the red blood cells, the nutrients they contain are returned to the blood plasma, and captured in the bone marrow for production of new blood cells.
(This pattern is common in a lot of systems, by the way: Even though the liver is the primary organ to break down toxins, for instance, most cells in the body has some limited capability for doing so; this is true of many functions.)

Ref:

http://bril2002.narod.ru/bllod56.html
https://en.wikipedia.org/wiki/Drug_metabolism#Sites


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Evolution of complex organs
If it evolved, how is a feature selected through a long time span with useless function before the feature becomes complete?
For example, an eye is a very complex organ consisting of countless small features. According to evolutionism, every such small feature should be formed by evolution over long time. But most intermediate features would be useless until the small incremental features are accumulated to provide any useful function good enough to be selected by nature. How do evolutionists explain this intermediate useless features and natural selection? I would appreciate if someone doesn't direct me to another long article but provide an essential succinct explanation. (think of all the organs' intermediate state.. would they survive?)

You really should try to write a short comprehensible title. And this is a question and answer forum, not a debating society or a text book. If I suggest you read The Blind Watchmaker this is because Dwarkins went out of his way to argue this very point in that book. Why should we provide you with a summary? In any case, as I believe you already stated that your attitude to evolution was based on religious belief, you're not likely to be convinced by argument.

This question has been asked many times on this site. See for example http://biology.stackexchange.com/questions/49209/how-did-the-cardiovascular-system-evolve

"an essential succinct explanation" of a complex process is never helpful. Learn about it if you really want to know what it's all about. As a Christian, learning molecular biology and evolution actually made me appreciate the complexity of creation and the compassion shown for the adaptability of creation to change. Read something by Francis Collins, a believer and the head of the Human Genome Project and current head of the National Institutes of Health. It's enlightening.

@anongoodnurse I disagree that "an essential succinct explanation" is never helpful. Having a very basic framework on which to build a deeper understanding can be, and is, vital. While 'Simple systems develop, interact, grow interdependent.' is utterly simplistic, it captures the thrust of the process and gives something to build on. Simple explanations should not be dismissed so readily.

You're working under the false and foolish assumption that intermediate traits are useless and should be selected against.

A little bit of terminology first
"evolutionism" refers to a set of beliefs from the 19th century. Evolutionary biology is much more than "evolutionism" and I suppose you are more interested is the current day understanding rather than a historic perspective on the question, is that right?
An "evolutionist" is a person that believes in evolution without necessarily understanding it (as by opposition to "creationist"). Someone who study evolutionary processes is called an evolutionary biologist (or often evolutionary geneticist although it does not exactly refer to the same field).
Issue with the question
It is a very standard question as it is a common fake argument from religious extremists that refuse to accept the theory of evolution. A good answer is necessarily long as (1) there are a number of processes of interest and (2) within the question it is clear that the person asking it has very little understanding in evolutionary biology. I will try to keep as introductory and short as possible. Asking for a short answer for this question is like asking for the name of the most populated city in the USA and authorized to use only one word in the answer (while "New York" is in two words).
Answering to a specific case
For the reasons explained above, it is often easier (faster) to explain for a specific case than in theory for a general case. Here are two examples from Biology.SE

How did the cardiovascular system evolve?
When did vision evolve for the first time? and What is the minimum eye?

Source of information
There are good books designed for people that know nothing to evolutionary biology to get an introductory answer to that question. The Blind Watchmaker is one such book for example. More generally speaking, one might want to have a look at  Understanding Evolution by UC Berkeley, a very introductory source of information on evolutionary biology.
Key Concepts to answer your question
Quickly speaking here are a series of quick concepts that are necessary to understand in order to answer this question.

Genetic drift

There are a number of different forces that affect evolutionary processes. Layman often think of natural selection as being the only force causing evolution but this is wrong. Genetic drift refers to the random sampling of individual at one generation to build up the successive generation. The relative importance of drift to natural selection in driving evolution of a population depends on the effective population size. Have a look at Why is the strength of genetic drift inversely proportional to the population size?.
Typically a phenotypic feature that explain little in the variance of fitness in the population might well increase in frequency in the population just through drift.

Fitness effect of intermediate states

It is common for layman to assume that intermediate states ought to be deleterious. This is a typical logical fallacy called argument to ignorance. In reality the intermediate states might well be neutral or only slightly deleterious (and therefore be mainly affect by genetic drift) or might even be beneficial.

Existence of intermediate states

Darwin framed his theory into the idea that evolution is a very gradual process. As we know today, this is far from being true. Evolution can actually occur through a big steps. There are single mutations that double the amount of genetic material, there are single mutations that completely affect the physiology or anatomy of an individual. There are cases of horizontal gene transfer (transfer of genetic material between species) as well that can cause sudden important change without having to get through intermediate stages. It is sometimes wrong to assume that there must be intermediate steps.

Phenotypic flexibility

While you haven't raised this question, a common creationist argument is to say that if a mutation occurs to make a bone a big longer, then one organism would simultaneously need mutations that would make muscles, nerves and other tissues longer accordingly. In reality our developmental process is quite flexible to an environmental change or to a mutational change. This flexibility is very much used in medicine and agriculture.

Why do we talk about the "Theory" of evolution
This is just a sidenote but you might want to have a look at this post

Thank you for explaining the down vote so that I can improve my post accordingly. Note that the downvote appeared about 10 seconds after I posted my answer. It seems therefore impossible that the one who down voted had time to read my answer.

Not the down voter, but it bears mentioning that it's 'beliefs', not 'believes', also 'believes', not 'believe'.

Sure, I explained why the answer has to be of a certain length.

While I agree that your answer is illuminating, thorough and good, the core concept I think can be expressed in a shorter phrasing: 'Simple stuff developed, interacted, got more complicated.' It's not a complete answer, nor even ultimately a satisfactory one, but it does get a core point across, and leaves something to build on. Biology is necessarily full of these kinds of simplifications, because life is just… It's just all over the place, man. It's crazy. Complete lunacy. A good and complete answer can't be shorter, but a very rough and ultimately helpful outline can be, I feel.

I'm not the down voter. I read your answer but again another long not-convincing words evading my core question. I'm on something else but will try to add more comments later. I already read about eye evolution but not convincing at all. Still seems like a far-fetched theory which fails to explain things.

You should probably follow an introductory course to evolutionary biology then and you will be able to read more advanced explanations. I also think that going through example specific would help a lot (but I recognize the interest of a question that seek for general explanations). Typically, you said that something still remained unclear to you about the evolution of the eye so you might want to investigate this particular subject in a post.

my question is not about the eye, can any one suggest any 'intermediate organ?' don't you all think we should be seeing many such intermediate organs having meaningless features?

To put it succinctly: None of the parts of any complex organ present in humans today appeared as they are now.
The parts of the organs we have now are useless in isolation because they have over the last ~500 Ma developed to rely more and more on each other, becoming more and more interdependent.
To use the eyes as an example, the very earliest ones (some of which are still found today, in mollusks, for example) were just light-sensitive skin spots or light-sensitive clusters of core cells in the nervous system. Additional features developed around these, and over time became more interdependent.

The question was not specific to the eye and discussion on the evolution of the eye already exist on Biology.SE

@Remi.b: The eye makes a good case study. And a discussion on the issues with the underlying question already exists on Biology.SE (I assume).


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Do our blood vessels exude chemicals?
I watched a youtube video explaining how mosquitoes detect our blood vessels through "chemicals that our blood vessels exude naturally"
I was wondering if it's true that our blood vessels exude any chemicals, and which chemicals are they.
[Link to the video in case anyone is interested https://youtu.be/rD8SmacBUcU]

If so, it's probably more accurate to say that mosquitoes have developed a way to sense chemicals our blood vessels exude, not that our blood vessels exude chemicals mosquitos can sense. It's a subtle difference, I'll agree, but kind of important.

@WillihamTotland Thanks, i edited out the mosquitoes part in the title, since my interest is really whether or not our blood vessels do exude any chemicals.


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Molecular Logic GATE
Currently either PET-Fluorophore or FRET is used as output of the molecular/DNA-based logic gate. Likewise, in a logic gate, lets say YES GATE, you provide an input to the logic gate and in return you got fluorescence. Please help me understand what other transfer method can be used as the output. I want to develop a complex system i.e. connect multiple logic gates with each other which, definitely, cannot happen if molecular logic gate would return output such as fluorescence, can any other method be used?
Thanks in advance

You have to be more specific than this.


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Are there dichotomous keys for identifying medical conditions?
I know dichotomous keys are often used to identify flora and fauna.
I was wondering if they are also used in medicine for identifying diseases -- are they? If not, why not?

For histopathology they use them all the time to describe cells and tissues, very much as they are used to describe biological entities.  Characteristics like size, cytoplasm to nucleus ratio, grouping, staining characteristics, immunohistochemistry and now molecular attributes are all used to categorize a cell of interest.  For cancer, the identity of the malignant cell is crucial to diagnosis and subsequent effective treatment - based on successful treatments used in the past for people with that type of cancer.
Here is a histopathology dichotomous key I found at Noelways.com

There are several doctors that post on this site, so hopefully one of them can give a better answer. Anyways, several years ago I took a certification program as an emergency medical responder (basically the lowest level of EMT in my area). Various dichotomous keys are used to assess patients. These were not diagnostic but rather used for determining correct patient management. For example, here is a key for airway management. Obviously, these would be committed to memory.

I think the equivalent concept in medicine is the differential diagnosis.

Welcome to the site. We are looking for longer, informative answers. See the guide: http://biology.stackexchange.com/help/how-to-answer

I grant that longer answers are more useful, but it's all I had, not being a doctor. Should we have waited three months instead, for the more helpful and complete answer? I actually don't see anything on your help link that refers to length of answer. In fact, I would argue that my answer falls under "Have the same problem?", which says "Help us find a solution by researching the problem, then contribute the results of your research and anything additional you’ve tried as a partial answer. That way, even if we can’t figure it out, the next person has more to go on." (We can take this to Meta.)

Sadly, no. In plants, you know exactly the number of sepals, the number of petals, the shape of leaves, the type of pollination and other variables used in 'travelling' through the key.
Equivalently, a dichotomous key in medicine would require that a patient with a certain disease display all of the signs and symptoms so-and-so (eg. belly pain, vomiting) and none of the signs and symptoms this-and-that (eg fever and cough) for any given disease. Very very sadly, this is not the case.
As an example, appendicitis: in the typical clinical picture, a patient presents with dull pain around the navel for a few hours with loss of appetite, before progressing to sharp right lower quadrant pain with a low fever and nausea. Simple? No. This presentation appears in about 30% of patients with proven appendicitis, the rest may or may not have had pain around the navel, may or may not have lost their appetite, may or may not run a fever that may or may not be suitably low-grade, they may or may not have been nauseous, they may or may not have vomited, they may or may not have accompanying malaise, some even show up without the basis for diagnosis (sharp right lower quadrant pain)...
To make things even more complicated, there's a significant number of patients who DO present with the classical signs of appendicitis (including the obvious appy symptom of sharp lower right quadrant pain) or dangerously similar, but don't have it. What do they have? Your guess is as good as mine, the differential diagnosis is loooooong, and includes things ranging from "OR RIGHT NOW BUT IN A DIFFERENT SPECIALTY!!!!" to "Don't you dare take that patient to surgery, it could kill them!"
And that's just a 'simple' appy. There's a reason they call it the art of medicine.

Interesting perspective. But in my mind, anyway, it's a number of dichotomous keys that overlap. This comes together in the differential. It all happens on almost a subconscious level after many years of experience, and becomes "a gut reaction" (which is really not intuition at all), that which you call art. But to say there are no dichotomous keys in medicine is an oversimplification for sure.


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What does the phrase 'background level' mean?
I was reading BIOS Biochemistry and stumbled upon a phrase 'background level' in the following excerpt $-$

The lac operon contain lacZ,lacY and lacA genes encoding $beta$-galactosidase, galactoside permease and thiogalactoside transacetylase, respectively, preceded by an operator site and a promoter. The operon is transcribed by RNA polymerase to produce a single polycistronic mRNA that is translated to produce all three enzymes. When lactose is present the background level of $beta$-galactosidase converts some lactose to allolactose, which induces transcription of the lac operon.

What is meant by background level? Does it refer to the basal level of transcription, the constitutive transcription of facultative genes?

Why do you see the constitutive transcription of a gene as wasteful? These fulfil usually important roles...

The phrase “background level” is generally used in an experimental context where you are measuring the effect on a variable of some agent or stimulus. You might expect that your control condition(s) — without the stimulus — would give you a measurement of zero, but often that is not the case, and one needs to subtract this control value — often referred to as ‘background’ — from the experimental value.
Such background values can be real — e.g. background radiation — or artefacts caused by fundamental limitations in the measuring system used. Generally the implication is that their origin is unknown or is not specific. That is why I think that the use of the term ‘background’ in the context of the lac operon is somewhat unfortunate. I would have used (and encourage you to use) the term ‘basal level’ instead*. As the text states, there is a low — but specific and necessary — expression of β-galactosidase in the non-induced situation, so that when lactose is added some of it can be converted to the inducer, allolactose, which will then result in the synthesis of the greater amount of β-galactosidase needed to deal with the rest of the lactose.
*Footnote
In fact I hate the term ‘level’ except for water in the bath tub, and I would have used ‘amount’ or ‘activity’, but that’s not the point at issue here.

Love the footnote of you answer... I also greatly dislike the word "level" because it is not very specific and can mean different things in different situations. Many individuals use the word "level" when they more accurately should be saying "concentration".

Concentration is a measure of the expression level. I, however, do concur that people use this word casually which would is likely to mislead others. "Background level" is not a suitable usage at all.


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When does the first "random mutation" of DNA (have to) occur?
When reading about how evolution happens, "random mutations" are often spoken of.
As far as I understand, "random mutation" refers to the unsuccessful self-replication of DNA (the new version of which is then passed on correctly). But when does this change happen? During fertilization? Shortly before (in the sperm or egg itself) or shortly thereafter? And what is the last possible time for that to happen so that it gets passed onto every cell in the body and eventually brings forth a new physical trait?
I hope the questions make sense, I don't have a lot of background in biology.
Edit for completeness: When is the earliest possible moment for a mutation to take place? (A mutation that will ultimately make it to the offspring and eventually cause a new trait.) Is it in the ovaries/testicles or even before that?

I think you will do better not to put things like random mutations in scare quotes. It immediately puts you in a category hostile to science.

Random mutations happen everywhere in the body all the time. Most are harmless, some cause problems, some cause cancer. Some are beneficial. If a beneficial mutation occurs in the germ cell line, it will be passed on to the offspring. Depending on how beneficial it is, it can spread like wildfire (the mutation allowing lactase to continue to be expressed after infancy is a good example of this, as is sickle cell trait); if it is harmful, the carrier may die before birth, in infancy, etc. If it causes a later onset disease (e.g. early Parkinson's)1, the carrier has time to mate, reproduce and pass the disease on to their offspring. More and more diseases are being found to be genetic in nature now that genetic studies are so much easier to perform.
Again, for a mutation to be passed on, it must occur anywhere in the germ cell line of a parent, right up to the last stage before being released as an ova or a sperm cell, during fertilization, or during the very early stages of embryonic development in cells genetically programmed to become germ cells. If it occurs after fertilization, it will not affect that person, but its offspring. Depending on how early the mutation occurs, it may affect other parts of the reproductive system as well.
If a mutation happens in an embryo in a non-germ cell line, it may affect that person mildly, profoundly, not at all, or the embryo may die if it is a deleterious mutation in a critical organ system, say the heart.
But you need not put random mutations in scare quotes. I'm pretty sure you don't trust me, but they happen all the time, in every tissue, in you yourself as well as in everyone you know and everyone you don't know. And, by the grace of God, many of them can be repaired, and we don't ever have any ill effects from them. Alas, not all are repaired, and some lead to cancer.
Hereditary Early-Onset Parkinson's Disease Caused by Mutations in PINK1

Thank you for this great answer! I'd love to upvote, but it doesn't let me. The first three paragraphs make a perfect answer in terms of what information I was looking for. Though the rest, dunno where that came from—was it because of the quotation marks? Haha, they were partly in the sense of "seeing this term often but not sure if established scientific term hence quoting it" and partly "not sure if this is what I want to ask about". Eventually comparable to how some technically less versed person might put quotes around "tablet" or "smartphone". Powerful little fellas.

The question had nothing to do with faith. Why include it in your answer.

I agree with @Floris comment. I think you let yourself react too much to the quotes around the term "random mutation" :) Also, you say Science and faith are not mutually exclusive. This is a question of philosophy and not science and should not be present on this website (or only as a tiny note that is clearly label belonging to philosophy and only if obviously aligned with the interest of the OP). Finally, not to be too picky but in the middle of these discussion, the use of the expression grace of God sounds quite inappropriate.

@Remi.b - That is a bit pickly. Have you ever heard the expression, "There but for the Grace of God go I?" It doesn't have a necessarily religious connotation anymore.

@KarloGrba - Sorry for the assumption!

@Karlo Grba, Hi, I like answers like this which is to the point. I had this question in mind for a couple of days. When biologists say humans have about 65 mutations per generation, it should actually arise mostly during the fertilization through meiosis and before large scale celluar differentiation which is a very short term like a few days. After the gametes are formed, mutations should be repaired like other normal cases(mutations are minority already). Is this what biologiests think? (I mean, mutations effective for evolution takes only in couple of days..!!)

You need to understand that whenever a cell duplicate there is a DNA replication process, which means even when you are growing up there is DNA replication process, whatever or wherever you are there is DNA replication because cells in your body don't stop duplicating, which means every cell duplication hold a risk potential of causing a DNA mutation but that potential's probability is as low as one in a billion cell duplication and even if there is any mistake in the DNA-replication process the DNA-Polymerize-enzyme have repairing abilities which correct the mistakes, well sometimes even  DNA-Polymerize-enzyme don't repair these mistakes which cause a disorder in some gene's task, these disorders might be helpful and make the creature grow faster or reproduce faster, or it might be harmful and cause diseases or some kind of three hand human or any kind of disorder and that depends on which gene that has been affected by the mistake in the DNA-replication, that means if the gene was in charge of the cell's duplication process this might make the cell duplicate forever and cause cancer, on the other hand, most of the times the mutation doesn't happen normaly because DNA-Polymerize-enzyme failed to do it's job but it happens because of some chemicals or even being exposed a lot of time to the sun rays. Bear in mind that fertilization or anytime before or after it have anything to do with DNA mutation as far as I know, anyway I might be mistaken, I have answered you by the information I got in the school.

so most people already know cells undergo muation and it is repaired. Of course these most (99.999%) mutation has nothing to do with evolution because it's not in gamtes cell and not related to reproduction. THe mutation in the gametes only affect next generation and the mutations before large scale cell differentiation of the gametes only affects DNA pass-down to the next generation, which is during only several days or weeks? I think this is against our intutition with the mutation proability and "65 mutations per generation" measurement.


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(Bioinformatics) Protein-Protein Software Prediction
I'm trying to figure out Protein-Protein interaction of two proteins without known crystallography structures. Any way software can predict this without the known structure? The problem is most software that does it is just textmining through articles, I was seeing if they can do some sort of prediction based off of just known sequences and other trivial things?

What options have you tried so far? There a lots of options, but it depends on what biological question you're asking, and the resources available to you.

Based on what I know you won't be able to run docking simulations on a sequence. The reason being our technologies for predicting 3D structures from sequences are not accurate enough to determine biological activity. Currently there is a competition every year for protein structure prediction software and I'm almost certain if someone comes up with a 100% accurate one there will be a nobel prize in it for them. Software that could predict structure from sequence accurately would radically accelerate molecular biology research.

This review about protein docking will hopefully get you started.
Xue, L. C., Dobbs, D., Bonvin, A. M., & Honavar, V. (2015). Computational prediction of protein interfaces: A review of data driven methods. FEBS letters, 589(23), 3516-3526.
There is a page where they provide a short description about the different algorithms used, as well as links to the web servers. I also believe that most of these website should have a downloadable source code that you could compile and use on your own computer/cloud.
Here is a brief summary of the main methods highlighted by the paper:
Homology-based methods. In this approach, biological properties of a query protein are inferred from its homologs. The assumption here is that homologs share significant similarity in their sequence, structure and functional sites. Therefore, this approach performs best when close homologs are available.
Template-free machine learning methods. In this approach, machine learning algorithms are used to classify a target residue as either interfacial or non-interfacial, based on properties of both the target residue and the neighbouring residues. This approach is best used if there is limited availability of homologs, or when templates are not available or of poor quality.
Conclusion: If you have the sequence data available, then the 2nd approach seems most appropriate. You could also apply both methods and see the extent of agreement/disagreement between the methods, i.e, you could use the machine learning approach to detect the interfaces, and subsequently validate your docking predictions based on sequence data, if close-enough homologs are available.

Great succinct answer for a pretty vague question!


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Can a zombie apocalypse really occur?
Now, before you flag this question as blatantly off-topic, I claim to have a scientific basis for this(!): not some drug or remote control, but parasitic infection.
While reading about behavior altering parasites and parasitoids, I found this:

Parasites that induce behavioral changes in their hosts often exploit the regulation of social behavior in the brain...For example, Toxoplasma gondii attaches to the hypothalamus rather than target a specific cellular pathway; this broad targeting leads to a widespread increase in host dopamine levels, which may in turn account for the loss of aversion to cat odor...This rise in dopamine levels induces a loss of aversion to cat odor in the rats, increasing the risk of predation by cats, T. gondii’s definitive host.

Now, if a parasite can prevent mice from being afraid of cats, how hard would it be for another parasite to prevent humans from caring about each other's life(!)? Can a parasite develop some method by which it can alter behavior of humans in such a way that they just start killing each other for no reason? How easy/hard would it be for a parasite to do so?
Note: although it is just a curiosity question about whether it is possible or not, giving some description of neural pathways which stimulate social behavior in humans and how they are regulated would be much more appreciated.

interesting question, however you might still want to consider posting this question on skeptics.se

@jordizambrino well I didn't  wish to involve skepticism in the question, it is as general as was yours "can magnetoreception occur in humans?" Also, (if you've given close vote) can you please explain how the question is opinion based so that I can improve it?

First of your questions is partly based on skepticism, secondly in my question on magnetoreception I cited a paper by nature (nature.com/nature/journal/v301/n5895/abs/301078a0.html) which suffices as an appropriate source and lastly I did not vote to close this question as I am interested in which direction this question will go.

Okay let me clear this out ( as it seems to me that your opinion would be shared by many others) firstly, as I say in the question that its mere curiosity about whether its possible or not, second I've also cited a wikipedia paper that it occurs in mice, so can it occur in humans (just like you cite that cryptochromes are there in humans so can they attain magnetoreception). Anyways thanks that you didn't flag it, but an upvote won't hurt ;)

Zombies are reanimated corpses, not just people who murder other people for no reason. There are many diseases and conditions that can possibly lead to people losing certain inhibitions and potentially unpremeditatedly killing other people. I suggest you reword the title to reflect the actual question.

@harryvervet I don't actually know what to call it then. I saw a movie in which some people took an infected drug which made them zombie, and the ones who killed them also called them zombies. So I thought it would fit here.

To me the question is likely going to require a primarily opinion based answer

Sorry guys but I just can't understand how the answer would involve opinion. Just some description of what neural mechanisms would need to be affected to bring this condition would be more than sufficient.

The OP specifically asks for a scientific based answer.

There are many examples of parasite manipulation in nature, if you want more examples you can look up the paper of Lefevre and Thomas (2008). I think the key is, in order for a parasite to develop such behaviour, that it should be giving them a fitness advantage. So I don't think it would ever happen for no reason. The paper discusses a few examples where the manipulation results in a higher transmission rate by the parasite.
I guess that because parasite manipulation is happening in many other organisms, it's probable that it happens to some extent in humans too. There are for example indications that when we are infected with  malaria, the malaria parasites can change our odour profile to make us more attractive to mosquitoes, thus increasing it's transmission (Batista et al. 2014, De Moraes et al. 2014). There are also indications that our gut microbiota have an influence on our brain and behaviour, regulating anxiety, mood, cognition and pain, by communicating with our CNS (Cryan and Dinan 2012).

You've given a really nice answer, but I'm gonna wait for some time to see if I get some other response :)

If there are drugs that can cause this kind of disorder you described, then it is possible to engineer a microbe, that can produce these drugs and maintain a chronic infection, which does not necessarily kills the host.
Walking dead is not possible, human bodies cannot move with rotting muscles or without muscles, so you won't see real zombies, just insane ppl.


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Outbreeding depression in humans
Is there any evidence of outbreeding depression in human beings?

@Remi.b - why would this be a dupe? This question has nothing to do with the definition of species, but with the possibility to eliminate the genetic component of depression. I actually like this question a lot. +1

@AliceD The currently most upvoted answer provided in Does it make sense to classify all humans in a single species? specifically target the this question.

@Remi.b and is the convention then to close this one? I have seen many (still open) questions that are answered by answers to other questions.

@AliceD Ok. So, do you think I could just copy-paste the section 'Do we have documented cases of outbreeding depression?' of my answer at the other post to make the answer here? Keeping this post open eventually allow others to target more specifically this issue here while they can't on the other post that is a little bit broader in sense, right?

@Remi.b - worth a meta question isn't it? I can imagine this has made it to meta previously. I can take a look into it later. And copy-pasting, no. With additional targeted references to this specific question you can surely re-use your previous material. I do that all the time, but only as a starting point though. I would strongly encourage you to do that. Closing questions is so easy. Writing new original answers is more difficult, but so more rewarding! Thing is, strictly spoken this is no dupe. Overlap is everywhere. This question is more specific and imo better than the other.

Ok, I removed my close vote. I copy-pasted my answer. I did not add any info (or reference) though as the whole point of the question is to try to find more references and I already tried and failed to find other references of interest. Thanks Alice

Answer below is copy-pasted from the section Do we have documented cases of outbreeding depression? of my answer here.
Many cases of inbreeding depression have been documented in humans (McQuillan et al. 2012, Strauss et al. 2013, Lettic et al. 2008, Gellera et al. 1990) but cases of outbreeding depression seem much rarer if any!
I spent some time screening through the literature searching for potential evidence of outbreeding depression. The only paper I found is Udry et al. 2003.
Udry et al. 2003:

First, note that they do not place their results in the context of our present discussion and do not talk about outbreeding depression.
They report that children of "mixed-race" in US colleges report having more behavioural troubles. One would obviously note that there could well be true that "mixed-race" children experience a different environment (incl. social environment) than "non-mixed-race" children. Such results therefore does not suggest the existence of any outbreeding depression.
They also reports more skin problem in mixed-race children. Unfortunately, 1) their p.value is only slightly significant and 2) they track tens of variables without correcting for multiple comparisons and only one came out significant suggesting it is likely to be a false positive.

So, in short: No, there is little to no evidence of outbreeding depression in humans
It is not impossible that there is a publication bias in which researchers looked for inbreeding depression more than for outbreeding depression but I doubt it would be the case. Such bias seems possible only if the outbreeding depression, should it exist, would be very slight and hard to detect outside a rigorous scientific study. In essence, such potential publication are impossible to detect.

Great! +1 I am a huge fan of digging up old questions and with another vote you'll get your well-deserved revival badge. I love this :)


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How does TYRP1 affect the synthesis of black and brown eumelanin (on a biochemical level)?
TYRP1 (aka B-locus) is a gene in dogs that determines whether black or brown eumelanin is produced (assuming eumelanin is produced at all which is determined by the MC1R gene). I've looked at many papers and flow charts and now i have a contradiction: DHI seems to be the molecule that gives eumelanin a black color and DHICA a brown color. According to many flow charts, TYRP1 seems to be involved in the polymerisation of DHICA (not DHI). Mutations that cause a loss-of-function of TYRP1 will cause dogs that carry these mutations (homozygous) to have brown fur. But if TYRP1 is important for polymerisation of DHICA to brown, why does a loss-of-function of this very protein cause dogs to have brown coat color?
Where did I get it wrong?

The actual coat color is determined by the ratio of the products of two genes: Tyr and TyrP1. The first oxidizes DHI to Indole-5,6-quinone and forms brown pigment, TyrP1 on the other hand oxidizes DHICA to Indole-5,6-quinone carbolic acid, which forms black pigment. See this pathway diagram (from here):

So loss of TyrP1 activity is not harmful to general pigmentation but prevents the formation of black color, while the inhibition (or loss of function) for Tyr will lead to albinism, since no pigment precursors (from Tyrosine to DOPA can be formed.
You may also be interested in this paper: "TYRP1 and MC1R genotypes and their effects on coat color in dogs."

Thank you! Then, my error was that DHICA forms black eumlanin and not brown.


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What decides between the synthesis of eumelanin and pheomelanin on a biochemical level?
MC1R is a very well known gene where a loss-of-function mutation will cause the synthesis of pale/redish pheomelanin instead of black/brown eumelanin. MC1R is only a receptor which doesn't directly participate in the synthesis. it affects the expression and transcription of several important enzymes for melanin synthesis (Tyrosinase, TYRP1, TYRP2).
In one study (Ito, 2003) they proposed that increased tyrosinase activity and decreased cysteine levels would promote the snythesis of pheomelanin. Since MC1R controls the expression and transcription of tyrosinase I think it makes that mainly the increased tyrosinase activity is responsible for the decision between eumelanin and pheomelanin.
The question is whether this is correct or false or if we just don't know yet.

Let's have a look at the pathway first (this figure is figure 2 from reference 1), which shows the basic pathway of pigment biosynthesis:

The first important step, the oxidation of the amino acid tyrosine to Dopaquinone (DOPA) by the tyrosinase is the same for both pathways (eumelanin and pheomelanin production) and rate limiting.
The important step is the next one: Either the formation of Cyclodopa (for eumelanin) or Cysteinyldopa (for pheomelanin). As long as the concentration of cysteine in the melanocyte is above 13µM (see reference 1) the formation of pheomelanine is favored and biochemically much faster than the cyclisation of DOPA.
If there are high levels of tyrosine and normal to low levels of cysteine, the cysteine will be depleted at some point and only eumelanin is made.
The opposite will happen if either a lot of cysteine or little tyrosine is available. It will also happen, when the available tyrosine cannot be oxidized into DOPA when there is little or reduced Tyrosinase activity.
And this is actually what happens in the case of the MC1R mutation. MC1R is a receptor on the pigment producing cells which regulates the production of pigment upon external signals (as UV radiation to the skin) (see reference 2 for more details). When mutated is is not or much less functional leading to much less (or no) signals to the downstream gene (MITF) which regulate the enzymes for the pigment production.
Low signals lead to low tyrosinase production which then can only produce little DOPA. Since the cysteine stocks of the cells will not be depleted then, only pheomelanin is produced causing people with MC1R mutations to be red haired and having light skin and freckles.
References:

Chemistry of mixed melanogenesis--pivotal roles of dopaquinone.
MC1R, Eumelanin and Pheomelanin: their role in determining the
susceptibility to skin cancer