Aphorisms


There's nothing so bad, that adding government can't make it worse. -- The Immigrant

Government is not the solution to our problem; government is the problem. -- Ronald Reagan

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Read the next two together:

Every collectivist revolution rides in on a Trojan horse of 'Emergency'." -- Herbert Hoover

This is too good a crisis to waste. -- Rahm Emanuel

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Government is the great fiction through which everybody endeavors to live at the expense of everybody else. -- Fredric Bastiat, French Economist (30 June 1801 – 24 December 1850)

In general, the art of government consists of taking as much money as possible from one party of the citizens to give to another. -- François-Marie Arouet, a.k.a. Voltaire, (21 November 1694 – 30 May 1778)

The problem with socialism is that, sooner or later, you run out of other people's money. -- Margaret Thatcher

The inherent vice of capitalism is the unequal sharing of blessings; the inherent virtue of socialism is the equal sharing of miseries. -- Winston Churchill

Monday, September 21, 2009

#26: Evolution III

This is actually a response to two comments left by Jeff. I add it as a separate post only because of its length and because I think it sheds further light on the issues in the two prior posts.

Greetings, Jeff, glad to read your contribution to my questions. As I understand the theory, there are two explanatory theses. The first is the thesis that there are random mutations. The second is that the creatures with adaptive mutations survive, while the others do not.

The example of evolution in action that I find most persuasive is that of the development of anti-biotic resistant bacteria. But even in this example, there are two possible stories to be told, either of which might be true, or both.

Let’s assume a population of bacteria B such that 95% of these bacteria succumb to anti-biotic C. This means that even after a round of C, there are still 5% of the original population left in the system, RB, which cannot be killed with C.

Now, some theorists claim that there is such a thing as environmental “room” such that organisms will automatically breed to the limits of that “room.” In this case, that means the original 5% will breed to fill the room vacated by the now defunct 95%.

The second possible story is this. We start with population B, but do not assume that it contains 5% RB. Instead, we assume that C either kills members of B OR it alters the DNA of some members in such a way as makes them resistant. The only advantage of this story is that it doesn’t rely on random mutations (or random mutations alone).

If all of this is true, then this is a simple model of natural selection.

In either case of this simple model, the presence of the adaptive property or feature of the organism has to be explained. It is here that I’m not persuaded that the theory is fully defensible.

You say that we should be talking about a simple organism, not a raptor. Fine. And here you say we just need to assume a single photosensitive cell. OK. But then you go on to add a causal connection to attractive or aversive action, and this seems already fairly complex to me. How do we assume this random mutational activity takes place? Do we assume that nature produces quite literally every conceivable variation on every creature it spawns from the simplest on? This would mean photosensitive cells appearing at one time on one creature at least for every location on and in the body. Of course, the same goes for every other sensory kind, including ones of which we have no experience. Surely this did not happen. Have we found remains of creatures with eye sockets where the navel would normally be?

And is it really true that the locations of eyes on the world’s creatures is actually optimal? There are critters with stalked eyes, which seems a pretty good design. But wouldn’t a critter with four stalked eyes have an advantage over one with just two? And why, just in general, have we never found a trace of an animal with more than two eyes?

Then, in addition, the mutations in the theory should be heritable ones in order to produce a new and better adapted population. But this would involve a further mutational change at the chromosomal level, no?

What seems to be the case (though it may well not be) is that there is some other mechanism that limits or directs the mutations. The “mutations” assumption, thus, seems to need elaboration in order to avoid being nothing other than a baptism of ignorance, as Russell would say.

I have a similar problem with the notion of “genetic drift.” You write:

“More likely than these theories is the case for non directed genetic drift. Instead of use it or lose it, a deletory mutation probably occurred in the lineage of cave fish (once they had moved to the caves). Being that the mutation was neither adaptive or non adaptive it would neither be selected for or against. However, natural selection is not the only way a population can change. Sometimes when there is no selective pressure a population can drift due to chance. These changes tend to occur very slowly and can drift back as well. It may even be that there is a higher probability of mutation at on of the genes determining cave fish sight, such that in the absence of positive selective pressure drift is more likely to occur.”

If what happened was a “deletory mutation,” then it would seem that the blind and sighted fish would have equal survival ability and we should find both populations present side by side. This is not what happens. So the explanation must lie with “genetic drift.” But I am not comfortable with this doctrine for reasons similar to those against “mutation.”

“Genetic drift” seems to be a doctrine quite similar to “global warming” in that it is consistent with anything that happens. If a feature disappears, it’s due to genetic drift; and if it doesn’t disappear, then there was no drift. If the blind fish have non-functioning eyes, we assume that these eyes are vestigial, which means that they were fully functioning products of the evolutionary process at one time. Apparently, they lost the sightedness, but the non-functioning organ remained. This means that sight “drifted” away, but the organs did not. Why would the “drift” discriminate in this way?

You said once that you thought that the Dawkins story about evolution really taking place at the cellular level addressed these questions, but I didn’t understand how at the time (still don’t). Do you still think this?

11 comments:

  1. Couldn't genetic drift also be explained by the fact that, in losing its sight, one of the fish's other senses was enhanced and this provided an evolutionary advantage?

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  2. Hello, Asher. If one of the other fish's senses was enhanced, this also would have to have taken place through the process of natural selection (which is still unexplained in detail). And even if natural selection enhanced one of the fish's other senses, this still would not explain why sight disappeared. Genetic drift seems to be just the doctrine that *sometimes* characteristics disappear (or *appear*?) just on the basis of random chromosomal mutations.

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  3. I believe that the theory of genetic drift is a very good one with lots of substantiating evidence. It is not hard to conceive of either at a genetic level. We do have a genetic mutation machine built into DNA replication. When one cell splits and becomes two the DNA in the first cell must be copied and then partitioned into the second cell. This copying process is not 100% and varies greatly between species and plays a significant role in certain cancers. Thus, we naturally are producing mutated cells all of the time. When this mutation occurs within the germ line it becomes heritable. Must mutations don't have a significant impact because they either occur within the non gene regions of DNA or they cause a substitution of an Amino Acid (the building blocks of proteins) that does not change the function of the protein.

    If anyone of us were to have the genetic code in a skin cell read it would be different than the genetic code in our sperm cells and this is because of mutations.

    It is when the mutation causes a functional mutation that a functionally different protein is produced. Thus, a protein that functioned as an electron receptor (as a lot of proteins do in cellular processes) could become a photon receptor. However, positive functional changes are a lot less common than negative functional changes. Luckily, as it is easy to imagine, the serious functional changes usually will cause something wrong with the developmental process and cause terminated pregnancies. Some changes just give a disadvantage (as in most of our diseases) that in organisms other than humans usually lead to a decreased chance in finding a sex partner and thus decreased chance of passing on the genes. NOW TO GENETIC DRIFT. When a mutation occurs in the germ line that is neither benificial or harmful (and they occur all the time) then they will not be selected against. In the case of the species of blind fish in mexico, there are different variations of blindness that occur either as a lack of sight or as a lack of development of the physical structure of the eye, or as a lose it or use it phenomenon (skin growing over the eye). This is not to say that there are not also seeing cave fish that have not lost their sight. Thus, in the first two types of blindfish (sight loss and structural loss) the best explanation seams to me to be that they just lost it due to drift. Let us say that every 5th fish born in the cave or on the surface is born blind. The ones on the surface are selected against but the ones in the caves are not. Over time the ones in the cave will all be blind as the mutation can not as easily go the other way. This is because there is only a few genetic sequences that can lead to sight and a million that don't. This is the way it works. Out of the five fishy kids one is blind. All of these fish have children. In generation 2 one fifth of the sighted fishes kids are blind plus 100% of the blind fishes. Over all the # of blind fishes increases without a negative selective pressure over each generation.

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  4. Asher is also right to suggest that there may be selective reasons for the loss of sight as well. These include the fact that eyes are easily infected and that not using eyes enables the animal to use a finite amount of energy is other ways.

    Genetic drift does not do so well with gain of function mutations as they are so much less frequent and easily reversed by subsequent mutations. Thus, unless there is a benefit to a gain o function mutation it will not stay in a population. This is why we do not see all the wacky things J.P. mentioned. Note as well that evolutionary gains are always constrained by the organism as it exists. A third eye thus could not develop on a human because of a processing constraint. there are however animals with eyes at different locations and with different numbers (such as the three eyed beetle.

    Here are two examples of evolution (that can be observed) that I think are really elegant.

    1. If you are to grow a colony of bacteria from a few bacteria containing the same DNA certain bacteria in the colony will develop interesting features. Lets say that first few bacteria were all lactose intolerant so that if you fed them only lactose they would die. The same is not true of all individuals in the colony.
    If you let the colony grow and then add lactose something interesting occurs. At first it looks like you have wiped out the bacteria. But if you wait a couple of days a new colony has formed that is lactose tolerant and perfectly happy to grow only lactose coated plates. More over they contain altered genes from their ancestors to enable them to digest lactose.

    This example mirrors the one J.P. used in his post regarding bacteria and antibiotic resistance. What I don't understand about J.P.'s comments is why a theory that doesn't involve random mutation is advantaged considering we know that random mutations occur all the time. Second I don't understand what is meant by "the presence of the adaptive property or feature of the organism has to be explained." I assume what is meant is the feature which confers resistance must be explained. If this is what is meant I assure you the answer is known. As I understand it, two types are easily identified "chromosome shifters and plasmid encoders." The mechanisms get complex but still follow evolutionary principles. The likelihood of the antibiotic inducing the mutation is low considering the mechanism of action of the antibiotic.

    #2 This is a human example. Sickle cell disease is a disease that primarily effects black people. It occurs due to a genetic mutation in the hemoglobin (protein found in blood) gene that cause the protein to form chains that cause red blood cells to look like Bananas. However, you don't get sickled red blood cells unless you have two copies of the mutation (one from mom and one from dad). If you have one functional hemoglobin gene then sickled cells are not produced: a situation called a carrier. Interestingly, carriers of the sickle cell gene have a powerful immunity against malaria. Also interesting is the fact that the prevalence of the gene mirrors the distribution of malaria. Thus, African and Indians and italians get sickle cell but people from trinidad do not.

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  5. Hullo Jeff, Thanks for helping out with clarifying information. With respect to you first post, it still doesn't address why genetic drift would not remove the eye structure as well as the sight. That's been my puzzle.

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  6. Ob your second post. The beauty of the resistance example and your intolerance example is that the action of natural selection is very clear. If you kill all the x's with y, then all you'll have left will be x's without y. No problem. The issue seems to be with how x's came to have y at all -- "positive" mutations. Now you indicate that there are several reasons why positive mutations are less likely to reproduce. But it would seem that even the presence of these reasons requires further elaboration on ultimately as clear a way as the viral and bacterial examples.
    I'm also unclear as to what exactly the sickle cell example illustrates about natural selection. Good stuff!

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  7. PS DID NOT know there was a "three eyed" beetle! Damn, what a critter! How are the eyes placed? One on the belly button?

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  8. On the issue of sickle cell: Natural selection in this case has selected for a genetic mutation that has led to a positive adaptation in the heterozygote (one gene only state) and a negative adaptation in the homozygote state. What is interesting is that the presence of the mutation within the population is only selected for in the geographical region that confers the positive adaptive attribute. What is more interesting is that in african and indian communities that have not lived in a malaria zone for a long time the prevalence of the sickle cell mutation is decreased because it is ONLY negatively selected for (as in the homozygotes die at an early age eliminating their genes from the pool).

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  9. I take it that what you are saying is that natural selection has created a situation in which the mutation can either protect you from malaria or kill you. This seems to be a case of nature's unintended consequences. It changes a cell in such a way that if the animal reproduces with another who does not have that mutation, the offspring is malaria resistant; but if, by chance, it reproduces with another who has the mutation, the offspring gets sickle cell anemia.
    Since I don't know the distribution of animals with the mutation relative to those without, it's difficult to estimate the advantage of the mutation to the population. Clearly, this setup will not produce a population immune to malaria since immunity requires one parent with and one without the mutation. Unless, of course, once an animal is immune, it passes this on to its offspring regardless of its mate's status on the mutation. This, I do not know.
    But, if immunity requires one of each, then I cannot see how the example sheds light on the role of natural selection.

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  10. Hello Jeff, I’m tempted to concede the point to your superior knowledge, but must say that after all the explanation, my qualms persist. This is probably due to my not being able to follow the details of your explanation. Yet, even this would make an important point, namely that natural selection loses its intuitive plausibility when attention is paid to its details. This doesn’t mean that I think the theory false, just one that is far more complex in actual detail than its marketing would initially suggest.
    My credulity lags now at precisely the same point as when I began. I still cannot see how natural selection can work when the adaptive value of a mutation is infinitesimal. And, it seems to me, that all successful positive adaptations must begin as infinitesimal mutations.
    In effect, the presence of a functional eye must be the accumulated effect of countless infinitesimal incremental mutations, each of which is heritable. Even if we assume a heritable photosensitive cell occurs on an organism, that is scarcely sufficient to make it sufficiently more adapted than its fellows. There has to be an additional mutation that somehow links that cell to an adaptive behavior in response to light. In addition, there must not be other creatures in the environment more adapted for survival than the one with the photosensitive cell.
    I guess that it seems to me that in the detail, the theory is laden with ad hoc assumptions just to keep it working. But nature is not tidy, there is no reason a messy theory should not be true. I’m guessing that someone has already done this, but if not, it would be interesting to try to create a computer model of the evolutionary process to see just how much has to be built into it to yield results like the ones we actually encounter.

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  11. I think that your hesitations are intuitive and very relatable. I have to agree that natural selection requires molecular justification and that for me it was only in studying and observing examples of cellular processes that I have really come to appreciate the theory of natural selection.

    A few notions that I have noticed throughout my studies in cellular biology have particularily helped. For one, the fact that very small molecular changes can have very significant consequences for an organism has been a common theme. To go along with this point (and perhaps a seperate point on its own) is that a lot of the basic elements of cells are used over and over again in slightly different ways to produce dramatically different effects. For instance, the molecules that control the peripheral immune response in blood and tissue are the same molecules that mediate the storage of spatial information in the hippocampus. The pathways are the same except for slight variations in triggers and in end products. Another example is that molecules that are highly important in differentiating cells in development (skin cells and gut cells ect.) play a pivotal role in determining the differentiation of a specific synapses in neurons (synapse = connection between two neurons). This differentiation, like differentiation in development, also involves a pattern of protein expression but is not mediated at the genetic level. The main point is that slight modifications in small details can change the function of a cellular system draumaticaly.

    Another notion that I have observed is that different functional cellular processes can have very similar principals. Thus, the way in which light is transmitted as useful information for the brain is very similar to the way touch is transmitted. When I see these patterns it becomes easier to understand how a small cellular change (the creation of a signalling molecule with slightly different properties) can lead to the a set process taking on a different functional role. Therefore, it is not the case that the photo sensitive cell and its integration into a central nervous system which can cause a behavioural response all magically had to appear at the same time - of course this would be impossible. Rather, it is likely that photosensitivity was gained from a slight variation in an already integrated system. Possibly a baroreceptor cell that had a integrated response to touch changed in just a way that was is no longer sensitive to touch but rather to light. Now this raises the question about how the touch receptor became integrated in the firsrst place. Yet again, very plausable and understandable explanations are available about how an integrated group of cells could have developed where the environmental trigger for one cell can produce a reaction in another.

    My basic point is that it is not useful to think of functional systems as discrete entities that evolved seperately. What is more important to figure out is how did a feedback loop develop or how did cellular connectivity arise? Realistically once you can understand how these basic underlying processes could have arisen through natural selection then the rest of the story takes on a different dimension. It becomes more important to understand how different functional processes arose as slight varients of a more basic evolution event.

    Finally, I will admit that a complete explanation of evolutionary events of the past is never possible. It always involves the imagination and never involves actually observing the changes in progress. What I find convincing is that you can observe rapidly reproducing organisms adapting to changing environments now. Natural selection is attractive for other reasons as well. It contains a vast explanatory power when it comes to understanding differences and similarities between species and between members within a species.

    Jeff

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