Is evolution true as Darwin said?

I saw an excellent public science talk a few weeks ago. The speaker presented 5 questions which, if you answer yes to, you can only come to the conclusion that evolution exists. Firstly though we should define evolution: Evolution is the change in the inherited characteristics of biological populations over successive generations.

It was one of the best arguments I've seen put forward so I'll try to recreate it here. Put this to them and see what they say - and just in case they say no to any, I've put answers in for you ;) There is no hard evidence for the first four points because they are so damn obvious that if people say no, even after a logic based argument, then all they will ever say is no, they shouldn't need a scientific paper.

1) Do individuals reproduce?

The answer to this is undeniably yes, you were the result of reproduction. Reproduction exists.

2) Is there variation among individuals?

Yes, again this is undeniable. Do we all look and act the same? No. Are some people taller than others? Yes. Some more physically fit than others? Yes. Is everyone's hair or eye color the same? No. See, undeniable. Variation exists.

3) Do some individuals die before they get to reproduce?

Obviously yes. Children unfortunately die (of natural causes) which means they do no get to reproduce. Just go look in a cemetery or open the obituaries page of you newspaper and you'll likely find some one who died before they could have reproduced. Some people also never reproduce, because of life choices or fertility problems. Variance in reproductive success exists.

4) Do offspring resemble parents?

The answer to this is also yes, when two humans reproduce they (normally) produce something that resembles a human. And when that human reaches maturity they will likely look a more like their parents than a random stranger. Personally I was looking at old family photos recently and I honestly though I had found a picture of me marrying my mother, that's how similar my dad and I look. Heritability of variance exists.

5) Does heritable variation lead to differences in reproductive success?

If you've answered yes to all of the above then you really should be answering yes to this one too. As a hypothetical illustrative scenario, imagine two male deer. One has big antlers and one has small antlers. The size of antlers is largely genetically determined. The male with big antlers is seen as more attractive by a female. She chooses to mate with him. She gives birth to his offspring (n=2, 1 male 1 female) who inherit his genes for large antlers. This repeats with several females in the population (n=10). The smaller male has fewer mating events (n=2) and therefore sires fewer males in the next generation. The next generation contains more males with large antlers (n=10) than small antlers (n=2). This is evolution, the change in the inherited characteristics of biological populations over successive generations.

Another example is humans. We know some men have low sperm counts leading to low probability of successful mating. Further, we know that male infertility can be genetically caused for example by Y-linked genetic defects. Therefore we can expect that males with low sperm counts, caused by Y-linked defects, will have fewer offspring than a healthy male (given equal opportunity to mate) and because all males inherit their fathers Y chromosome they too will have low sperm counts. They will be represented at a lower level in the population's next generation. Again, this is evolution.

Speciation:

It then doesn't take much to jump from this to speciation. It involves the introduction of isolating mechanisms. These can be things like geography (allopatric speciation), or sympatric mechanisms like morphology, behavior, or any trait which prevents one group of individuals mating with another.

I'll illustrate first, and take the more difficult type - sympatric speciation. Again imagine our deer population. This time there is variance in sperm morphology, and female reproductive tracts. Males can produce two different types of sperm, one (male type S) is a slow moving but more resistant to the hostile female reproductive tract (because it is resistant to all types of antibody the females can produce), the other is faster (male type F) but less resistant (because it is resistant to only some of antibody the females can produce). Female reproductive tracts vary in the number of different antibodies they produce, one produces "all" that can be produced (female type R) and the other only a subset of the full array (female type W).

What will happen is that type S males will be more successful when mating with type R females because their sperm survive (whereas type F males have no sperm fertilizing the egg). However, type F males will be more successful in sperm competition than type S when mating to type W females. Repeated over many generations, these incompatibilities will cause distinct mating groups which do not overlap, i.e. species.

In reality it is much simpler to demonstrate this with allopatric speciation. Here two groups of one species become isolated by a geographical feature, like a river. Over time these populations evolve differently (because genetic mutation is random and selection might differ on opposite sides of the river). When they get the opportunity to mate after X generations, they can't because they have evolved genetic incompatibilities (offspring fail to survive, eggs can't bee fertilized).

One of the absolute classic examples is an experiment using fruit flies by Diane Dodd. In her experiment she reared a population in two groups, one on starch based food, and one on maltose based food. After many generations (35 I think) the two groups showed mating preference, which is a reproductive isolating barrier, within their groups (mating pairs were more often formed from within treatments). Here is the paper.

Picture from http://evolution.berkeley.edu/

dna - What is the fiber axis in the Watson and Crick paper?

Short answer:
The term fiber axis is not in reference to the DNA model, it comes from the experiments that Watson and Crick used to guess their model. The fiber axis is basically the dimension along the length of the DNA strand.

Longer:

Watson and Crick created their model of DNA based on the esoteric experiment called X-ray fiber diffraction. To collect fiber diffraction data ( gathered by Rosalind Franklin actually) DNA is pulled out of a cell lysate and washed with buffer. It looks like a clear, liquid, string of snot (a technical term that is). Its stringy though because the long DNA molecules pull out and create viscous fluid where the DNA is pulled along the length of the snot fiber. Because the DNA is ordered in this one dimension, if you shoot a beam of X-rays through it, it creates a pattern on film that looks like this:

As you can see its got a nice X-shaped pattern. The DNA in the fiber is mostly aligned along the fiber, in the up and down direction. Because this is so, the spacings between the different layers is due to the spacings between the DNA bases and the x-pattern comes from the fact that DNA forms a double helix.

Some misc details - you have to use X-rays because their wavelength is about the size of an atomic bond and this is the scale of model Watson and Crick and Franklin and Wilkinson were trying to find.

The fiber axis is along the y axis (top to bottom) because the trail of DNA snot hangs down - it will sag if you hold it an angle.

Rosalind Franklin was a great experimentalist and she realized that the DNA snot trail dries out over time as the experiment would go on for days. She set up a moist stream of hydrogen gas blowing over the DNA strand during the X-ray experiment and so was the only experimentalist who obtained what we now know to be the true result - double helical DNA. As it dries out, DNA interconverts to the Z-DNA form I believe, which does not have the x-pattern and also confuses things because the result is a smear of the DNA helix converting from one form to another.

Francis Crick had actually predicted the X-pattern for helices. The structure actually required these two to come together to get the answer while the American genius Linus Pauling was working hard in California on the structure as well and would have won too if he understood how to keep his snot properly damp.

The reference for nearly all of this is Watson's somewhat self-centered but historically accurate book "The Double Helix".

After some surprisingly difficult Googling, I can't found a picture of DNA fiber... picture below. You can make some yourself from the protocol listed here and some saliva, soap and other common household items.

Neuroscience of temperature regulation and perception

I've found a good resource for this--an open-access review by Nakamura, "Central Circuitries for Body Temperature Regulation and Fever." In it, the author provides a nice summary figure of the circuitry involved in temperature regulation (see below). As I suspected, the hypothalmus is pretty central to temperature regulation. I had forgotten about the involvement of the peripheral nervous system in responding to environmental temperatures, which, now that I think about it, makes some amount of sense, but is still pretty interesting. It appears that there's a difference in the specific circuitry and neurotransmitters used in responding to warm and cold temperature (especially GABA v. 5-HT), so I think a reasonable hypothesis regarding the basis of individual differences in the perceived temperature of an external environment might be differences in peripheral 5-HT systems (in addition to differences in body composition). Perhaps someone with a background in the peripheral nervous system could speak to this better than I can, but single nucleotide polymorphisms (SNPs) leading to differences in central 5-HT systems has been an active area of research in the neuroscience community of late (e.g., Nordquist & Oreland, 2010, Gonda et al., 2010), which I think lends some face validity to this idea.

biochemistry - What exothermic reaction distinguishes warm blooded animals?

While all animals and even plants generate heat from chemical reactions or mechanical motion of their tissues (like muscle tissues), warm blooded animals have brown fat which has the unusual ability to generate heat directly from metabolic energy.

The particular chemical process you are looking for is performed by uncoupling proteins (UCPs). They reside in the mitochondria and rather than use the proton gradient in the mitochondria to generate ATP, UCPs pass protons through the membrane and generate heat.

Brown fat is brown because of a relatively large iron content associated with many extra mitochondria (brown adipose tissue appears to be derived from muscle cells and not white adipose tissue). Its a heat generating organ in humans, particularly infants.

genetics - Expression of an ancestral gene

Your updated question is still very vague, but I'm going to assume it is basically: "Why would the ancestral version of a gene be mistaken for a more recent version than the modern gene?"

If this is incorrect, please let me know and modify your question to clarify.

The simple answer to that question is that the mutations that occurred after the Ancestral gene resulted in less apparent divergence than the LCA (last common ancestor), which would cause the Ancestral gene to seemingly have more polymorphisms - and the general assumption is that the more polymorphisms (mutations) that a gene has undergone, the more recent it is.

So let's say you have the following DNA sequences:

5' - AAAT - 3' = LCA (Template)

5' - AAAG - 3' = Sample 1 : # Differences = 1 Nucleotide

5' - AACG - 3' = Sample 2 : # Differences = 2 Nucleotides

The general assumption is that the larger the difference from the LCA, the more mutations have occurred over time. So, under the general assumption, Sample 2 is probably the most recent version of the sequence.

However, and this is what I think is the answer to your question, because mutations can occur in any order and at any place in the genome, it is entirely possible for the third (from left) Nucleotide to have followed this mutation path: A -> C -> A

That would make Sample 2 appear to be more recent than it is because it essentially mutated "back" to the LCA version of the gene, despite being a linearly older version than Sample 1. In this way, an Ancestral gene can be mistaken for a more recent evolution of a gene. This is also why genomic data is never as strong as when paired with fossil records or other corroborating data that also aligns with the genomic data's proposed timeline; though the odds of a mistake being made grow exponentially less as more of the genome is compared and analyzed.

With very recent mutations; on the scale of hundreds to thousands of years, it's sometimes necessary to analyze thousands of base pairs to calculate an adequately confident answer.

metabolism - What are the differences between white and brown adipose tissue?

Not sure what you are asking, except to add to the list?

Its worth mentioning that brown adipose tissue is the only organ in the human body whose primary purpose is to generate heat. We are warm blooded, but the body temperature is regulated by other organs generating heat while they do work (like muscles or I suppose the stomach, kidney, etc).

Brown Tissue is supposed to not a juvenile attribute - doesn't show up in adults to the same extent (usually being limited to neck and upper chest.

Brown Tissue is thought to be present in only critical areas of the body - even in infants. Its found in the inner body cavity around vital organs.

The color comes from the large number of mitochondria in the cells, which is where the heat is generated via uncoupling protein 1 (UCP1).

White adipose tissue is what we more commonly call fat tissue - its primary function is to store energy in the chemical form of long chain fats. Fat tissue as it grows can inhibit the function of insulin in the body, increasing insulin resistance.

You could almost call them 'good fat' and 'bad fat'

physiology - How do the lungs act as a sieve to trap blood clots?

Just as an intro...

The heart pumps deoxygenated blood from the right ventricle, through the pulmonary arteries (pic) which then eventually split into small capillary networks that surround the alveoli. The alveoli are formed by the trachea eventually branching off. So when you breathe in, the alveoli become filled with higher levels of oxygen.

The blood then becomes oxygenated and returns to the heart via the pulmonary veins to be pumped to the rest of the body.

The deoxygenated blood becomes oxygenated because there is a difference in oxygen and carbon dioxide concentration between the capillary network (O2 low / CO2 high) and the alveoli (O2 high / CO2 low) and so gas diffuses across because of the difference in concentrations (pic).

Physiology textbooks explain these mechanisms but for blood clots in particular, you'll need to check out a pathophysiology book.

Blood clots

When a blood clot travels to the lungs, it's referred to as a pulmonary embolus or PE.

Most of the time (90%), pulmonary emboli are formed in deep veins of the lower leg. These then travel to the pulmonary circulation system.

Large emboli block larger vessels - the pulmonary arteries and their branches. The smaller ones travel further into the network.

Patients can sometimes be asymptomatic and the emboli can at times resolve on its own. The extent of the severity of a PE is determined by:

• how much blood flow is obstructed;


• how long the embolus has been there; and


• presence other underlying lung or heart disease.

There are a number of things that a PE can cause physiologically.

Reduced Gas Exchange - alveolar dead space occurs when an alveolus is ventilated, but not perfused with blood. This, along with other factors, cause varying levels of hypoxemia (lack of oxygen).

Pulmonary Infarction - in a small amount of cases loss of blood flow to lung tissue can cause tissue death. This is fairly uncommon.

Right Ventricular Failure - if there is a large enough blockage (> 50 - 60%), the pressure in the pulmonary arteries increase. Subsequently, the load on the right ventricle is higher.
So in acute cases, the ventricle hasn't had time to adapt (hypertrophy) and so the right heart can fail.

At any rate, the haemodynamic balance can be disrupted when a PE is present.

In the elderly or people with underlying disease where their lung function is already decreased, PEs can have a significantly larger effect because they can't compensate. There are many more important points related to this but hopefully this is a useful (very) basic overview.