The Ghost of Paley
Posts: 1703
Joined: Oct. 2005
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First, here's a summary of Denton's position by someone sympathetic to Intelligent Design:
| Quote | Attempts to dismiss the argument that DNA sequence comparisons imply common descent have been published by critics of Evolution. The most popular one is explained by Denton in Ref. 13 and was used in the popular creation textbook Ref. 14. Denton presents Table 7 of 21 different organism which shows the percent of the number of AA which are different amongst all of the AA sites in the Cytochrome C molecule for each of these 21 organisms. Table 3 shows that of the 110 AA sites in the Cytochrome C, 10 AA sites are different so Denton’s table would report a 100/110=91% value for the human to mouse comparison. The 21 organisms in Denton’s table essentially cover the whole range from humans to bacteria. Denton’s orders the organisms in his table according to the time from the proposed divergence from a common ancestor with the most recent ones on the top of the table and the most ancient divergence at the bottom. Thus, moving up the table means that according to evolution the species are expected to be more closely related and developed from a common ancestor more recently according to evolution. Since the relatively simple bacteria are considered some of the first organisms to evolve and the more complicated humans are some of the most recent, Denton’s table provides an opportunity to investigate the trend through time for the proposed sequences of development of organisms through evolution.
[see table 7 -- Paley]
Denton acknowledges his table does indicate that the percent differences get smaller the more closer the organisms are related. Denton's points out that the general pattern from the sequences indicate the same standard hiearchial topological categories that biologist Linnaeus came up with before Darwin proposed the theory of evolution. For example, within jawed vertebrates the group of terrestrial (land) organisms, amphibia, reptiles and mammals are more closely related than non-terrestrial organisms (fish). Within these groups such as mammals, there are groups of mammals such as rodents or hoofed animals that are consistently more closely related to each other than other groups of mammals. Denton and evolutionist would agree that the DNA sequences imply a pattern which is consistent with the standard hiearchial topological categories. The disagreement comes from Denton's claim that the pattern implies no transitional forms; therefore, the pattern does not indicate evolution.
Denton makes the case for no transitional forms being implied by pointing out that no sequence or group of sequences can be designated as intermediate with respect to other groups. "of the remaining Eukaryotic cytochromes, … all exhibit a sequence divergence between 64 and 67 percent." Since all the sequences have about the same difference in this comparisons Denton correctly points out that this indicate that none of them stands out as a transitional form, " … It means that no Eukaryotic cytochromes is intermediate between the bacterial cytochrome and the other Eukaryotic cytochromes" Denton goes on to say that this implies there is no transitional form; thus, the "missing links" are truly missing. |
But as the author proceeds to note:
| Quote | The fundamental flaw in this argument is that the sequence comparisons made in Denton’s table are from modern organisms not extinct ancient ones. The DNA sequences are taken from organisms that are alive today. Evolution proposes the common ancestor of the modern bacterial cytochrome and the other Eukaryotic cytochromes lived hundreds of millions of years ago. This would be some ancient bacteria which diverged from the path that led to the modern bacteria and started the path that led to the other Eukaryotic cytochromes. If this ancient bacteria could be compared to the other bacteria it diverged from then their sequence would be quite similar as Denton expects. The problem is Denton was expecting the modern organisms to have similar sequences which is not appropriate for this case because evolution proposes that the divergence from the bacteria occurred hundreds of millions of years ago. Because of the redundancy in the Cyctochrome C AA sequence there is no constraint to keep the sequences from changing. Naturally, the Cyctochrome C AA sequences have been continuing to change between all the different species since the time they diverged. Thus, there is no reason to expect any of the modern species compared to the modern bacteria to have an AA sequence that matches more closely to the modern bacteria. Therefore, the reason why Denton did not find the missing link in his table is because his table only has modern organisms. The transitional Cyctochrome C AA sequences if it did exist most likely became extinct hundreds of millions of years ago.
Denton is aware that it is the ancient organisms that are expected to have the most similar sequences, but claims that there is no evidence that this assumption is correct. There is good reason to expect that the more ancient organisms are expected to have more similar sequences. Based on the reasonable assumption that organism have always developed mutations, it is expected that organisms collected more and more variation over time even if their morphology remained the same over time because of the high level of redundancy in the DNA and AA sequences. Since it is very difficult if not impossible to get the sequences for these ancient organisms because they died out a long time ago, it is not appropriate to expect to study these ancient sequences directly. However, they can be implied. Even though no common ancestor or transitional organism is found in the table, Denton’s Table does imply a common ancestor because going up the table the sequences consistently become more similar. Evolution predicts this trend because going up the tables means the proposed common ancestor is more recent. Some creationist would object to this by arguing that this is also expected from fundamental creation because the more similar the organisms the more similar the sequences should be. While this may be true when comparing all the DNA of the different organism; however, there is no biological reason for this to be true when comparing just the DNA sequence for the Cytochrome C protein. As previously pointed out in section 5, many different cytochrome C AA sequence produce the same function; thus, there appears to be no requirement for the designer to specifically make the cytochrome C AA sequence similar. In fact only 14% of the sites are required to be the same according to Table 3.
Denton goes onto to point out that evolution could explain his table of data if there is a sequence change or mutation rate that is constant over time. The theory that mutation rates are fairly constant over time; thus, sequences difference can be used to measure time from divergence has been labeled "molecular clock". Denton points out that the mutation rate is not expected to be constant for the organisms in his table because they involve species with a very large variation of reproduction rates. Denton expects that mutation rates would be related to the number of generations which means that those species which regenerate quickly such as flies will develop mutations in the population in a much shorter amount of time then humans would. Since Denton’s table indicates that the mutation rate was constant with time rather then related to the number of generations, he concludes that the data in his table cannot be successfully explained by evolution. It appears to me that evolutionist have not yet figured out the molecular clock. Determining what caused mutations when they occurred and how often is very complicated problem; thus, it is not surprising that evolutionist have not yet developed a mature understanding of how the differences in the sequences came about. However, the determination of common ancestors does not require having this issue be resolved. As explained in section 5 it is possible to infer common ancestors from the similarities in the sequences.
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All bolding mine. (Incidentally, one of Deadman's sources supports this idea with purty pictures. Admittedly, the author of this piece is an idiot, but ya gotta work with what ya gots.  )
Scientists have made progress in quantifying the degree to which metabolism and body size affects the molecular clock. But before discussing this, here are a few observations:
| Quote | The generation time argument is a bit bogus for several reasons. First, mutation rates are based on changes per cell division (replication) and not generation time. Thus, in mammals such a mouse, there are about 50 cell divisions between zygote and gamete and the organism reproduces in about 100 days. Thus, there is, on average, one mutation-causing replication event every two days. This is no more than the average "generation time" of single-celled organisms such as yeast or bacteria. (Bacteria divide once every few days, at most, contrary to what most people believe.)
The second reason for skepticism is that for most of the history of life the "generation time" of different organisms isn't that much different. Large terrestrial mammals, for example, have only been around for about 15% of the time since single-celled life began.
Molecular biologists and population geneticists have thought about these things. They conclude that the evidence favors the idea that phylogenetic trees are due to fixation of nearly neutral alleles by random genetic drift. This explains the molecular clock.
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Now here's an attempt to model the effects of body size and metabolism on the molecular clock:
| Quote | Here, we present a model of nucleotide substitution that combines theory on metabolic rate with the now-classic neutral theory of molecular evolution. The model quantitatively predicts rate heterogeneity and may reconcile differences in molecular- and fossil-estimated dates of evolutionary events. Model predictions are supported by extensive data from mitochondrial and nuclear genomes. By accounting for the effects of body size and temperature on metabolic rate, this model explains heterogeneity in rates of nucleotide substitution in different genes, taxa, and thermal environments. This model also suggests that there is indeed a single molecular clock, as originally proposed by Zuckerkandl and Pauling [Zuckerkandl, E. & Pauling, L. (1965) in Evolving Genes and Proteins, eds. Bryson, V. & Vogel, H. J. (Academic, New York), pp. 97–166], but that it "ticks" at a constant substitution rate per unit of mass-specific metabolic energy rather than per unit of time. This model therefore links energy flux and genetic change. More generally, the model suggests that body size and temperature combine to control the overall rate of evolution through their effects on metabolism.
[...]
Here, we propose a model that predicts heterogeneity in rates of molecular evolution by combining principles of allometry and biochemical kinetics with Kimura's neutral theory of evolution. The model quantifies the relationship between rates of energy flux and genetic change based explicitly on the effects of body size and temperature on metabolic rate. Although the model does not distinguish between the metabolic rate and generation time hypotheses, it accounts for much of the observed rate heterogeneity across a wide range of taxa in diverse environments. Recalibrating the molecular clocks by using metabolic rate reconciles some fossil- and molecular-based estimates of divergence.
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Building on previous work showing correlations of substitution rate to body size (6), these results show that all animals cluster around a single line that is predicted by our model. Note that the model quantifies the combined effects of body size and temperature. Analyses that consider these variables separately, like much of the previous literature, explain much less of the observed variation in substitution rates (Table 2).
[...]
These results also may have broader implications for understanding the factors controlling the overall rate of evolution. The central role of metabolic rate in controlling biological rate processes implies that metabolic processes also govern evolutionary rates at higher levels of biological organization where the neutral molecular theory does not apply. So, for example, the rate and direction of phenotypic evolution ultimately depends on the somewhat unpredictable action of natural selection. However, the overall rate of evolution ultimately is constrained by the turnover rate of individuals in populations, as reflected in generation time, and the genomic variation among individuals, as reflected in mutation rate (16, 24). Both of these rates are proportional to metabolic rate, so Eq. 1 also may predict the effects of body size and temperature on overall rates of genotypic and phenotypic change. Such predictions would be consistent with general macroevolutionary patterns showing that most higher taxonomic groups originate in the tropics where temperatures are high (25), speciation rates decrease with decreasing temperature from the equator to the poles (26, 27), biodiversity is highest in the tropics (28), and smaller organisms evolve faster and are more diverse than larger organisms (29).
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Here's an older article on generation times and a little background.
Even worse, however, is the fact that Denton's hypothesis has no way to account for phylogenies based on unitary pseudogenes, retroviral insertions, SINEs, and LINES. Worst of all, Denton's hypothesis doesn't address the stunning congruence between different phylogenetic trees.
In summary, the molecular evidence provides overwhelming support for evolution, and little help for creationism.
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Dey can't 'andle my riddim.
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Every, and I do mean EVERY experiment done and accurate observation made has supported evolutionary biology. Sure the theories that comprise evolutionary biology have been modified over the years, this is what we call progress in science. We change things on the basis of the evidence. The whinings of Dembski et al are really nothing more than a restatement of ideas already tried and already failed.