Good for Bayblab. Read a short summary of the issue at [Electoral Reform: Referendum 2007].
To be fair, it's only kamel (the smart one
One interesting thing that leapt out at me when reading this was the fact that, while many scientists now realize that it was a mistake to jump to the conclusion that there were massive amounts of "junk" in DNA (because they were trying to fit the research into a Darwinian model), they are on the verge of committing the same exact mistake all over again, this time with RNA.In order to understand such a bizarre question you have to put yourself in the shoes of an IDiot. They firmly believe that the concept of junk DNA has been overturned by recent scientific results. According to them, the predictions of Intelligent Design Creationism have been vindicated and all of the junk DNA has a function.
Hainzl, T., Huang, S. and Sauer-Eriksson, A.E. (2007) Interaction of signal-recognition particle 54 GTPase domain and signal-recognition particle RNA in the free signal-recognition particle.
Proc. Natl. Acad. Sci. (USA) 104:14911-6. [PubMed]
Halic, M. and Beckmann, R. (2005) The signal recognition particle and its interactions during protein targeting. Curr. Opin. Struct. Biol. 15(1:116-125. Review. [PubMed]
Maity, T.S. and Weeks, K.M. (2007) A threefold RNA-protein interface in the signal recognition particle gates native complex assembly. J. Mol. Biol. 369:512-24 [PubMed]
Chen, J., Jones, C.L. and Liu, J. (2007) Using an Enzymatic Combinatorial Approach to Identify Anticoagulant Heparan Sulfate Structures. Chemistry & Biology 14: 972-973.
Lindhardt, R.J. and Kim, J-H. (2007) Combinatorial Enzymatic Synthesis of Heparan Sulfate (review of Chen et al. 2007). Chemistry & Biology 14:972-973.
Secreted proteins are synthesized on the surface of the endoplasmic reticulum, and the newly synthesized protein is passed through the membrane into the lumen. In cells that make large amounts of secreted protein, the endoplasmic reticulum membranes are covered with ribosomes.©:L.A. Moran and Pearson/Prentice Hall
The clue to the process by which many proteins cross the membrane of the endoplasmic reticulum appears in the first 20 or so residues of the nascent polypeptide chain. In most membrane-bound and secreted proteins, these residues are present only in the nascent polypeptide, not in the mature protein. The N-terminal sequence of residues that is proteolytically removed from the protein precursor is called the signal peptide since it is the portion of the precursor that signals the protein to cross a membrane. Signal peptides vary in length and composition, but they are typically from 16 to 30 residues long and include 4 to 15 hydrophobic residues.In eukaryotes, many proteins destined for secretion appear to be translocated across the endoplasmic reticulum by the pathway shown in the Figure. In the first step, an 80S initiation complex—including a ribosome, a Met-tRNAiMet molecule, and an mRNA molecule—forms in the cytosol. Next, the ribosome begins translating the mRNA and synthesizing the signal peptide at the N-terminus of the precursor. Once the signal peptide has been synthesized and extruded from the ribosome, it binds to a protein-RNA complex called a signal recognition particle (SRP).
SRP is a small ribonucleoprotein containing a 300-nucleotide RNA molecule called 7SL RNA and four proteins. SRP recognizes and binds to the signal peptide as it emerges from the ribosome. When SRP binds, further translation is blocked. The SRP-ribosome complex then binds to an SRP receptor protein (also known as docking protein) on the cytosolic face of the endoplasmic reticulum. The ribosome is anchored to the membrane of the endoplasmic reticulum by ribosome-binding proteins called ribophorins, and the signal peptide is inserted into the membrane at a pore that is part of the complex formed by the endoplasmic reticulum proteins at the docking site.Once the ribosome-SRP complex is bound to the membrane, the inhibition of translation is relieved and SRP dissociates in a reaction coupled to GTP hydrolysis. Thus, the role of SRP is to recognize nascent polypeptides containing a signal peptide and to target the translation complex to the surface of the endoplasmic reticulum.
Once the translation complex is bound to the membrane, translation resumes and the new polypeptide chain passes through the membrane. The signal peptide is then cleaved from the nascent polypeptide by a signal peptidase, an integral membrane protein associated with the pore complex. The transport of proteins across the membrane is assisted by chaperones in the lumen of the endoplasmic reticulum. In addition to their role in protein folding, chaperones are required for translocation, and their activity requires ATP hydrolysis. When protein synthesis terminates, the ribosome dissociates from the endoplasmic reticulum, and the translation complex disassembles.
Horton, H.R., Moran, L.A., Scrimgeour, K.G., Perry, M.D. and Rawn, J.D. (2006) Principles of Biochemistry, 4th edition. Pearson Prentice Hall, Upper Saddle River NJ (USA)
Schaffitzel, C., Oswald, M., Berger, I., Ishikawa, T., Abrahams, J.P., Koerten, H.K., Koning, R.I. and Ban, N. (2006) Structure of the E. coli signal recognition particle bound to a translating ribosome. Nature 444:503-506.
[Hat Tip: Scienceroll who thinks that there are only two science bloggers who link to references properly. And I'm not one of them. Boo!]
One result of random sampling is that most new mutations, even if they are not selected against, never succeed in entering the population. Suppose that a single individual is heterozygous for a new mutation. There is some chance that the individual in question will have no offspring at all. Even if it has one offspring, there is a chance of 1/2 that the new mutation will not be transmitted. If the individual has two offspring, the probability that neither offspring will carry the new mutation is 1/4 and so forth. Suppose that the new mutation is successfully transmitted to an offspring. Then the lottery is repeated in the next generation, and again the allele may be lost. In fact, if a population is of size N, the chance that a new mutation is eventually lost by chance is (2N − 1)/2N (For a derivation of this result, which is beyond the scope of this book, see Chapters 2 and 3 of Hartl and Clark, Principles of Population Genetics.) But, if the new mutation is not lost, then the only thing that can happen to it in a finite population is that eventually it will sweep through the population and become fixed. This event has the probability of 1/2N In the absence of selection, then, the history of a population looks like Figure 17-17. For some period of time, it is homozygous; then a new mutation appears. In most cases, the new mutant allele will be lost immediately or very soon after it appears. Occasionally, however, a new mutant allele drifts through the population, and the population becomes homozygous for the new allele. The process then begins again.This is an important conclusion. It shows that alleles are fixed in large populations by random genetic drift. I'd like it a lot if people would stop saying that drift only occurs in small populations.
Even a new mutation that is slightly favorable selectively will usually be lost in the first few generations after it appears in the population, a victim of genetic drift. If a new mutation has a selective advantage of S in the heterozygote in which it appears, then the chance is only 2S that the mutation will ever succeed in taking over the population. So a mutation that is 1 percent better in fitness than the standard allele in the population will be lost 98 percent of the time by genetic drift.
The fact that occasionally an unselected mutation will, by chance, be incorporated into a population has given rise to a theory of neutral evolution, according to which unselected mutations are being incorporated into populations at a steady rate, which we can calculate. If the mutation rate per locus is μ, and the size of the population is N, so there are 2N copies of each gene, then the absolute number of mutations that will appear in a population per generation at a given locus is 2Nμ. But the probability that any given mutation is eventually incorporated is 1/2N so the absolute number of new mutations that will be incorporated per generation per locus is (2Nµ)(1/2N) = µ If there are k loci mutating, then in each generation there will be kμ newly incorporated mutations in the genome. This is a very powerful result, because it predicts a regular, clocklike rate of evolution that is independent of external circumstances and that depends only on the mutation rate, which we assume to be constant over long periods of time. The total genetic divergence between species should, on this theory, be proportional to the length of time since their separation in evolution. It has been proposed that much of the evolution of amino acid sequences of proteins has been without selection and that evolution of synonymous bases and other DNA that neither encodes proteins nor regulates protein synthesis should behave like a molecular clock with a constant rate over all evolutionary lineages. Different proteins will have different clock rates, depending on what portion of their amino acids is free to be substituted without selection.
I have tried to show that adapatationism can have virtues as well as faults. But this chapter's main purpose is to list and classify constraints on perfection, to list the main reasons why a student of adaptation should proceed with caution. Before coming to my list of six constraints on perfection, I should deal with three others that have been proposed, but which I find less persuasive. Taking first, the modern controversy among biochemical geneticists about "neutral mutations", repeatedly cited in critiques of adaptationism, it is simply irrelevant. If there are neutral mutations in the biochemist's sense, what this means is that any change in polypeptide structure which they induce has no effect on the enzymatic activity of the protein. This means that the neutral mutations will not change the course of embryonic development, will have no phenotypic effect at all, as a whole-organism biologist would understand phenotypic effect. The biochemical controversy over neutralism is concerned with the interesting and important question of whether all gene substitutions have phenotypic effects. The adaptationism controversy is quite different. It is concerned with whether, given that we are dealing with a phenotypic effect big enough to see and ask questions about, we should assume that it is the product of natural selection. The biochemist's 'neutral mutations' are more than neutral. As far as those of us who look at gross morphology, physiology and behaviour are concerned, they are not mutations at all. It was in this spirit that Maynard Smith (1976b) wrote: "I interpret 'rate of evolution' as a rate of adaptive change. In this sense, the substitution of a neutral allele would not constitute evolution ..." If a whole-organism biologist sees a genetically determined difference among phenotypes, he already knows he cannot be dealing with neutrality in the sense of the modern controversy among biochemical geneticists.Natural selection is the only explanation we know for the functional beauty and apparently "designed" complexity of living things. But if there are any changes that have no visible effect—changes that pass right under natural selection's radar—they can accumulate in the gene pool with impunity and may supply just what we need for an evolutionary clock.
This certainly seems to place Dawkins as an "adaptationist", one who thinks that all differences in phenotypes are adaptations. I was a little surprised by this, but the quote seemed clear, and I wasn't going to take the time to find my original.The next lines P-ter is referring to is the beginning of a new paragraph ...
Luckily, another commenter pointed out that The Extended Phenotype is searchable at Google Books [The Extended Phenotype]. And funny, the very next line after Moran stops quoting is possibly relevant:
He might, nevertheless, be dealing with a neutral character in the sense of an earlier controversy (Fisher & Ford 1950; Wright 1951). A genetic difference could show itself at the phenotypic level, yet still be selectively neutral.P-ter then continues with ...
Dawkins goes on to express some skepticism about some arguments for evolution by drift, but he's certainly not an "adaptationist" in the Moran sense.This is a very serious charge. I'm accused of deliberately distorting Dawkins' position by selective quotation. According to P-ter, Dawkins does not believe what he says in the quoted paragraph. (And elswhere, I might add.) According to P-ter Dawkins believes that mutations with a visible phenotype can be neutral. (We're not talking about one or two exceptions here, we're talking about the generality that applies to a significant percentage of mutations.)
I suppose I'm somewhat naive: distorting someone's argument through selective quotation is a classic creationist tactic, and Moran has written a bit about the propaganda techniques used by that crowd. Little did I know his familiarity is not of an entirely academic sort.
[1] As opposed to "pluralists", as he likes to call himself. For someone who (rightfully, in my opinion) is disdainful of "framing" (the view that scientists need to spin their results in order to resonate better with the public), he certainly knows how to frame.
He might, nevertheless, be dealing with a neutral character in the sense of an earlier controversy (Fisher & Ford 1950; Wright 1951). A genetic difference could show itself at the phenotypic level, yet still be selectively neutral. But mathematical calculations such as those of Fisher (1930b) and Haldane (1932a) show how unreliable human subjective judgement can be on the "obviously trivial" nature of some biological characters. Haldane, for example, showed that, with plausible assumptions about a typical population, a selection pressure as weak as 1 in a 1000 would take only a few thousand generations to push an initially rare mutation to fixation, a small time by geological standards. It appears that in the controversy referred to above, Wright was misunderstood (see below) ...A careful reading of Dawkins shows that the objection to his claim doesn't stand because people misunderstood Wright. Thus, according to Dawkins, characters that appear to be neutral really aren't.