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AGelbert

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Re: Darwin
« Reply #165 on: July 23, 2018, 12:30:51 pm »
Agelbert NOTE: Smileys added by yours truly.

.DarwinsPredictions

Evolutionary causes predictions

Mutations are not adaptive

In the twentieth century, the theory of evolution predicted that mutations are not adaptive or directed. In other words, mutations were believed to be random with respect to the needs of the individual. As Julian Huxley put it, “Mutation merely provides the raw material of evolution; it is a random affair, and takes place in all directions. … in all cases they are random in relation to evolution. Their effects are not related to the needs of the organisms.” (Huxley, 36) Or as Jacques Monod explained:

chance alone is at the source of every innovation, of all creation in the biosphere. Pure chance, absolutely free but blind, at the very root of the stupendous edifice of evolution: this central concept of modern biology is no longer one among other possible or even conceivable hypotheses. It is today the sole conceivable hypothesis, the only one that squares with observed and tested fact. And nothing warrants the supposition—or the hope—that on this score our position is likely ever to be revised. (Monod, 112)

Ronald Fisher 😈 wrote that mutations are “random with respect to the organism’s need” (Orr). This fundamental prediction persisted for decades as a recent paper explained: “mutation is assumed to create heritable variation that is random and undirected.” (Chen, Lowenfeld and Cullis)

But that assumption is now known to be false. The first problem is that the mutation rate is adaptive. For instance, when a population of bacteria is subjected to harsh conditions it tends to increase its mutation rate. It is as though a signal has been sent saying, “It is time to adapt.” Also, a small fraction of the population increases its mutation rates even higher yet. These hypermutators ensure that an even greater variety of adaptive change is explored. (Foster) Experiments have also discovered that duplicated DNA segments may be subject to higher mutation rates. Since the segment is a duplicate it is less important to preserve and, like a test bed, appears to be used to experiment with new designs. (Wright)

The second problem is that organisms use strategies to direct the mutations according to the threat. Adaptive mutations have been extensively studied in bacteria. Experiments typically alter the bacteria food supply or apply some other environmental stress causing mutations that target the specific environmental stress. (Burkala, et. al.; Moxon, et. al; Wright) Adaptive mutations have also been observed in yeast (Fidalgo, et. al.; David, et. al.) and flax plants. (Johnson, Moss and Cullis) One experiment found repeatable mutations in flax in response to fertilizer levels. (Chen, Schneeberger and Cullis) Another exposed the flax to four different growth conditions and found that environmental stress can induce mutations that result in “sizeable, rapid, adaptive evolutionary responses.” (Chen, Lowenfeld and Cullis) In response to this failed prediction some evolutionists  now are saying that evolution somehow created the mechanisms that cause mutations to be adaptive.

References

Burkala, E., et. al. 2007. “Secondary structures as predictors of mutation potential in the lacZ gene of Escherichia coli.” Microbiology 153:2180-2189.

Chen, Y., R. Lowenfeld, C. Cullis. 2009. “An environmentally induced adaptive (?) insertion event in flax.” International Journal of Genetics and Molecular Biology 1:38-47.

Chen, Y., R. Schneeberger, C. Cullis. 2005. “A site-specific insertion sequence in flax genotrophs induced by environment.” New Phytologist 167:171-180.

David, L., et. al. 2010. “Inherited adaptation of genome-rewired cells in response to a challenging environment.” HFSP Journal 4:131–141.

Fidalgo, M., et. al. 2006. “Adaptive evolution by mutations in the FLO11 gene.” Proceedings of the National Academy of Sciences 103:11228-11233.

Foster, P. 2005. “Stress responses and genetic variation in bacteria.” Mutation Research / Fundamental and Molecular Mechanisms of Mutagenesis 569:3-11.

Huxley, Julian. 1953. Evolution in Action. New York: Signet Science Library Book.

Johnson, C., T. Moss, C. Cullis. 2011. “Environmentally induced heritable changes in flax.” J Visualized Experiments 47:2332.

Monod, Jacques. 1971. Chance & Necessity. New York: Vintage Books.

Moxon, E., et. al. 1994. “Adaptive evolution of highly mutable loci in pathogenic bacteria.” Current Biology 4:24-33.

Orr, H. 2005. “The genetic theory of adaptation: a brief history.” Nature Review Genetics 6:119-127.
Wright, B. 2000. “A biochemical mechanism for nonrandom mutations and evolution.” J Bacteriology 182:2993-3001.


https://sites.google.com/site/darwinspredictions/mutations-are-not-adaptive
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AGelbert

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Re: Darwin
« Reply #166 on: July 24, 2018, 01:07:56 pm »
Agelbert NOTE: Smileys added by yours truly.


.DarwinsPredictions

Evolutionary causes predictions

Competition is greatest between neighbors

Darwin’s basic theory of evolution, by itself, did not account for the tree-like, hierarchical pattern the species were thought to form. Darwin was keenly aware of this shortcoming and wrestled with it for years. He finally conceived of a solution for why modified offspring would continue to evolve away and diverge from their parents. The principle of divergence, the last major theoretical addition before Darwin published his book, held that competition tends to be strongest between the more closely related organisms. This would cause a splitting and divergence, resulting in the traditional evolutionary tree pattern. (Desmond and Moore 1991, 419-420; Ridley, 378-379)

But no such trend has been observed. 🧐 In a major study of competition between freshwater green algae species, the level of competition between pairs of species was found to be uncorrelated with the evolutionary distance between the pair of species. As the researchers explained, Darwin “argued that closely related species should compete more strongly and be less likely to coexist. For much of the last century, Darwin’s hypothesis has been taken at face value […] Our results add to a growing body of literature that fails to support Darwin’s original competition-relatedness hypothesis.” (Venail, et. al., 2, 9) The team spent months trying to resolve the problem, but to no avail. As one of the researchers explained:

It was completely unexpected. When we saw the results, we said “this can’t be.” ::)  We sat there banging our heads against the wall. Darwin’s hypothesis has been with us for so long, how can it not be right? When we started coming up with numbers that showed he [Darwin] wasn’t right, we were completely baffled. … We should be able to look at the Tree of Life, and evolution should make it clear who will win in competition and who will lose. But the traits that regulate competition can’t be predicted from the Tree of Life. (Cimons) ;D

Why this long-standing prediction was not confirmed remains unknown. Apparently there are more complicating factors 🕵️ that influence competition in addition to evolutionary relatedness. 

References

Cimons, Marlene. 2014. “Old Idea About Ecology Questioned by New Findings.” National Science Foundation.

Desmond, Adrian, James Moore. 1991. Darwin: The Life of a Tormented Evolutionist. New York: W. W. Norton.

Ridley, Mark. 1993. Evolution. Boston: Blackwell Scientific.
Venail , P.A., A. Narwani , K. Fritschie, M. A. Alexandrou, T. H. Oakley, B. J. Cardinale. 2014. “The influence of phylogenetic relatedness on competition and facilitation among freshwater algae in a mesocosm experiment.” Journal of Ecology, DOI: 10.1111/1365-2745.12271.

https://sites.google.com/site/darwinspredictions/competition-is-greatest-between-neighbors

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AGelbert

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Re: Darwin
« Reply #167 on: July 25, 2018, 07:44:38 pm »
Agelbert NOTE: Smileys added by yours truly. 


.DarwinsPredictions

Molecular evolution predictions

Protein evolution

Protein coding genes make up only a small fraction of the genome in higher organisms but their protein products are crucial to the operation of the cell. They are the workers behind just about every task in the cell, including digesting food, synthesizing chemicals, structural support, energy conversion, cell reproduction and making new proteins. And like a finely tuned machine, proteins do their work very well. Proteins are ubiquitous in all of life and must date back to the very early stages of evolution. So evolution predicts that proteins evolved when life first appeared, or not long after. But despite enormous research efforts the science clearly shows that such protein evolution is astronomically unlikely.  ;D

One reason the evolution of proteins is so difficult is that most proteins are extremely specific designs in an otherwise rugged fitness landscape. This means it is difficult for natural selection to guide mutations toward the needed proteins. In fact, four different studies, done by different groups and using different methods, all report that roughly 1070 evolutionary experiments would be needed to get close enough to a workable protein before natural selection could take over to refine the protein design. For instance, one study concluded that 1063 attempts would be required for a relatively short protein. (Reidhaar-Olson) And a similar result (1065 attempts required) was obtained by comparing protein sequences. (Yockey) Another study found that from 1064 to 1077 attempts are required (Axe) and another study concluded that 1070 attempts would be required. (Hayashi) In that case the protein was only a part of a larger protein which otherwise was intact, thus making for an easier search. Furthermore these estimates are optimistic because the experiments searched only for single-function proteins whereas real proteins perform many functions.

This conservative estimate of 1070 attempts required to evolve a simple protein is astronomically larger than the number of attempts that are feasible. 👀 ;D And explanations of how evolution could achieve a large number of searches, or somehow obviate this requirement, require the preexistence of proteins and so are circular*. For example, one paper estimated that evolution could have made 1043 such attempts. But the study assumed the entire history of the Earth is available, rather than the limited time window that evolution actually would have had. Even more importantly, it assumed the preexistence of a large population of bacteria (it assumed the earth was completely covered with bacteria). And of course, bacteria are full of proteins. Clearly such bacteria would not exist before the first proteins evolved. (Dryden) Even with these helpful and unrealistic assumptions the result was twenty seven orders of magnitude short of the requirement.   

Given these several significant problems, the chances of evolution finding proteins from a random start are, as one evolutionist explained, “highly unlikely.” (Tautz)

Or as another evolutionist put it, “Although the origin of the first, primordial genes may ultimately be traced back to some precursors in the so-called ‘RNA world’ billions of years ago, their origins remain enigmatic.” (Kaessmann)


 


Quote
* Circular reasoning

Circular reasoning (Latin: circulus in probando, "circle in proving";[1] also known as circular logic) is a logical fallacy in which the reasoner begins with what they are trying to end with.
 

https://en.wikipedia.org/wiki/Circular_reasoning


References

Axe, D. 2004. “Estimating the prevalence of protein sequences adopting functional enzyme folds.” J Molecular Biology 341:1295-1315.

Dryden, David, Andrew Thomson, John White. 2008. “How much of protein sequence space has been explored by life on Earth?.” J. Royal Society Interface 5:953-956.

Hayashi, Y., T. Aita, H. Toyota, Y. Husimi, I. Urabe, T. Yomo. 2006. “Experimental Rugged Fitness Landscape in Protein Sequence Space.” PLoS ONE 1:e96.

Kaessmann, H. 2010. “Origins, evolution, and phenotypic impact of new genes.” Genome Research 10:1313-26.

Reidhaar-Olson J., R. Sauer. 1990. “Functionally acceptable substitutions in two alpha-helical regions of lambda repressor.” Proteins 7:306-316.

Tautz, Diethard, Tomislav Domazet-Lošo. 2011. “The evolutionary origin of orphan genes.” Nature Reviews Genetics 12:692-702.

Yockey, Hubert. 1977. “A calculation of the probability of spontaneous biogenesis by information theory.” J Theoretical Biology 67:377–398.

https://sites.google.com/site/darwinspredictions/protein-evolution


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AGelbert

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Re: Darwin
« Reply #168 on: July 26, 2018, 10:05:20 pm »
Agelbert NOTE: For those who are unfamilar with Histones, I am posting some info and a video to help make clear to you how absolutely essential they are to life. 

Quote
Histones are one of the specific proteins involved in cell division and cancer. Technically, the ball-like groups of histones are referred to as nucleosomes, but--for simplicity--the website will continue to refer to these groups as histones.

In more general terms, histones are the protein “balls” that DNA wraps around in order to help DNA coil itself and condense into a chromosome during interphase. In fact, the image of nucleosomes (groups of histones) strung along a strand of DNA is often referred to as the "Beads on a String" model.

In the image below, you can see the histones, drawn as gray spheres that attach to the DNA and each other as the DNA condenses into a chromosome that can be easily divided and transported during cell division.



We, however, are interested in just the histones, as pictured below:


The video below provides a good representation of what histones look like in the cell. The clip denotes the histones as groups of orange spheres wrapped in blue globular DNA. Courtesy of jccairs.


http://www.unc.edu/depts/our/hhmi/hhmi-ft_learning_modules/proteinsmodule/histones/index.html

You read that part about cell division, but, leaving the cancer issue aside for the moment, Histones have other vital functions. You all know what an anti-histamine spray is. Certain types of Histones cause the release of histamines (vasodilators - relax blood vessel smooth muscles and make them leaky) which give you a runny nose. It is an immune system response to get rid of something your body does not want. An anti-histamine spray counteracts that. You may not like that runny nose, but keeping it from running may not help in getting rid of some bacterial or viral agent attacking you, so please keep that in mind.

You also should know about the Histone that sends histamines to your H3 receptors when you eat sweets (they are located throughout your body). When those H3 receptors get hit too often, they become sensitized and more and more histamines are required to make the H3 receptors work. What work is that? It's calling for insulin to process the sugar. Eating too much sugar triggers a massive amount of histamines towards the H3 receptors. When the H3 receptors get overtaxed over a number of years, the person develops Diabetes.

I apologize for being so brief, but the point I wish to make is that we cannot function without Histones and that all of their functions are extremely fine tuned and targeted. Histones are an irreducibly complex part of the eukaryotic cell (Eukaryotic means true=Eu - karyot=nucleus versus Prokaryotic=bacterial cells - Pro=before) design.

They are either all there or they do not work. In the case of cancer, they work too much, which is also not part of their function. All biological functions work inside a life band of "not too little" and "not too much" activity. It is ludicrous to claim that any organism had a non-functioning partial group of all the histones that just randomly mutated to be an extremely precisely targeted tool of cell division and the immune system. Without Histones (and several other irreducibly complex parts of the celluar anatomy and physiology that work in precise harmony), there is no life because there is no cell division, period.  The fact thar Eukaryotic Histones can continue to function with several deleterious mutations, contrary to what evolutionary theory had predicted, strengthens the hypothesis of a robust original design, even though evolutionists are trying to talk their way around this.


Smileys added by yours truly.


.DarwinsPredictions

Molecular evolution predictions

Histone proteins cannot tolerate much change

Histones are proteins which serve as the hubs about which DNA is wrapped. They are highly similar across vastly different species which means they must have evolved early in evolutionary history. As one textbook explains, “The amino acid sequences of four histones are remarkably similar among distantly related species. … The similarity in sequence among histones from all eukaryotes indicates that they fold into very similar three-dimensional conformations, which were optimized for histone function early in evolution in a common ancestor of all modern eukaryotes.” (Lodish et. al., Section 9.5) And this high similarity among the histones also means they must not tolerate change very well, as another textbook explains: “Changes in amino acid sequence are evidently much more harmful for some proteins than for others. … virtually all amino acid changes are harmful in histone H4. We assume that individuals who carried such harmful mutations have been eliminated from the population by natural selection.” (Alberts et. al. 1994, 243)

So the evolutionary prediction is that in these histone proteins practically all changes are deleterious: “As might be expected from their fundamental role in DNA packaging, the histones are among the most highly conserved eucaryotic proteins. For example, the amino acid sequence of histone H4 from a pea and a cow differ at only at 2 of the 102 positions. This strong evolutionary conservation suggests that the functions of histones involve nearly all of their amino acids, so that a change in any position is deleterious to the cell.” (Alberts et. al. 2002, Chapter 4)

This prediction has also been given in popular presentations of the theory: “Virtually all mutations impair histone’s function, so almost none get through the filter of natural selection. The 103 amino acids in this protein are identical for nearly all plants and animals.” (Molecular Clocks: Proteins That Evolve at Different Rates)

But this prediction has turned out to be false. An early study suggested that one of the histone proteins could well tolerate many changes. (Agarwal and Behe) And later studies confirmed and expanded this finding: “despite the extremely well conserved nature of histone residues throughout different organisms, only a few mutations on the individual residues (including nonmodifiable sites) bring about prominent phenotypic defects.” (Kim et. al.)

Similarly another paper documented these contradictory results: “It is remarkable how many residues in these highly conserved proteins can be mutated and retain basic nucleosomal function. … The high level of sequence conservation of histone proteins across phyla suggests a fitness advantage of these particular amino acid sequences during evolution.  Yet comprehensive analysis indicates that many histone mutations have no recognized phenotype.” (Dai et. al.) In fact, even more surprising, many mutations actually raised the fitness level. (Dai et. al.)

References

Agarwal, S., M. Behe. 1996. “Non-conservative mutations are well tolerated in the globular region of yeast histone H4.” J Molecular Biology 255:401-411.

Alberts, Bruce., D. Bray, J. Lewis, M. Raff, K. Roberts, J. Watson. 1994. Molecular Biology of the Cell. 3d ed. New York: Garland Publishing.

Alberts, Bruce., A. Johnson, J. Lewis, et. al. 2002. Molecular Biology of the Cell. 4th ed. New York: Garland Publishing. http://www.ncbi.nlm.nih.gov/books/NBK26834/

Dai, J., E. Hyland, D. Yuan, H. Huang, J. Bader, J. Boeke. 2008. “Probing nucleosome function: a highly versatile library of synthetic histone H3 and H4 mutants.” Cell 134:1066-1078.

Kim, J., J. Hsu, M. Smith, C. Allis. 2012. “Mutagenesis of pairwise combinations of histone amino-terminal tails reveals functional redundancy in budding yeast.” Proceedings of the National Academy of Sciences 109:5779-5784.

Lodish H., A. Berk, S. Zipursky, et. al. 2000. Molecular Cell Biology. 4th ed. New York: W. H. Freeman. http://www.ncbi.nlm.nih.gov/books/NBK21500/

“Molecular Clocks: Proteins That Evolve at Different Rates.” 2001. WGBH Educational Foundation and Clear Blue Sky Productions.

https://sites.google.com/site/darwinspredictions/histone-proteins-cannot-tolerate-much-change


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