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Theory of Intelligent Design, the best explanation of Origins » Theory of evolution » Genetic entropy

Genetic entropy

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1 Genetic entropy on Sun Oct 18, 2015 10:00 am


Genetic entropy 1

The common understanding is that  the evolution, as a whole, of all species on the planet throughout history  has been the result of a general trend of increasing complexity.  By the standard ToE,  directionality in the history of life is commonly  framed in terms of six major evolutionary steps, or megatrajectories

(1) evolution from the origin of life to the last common ancestor of extant organisms,
(2) the metabolic diversification of bacteria and archaea,
(3) evolution of eukaryotic cells,
(4) multicellularity,
(5) the invasion of the land and
(6) technological intelligence.

evolutionary theory has traditionally held that very long periods of time are needed for natural selection to generate extreme differences in morphological organization like those seen in animal body plans. Each major transitional step would require  increase of genome complexity, and the arise of new genomic specified complex information through mutations and natural selection would result  directly in the increase of complexity of  body plans and new species.

The scientific evidence however points to a different picture. Several lines of evidence refute this darwinian prediction :

Kurland CG  et al write in their remarkable paper :  " Genomics and the irreducible nature of eukaryote cells " following:

Comparative genomics shows that, under  certain ecological settings, sequence loss and cellular simplification are common modes of  evolution. Comparative genomics has confirmed a lesson from paleontology: Evolution does not proceed monotonically from the simpler to the more complex . Comparative genomics, aided by proteomics of  cellular signature structures (CSSs)  such as the mitochondria , nucleoli, and spliceosomes, reveals hundreds of proteins with no orthologs (ortholog = two or more homologous gene sequences found in different species related by linear descent ) evident in the genomes of prokaryotes.

That is one of the reasons, why i doubt common ancestry is true. There is no reason to believe eukaryotes evolved from prokaryotes and archaea

Examples of ecological circumstances driving genome reduction are seen in many intracellular endosymbionts and parasites, which gain few genes but lose many genes responsible formetabolic flexibility The mitochondrion is even more extreme in its reductive evolution; its ancestral bacterial genome has been reduced to a vestigial microgenome supported by a predominantly eukaryote proteome. Genomes of modern mitochondria encode between 3 and 67 proteins, whereas the smallest known free-living a-proteobacterium (Bartonella quintana) encodes 1100 proteins. Taking Bartonella as a minimal genome for the freeliving ancestor of mitochondria, nearly all of the bacterial coding sequences have been lost from the organelle, though not necessarily from the eukaryote cell. The mitochondrial genome of the protist Reclinomonas americana is the largest known but has still lost more than 95% of its original coding capacity. This abbreviated account of genome reduction illustrates the Darwinian view of evolution as a reversible process in the sense that ‘‘eyes can be acquired and eyes can be lost.’’ Genome evolution is a two-way street. This bidirectional sense of reversibility is important as an alternative to the view of evolution as a rigidly monotonic progression from simple to more complex states, a view with roots in the 18th-century theory of orthogenesis. Unfortunately, such a model has been tacitly favored by molecular biologists who appeared to view evolution as an irreversible march from simple prokaryotes to complex eukaryotes, from unicellular to multicellular. The many well documented instances of genome reduction provide a necessary corrective measure to the often-unstated assumption that eukaryotes must have originated from prokaryotes.


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2 Re: Genetic entropy on Wed Nov 04, 2015 4:19 am


Genetic Entropy Confirmed 1

In Darwinian evolution, variations must add new information to produce innovations.  Neo-Darwinism ascribes those variations to genetic mutations.  In 2005, geneticist John Sanford (Cornell) argued that the accumulation of mutations always decreases fitness in a process he called “genetic entropy.”1The downhill trend is amplified by a number of factors, including selection interference and epistasis (interactions between mutations).2  Now, genetic entropy from epistasis has received support by two new papers in Science.
For mutations under epistasis to produce innovation, there must be a way for them to work together (synergistic epistasis).  This is often assumed but has not been observed.  Most experiments have shown beneficial mutations working against each other (antagonistic epistasis; see 12/14/2006), or causing even less fitness than if they acted alone (decompensatory epistasis; see 10/19/2004).  In a new paper in Science,3Khan et al, working with Richard Lenski [Michigan State], leader of the longest-running experiment on evolution of E. coli, found a law of diminishing returns with beneficial mutations due to negative epistasis.  The abstract said:
Epistatic interactions between mutations play a prominent role in evolutionary theories. Many studies have found that epistasis is widespread, but they have rarely considered beneficial mutations. We analyzed theeffects of epistasis on fitness for the first five mutations to fix in an experimental population of Escherichia coli. Epistasis depended on the effects of the combined mutations—the larger the expected benefit, the more negative the epistatic effect. Epistasis thus tended to produce diminishing returnswith genotype fitness, although interactions involving one particular mutation had the opposite effect. These data support models in which negative epistasis contributes to declining rates of adaptation over time.
Within the paper, they said, “We observed an overall negative relation, indicating that epistatic effects became more negative as the expected fitness rose.…”  Near the conclusion, they confirmed witnessing a type of genetic entropy: “A conspicuous feature of the mean-fitness trajectory for this population—and indeed for most experimental populations evolving in a constant environment—is that the rate of adaptation declined over time.”  The reason they gave was that “epistatic interactions contribute greatly to this deceleration by reducing the effect-size of the remaining beneficial mutations as a population approaches a fitness peak. In other words, epistasis acts as a drag that reduces the contribution of later beneficial mutations.”  No increases in adaptation or fitness were observed, and no explanation was offered for how neo-Darwinism could overcome the downward trend in fitness.
Another paper in the same issue of Science found similar bad news.  A group of researchers in Massachusetts put “diminishing returns” in the title of their paper.4  They introduced beneficial mutations into bacteria, but found them decelerating adaptation.  Their abstract said, “These results provide the first evidence that patterns of epistasis may differ for within– and between-gene interactions during adaptation and that diminishing returns epistasis contributes to the consistent observation of decelerating fitness gains during adaptation.”  Aware of the study by Khan et al,  they claimed that “across these two distinct model systems 7 of 10 alleles consistently showed antagonism, whereas only 2 exhibited synergy.” 
A look in both papers, however, showed no clear examples of evolutionary progress in the experiments, and certainly no new species arising.  In fact, the experiments were more a test of artificial selection—studying which mutants adapted to contrived laboratory conditions.  In addition, fitness gains were measured by reproduction rates which, in some cases of adaptation, might have deleterious trade-offs, such as metabolic cost.
Commenting on these papers in Science,5 three authors from University of Pennsylvania noted that, “In Evolution, the Sum Is Less than Its Parts.”  The figure caption explained, “The mutations conferred smaller marginal benefits in combination than they did individually. This antagonistic epistasis causesprogressively slower rates of adaptation over time.” Khryazhrimsky, Draghi and Plotkin referred to some microbe experiments that showed initial gains due to beneficial mutations (in isolated lab populations) that slowed to a crawl due to epistasis, or then “discover rare phenotypic innovations,” then diverge into populations that either coexist or compete.  More work will be needed, they said, to quantify these effects in the wild with different organisms, population sizes and natural ecologies. 
Though hopeful that evolution can march onward in spite of these genetic brakes, they admitted that “the prevalence of antagonistic epistasis measured by the two groups ensures predictable tempo of adaptation characterized by diminishing marginal returns.”  They pulled victory from the jaws of defeat, claiming that these experiments “represent resounding achievement for the reductionist approach to studying biology.
A pro-evolution article in Science Daily summarized the work of the first paper thorough the eyes of Tim Cooper [U of Houston], one of the participants.  “The more mutations the researchers added, the more they interfered with each other,” was one of the “surprising” results.  “It was as if the mutations got in each other’s way as they all tried to accomplish the same thing.”  Hopefully readers will pardon Cooper for the anthropomorphism.  “The effect of theirinteractions depended on the presence of other mutations, which turned out to be overwhelmingly negative.”  What does this mean for evolutionary progress?  “These results point us toward expecting to see the rate of a population’s fitness declining over time even with the continual addition of new beneficial mutations,” Cooper said.
In contrast to the depressing news in Science, three authors in Nature claimed hopeful news with mutations under epistasis.6  “Cryptic genetic variation promotes rapid evolutionary adaptation in an enzyme” was the optimistic title of their paper, but a close look at their experiment shows it was a case of artificial selection on ribozymes only.  It did not involve a real cell culture, and the gains from “cryptic variation” only showed adaptations to contrived conditions in the lab.  They explained the adaptation as a case of “pre-adaptation” or “exaptation” with mutations hiding out till an opportunity arrived for them to show some adaptation in the scientists’ contrived environments.  Their simplified model substituted for real evidence, because “this facilitating role for cryptic variation has not been proven, partly becausemost pertinent work focuses on complex phenotypes of whole organisms whose genetic basis is incompletely understood.”  Nevertheless, they claimed by extrapolation that “Our results highlight the positive role that robustness and epistasis can have in adaptive evolution.”  This paper came out in print a day before the pessimistic papers in Science.
Speaking of mutations, researchers at discovered “a chromosomal mutation responsible for a very rare condition in which people grow excess hair all over their bodies” (see Medical Xpress). While the benefit of such a condition might only count in the arctic, it shows that some mutations can have drastic effects.  Even if a hairy female could survive the cold, though, what male would want to marry her?   Such mutations would probably not become fixed in a population or else Eskimos would all have it.  Most mutations are nearly neutral and invisible to natural selection, as Sanford explained in detail in his book.  Because they are not eliminated by purifying selection, they therefore accumulate in the genome, dragging it into genetic entropy.  Mutations are not good material for natural selection.
1.  John Sanford, Genetic Entropy and the Mystery of the Genome (Ivan Press, 2005).
2. Ibid., pp. 109–111.
3. Khan et al., Negative Epistasis Between Beneficial Mutations in an Evolving Bacterial Population, Science, 3 June 2011: Vol. 332 no. 6034 pp. 1193–1196. : 10.1126/science.1203801.
4. Chou et al., Diminishing Returns Epistasis Among Beneficial Mutations Decelerates Adaptation, Science, 3 June 2011: Vol. 332 no. 6034 pp. 1190–1192, : 10.1126/science.1203799.
5. Khryazhrimsky, Draghi and Plotkin, In Evolution, the Sum Is Less than Its Parts, Science, 3 June 2011: Vol. 332 no. 6034 pp. 1160–1161, : 10.1126/science.1208072.
6. Hayden, Ferrada and Wagner, Cryptic genetic variation promotes rapid evolutionary adaptation in an enzyme, Nature, 474  (02 June 2011), pages 92–95, doi:10.1038/nature10083.
Only an evolutionist can find hope in this bad news. Re-read the 12/14/2006and 10/19/2004 entries to see evolutionary hopes get further dashed.  And even if an evolutionist can claim a real fitness innovation arose spontaneously, the organism will face newer and bigger hurdles (see04/09/2007).
Mutations are like weights on a swimmer, loading him down.  Beneficial mutations are so small, they are mere bubbles providing a tiny bit of buoyancy.  Now get other swimmers with weights clinging to him to illustrate epistasis; do you think he will evolve wings and fly?  Get real.  Even if one of them has lifeguard training, it will only delay the inevitable.  Remember, evolution has no direction and cannot see the shoreline.
Get John Sanford’s book; it will scare some genetic sense into any Darwinist.  Sanford was asked what has been the reaction to his book by Darwinists.  His answer was, “complete silence.”


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3 Re: Genetic entropy on Mon Mar 21, 2016 6:43 am


The book Genetic Entropy asserts there is a profound waiting time problem (see 2014 edition, chapter 9, page 133-136). This assertion strongly supports the previous work by Behe and others. Stated most succinctly, the waiting time problem is simply – there is not enough time for evolution to establish even the most trivial amount of new information. For example, in a typical mammalian population there is not enough time to establish within the population's genome as much information as would be equivalent to a specific "word" (string of nucleotides) in a specfic context. This waiting time problem was illustrated in the book Genetic Entropy using some simple calculations. The calculations were based upon the known human mutation rate (per nucleotide per generation), assuming a generation time of 20 years, a population size of 10,000 individuals, a 1% fitness benefit for all individuals that carry the newly created target "word" (i.e., a specific string of nucleotides), within a specific genomic location (context). These calculations showed that for such a population to establish even a single-letter word, on average, required about 18 million years. It was argued that as the word size increases linearly, the waiting time would increase exponentially.
The authors of the recently published paper tested these claims by employing state-of-the-art numerical simulation experiments to realistically enact the establishment of short genetic words within a model hominin population. These authors rigorously demonstrate that the waiting time problem is very real, validating the author's earlier mathematical approximations, and showing that as word size is lengthened, waiting times increase exponentially (Table 2 and Figure 2). This new paper shows that the waiting time problem is overwhelming – clearly showing that classic neo-Darwinian theory has failed in a profound way. Even given best-case scenarios (using parameter settings that are grossly over-generous), waiting times are consistently prohibitive, even for the shortest possible words. Establishment of a two-letter word requires at least 84 million years. A three-letter word requires at least 376 million years. A six-letter word requires over 4 billion years. An eight-letter word requires over 18 billion years.!latest-development/cqzd

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