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1. Eytan H. Suchard, "Genetic Algorithms and Irreduciblity," Metivity Ltd, email: Eytan_il at netvision dot com (2007) 

• Abstract Genetic Algorithms are a good method of optimization if the target function to be optimized conforms to some important properties. The most importantof a is thatthe sought for solution can be approached by cumulative mutations such that the Markov chain which models the intermediate genes has a probability that doesn‘t tend to zero as the gene grows. In other words each improvementof the gene -setof 0s and 1s follows from a reasonable edit distance - minimum number of bits that change between two genes -and the overa probability of these mutations does not vanish. If for reaching an improvement, the edit distance is too big then GAs are not usefuleven after millions of generations and huge populations of millions of individuals. If on the other hand the probability of a chain of desired mutations tends to zero as the chain grows then also the GA fails. There are target functions that can be approached by cumulative mutations but yet, statistically defy GAs. This short paper represents a relatively simple target function that its minimization can be achieved stepwise by small cumulative mutations but yet GAs fail to converge to the right solution in ordinary GAs. [ pdf | code ] 

2. Peter Borger, Evidence for the design of life: part 1—genetic redundancy. TIRIO, Germany. email: peterborger at hotmail dot com

• Abstract Knockout strategies have demonstrated that the function of many genes cannot be studied by disrupting them in model organisms because the inactivation of these genes does not lead to a phenotypic effect. For living systems, this peculiar phenomenon of genetic redundancy seems to be the rule rather than the exception. Genetic redundancy is now defined as the situation in which the disruption of a gene is selectively neutral. Biology shows us that 1) two or more genes in an organism can often substitute for each other, 2) some genes are just there in a silent state. Inactivation of such redundant genes does not jeopardize the individual’s reproductive success and has no effect on survival of the species. Genetic redundancy is the big surprise of modern biology. Because there is no association between redundant genes and genetic duplications, and because redundant genes do not mutate faster than essential genes, redundancy therefore brings down more than one pillar of contemporary evolutionary thinking. [pdf]

3. Peter Borger, Evidence for the design of life: part 2—Baranomes. TIRIO, Germany. email: peterborger at hotmail dot com

• Abstract The major difference between the evolution and creation paradigms is that the evolutionist believes that the natural variation found in populations can explain microbe-to-man evolution via natural selection (Darwinism), while the creationist believes it cannot. This is because the evolutionary, naturalistic framework requires something creationists hold impossible: a continuous addition of novel genetic information unrelated to that already existing. In the creation paradigm neither variation nor selection is denied; what is rejected is that the two add up to explain the origin of species. In part 1, I discussed genetic redundancy and how redundant genes are not associated with genetic duplications and do not mutate faster than essential genes. These observations are sufficient to completely overturn the current evolutionary paradigm and could form the basis for a novel creationist framework help us understand genomes, variation and speciation. In this second part, I argue and provide biological evidence that life on Earth thrived due to frontloaded baranomes—pluripotent, undifferentiated genomes with an intrinsic ability for rapid adaptation and speciation. [pdf]

4. Peter Borge, The design of life: part 3—an introduction to variation--inducing genetic elements. TIRIO, Germany. email: peterborger at hotmail dot com

• Abstract The inheritance of traits is determined by genes: long stretches of DNA that are passed down from generation to generation. Usually, genes consist of a coding part and a non-coding regulatory part. The coding part of the gene determines the functional output, whereas the non-coding portion contains switches and units that determine when, where and how much of the functional output should be generated. Point-mutations in the coding part are predominantly neutral or slightly detrimental genetic noise that accumulates in the genome, whereas point-mutations in the regulatory part of DNA units can induce variation with respect to the amount of output. Previously, in part 2, I argued that created kinds were frontloaded with baranomes: that is, pluripotent genomes with an ability to induce variation from within. The output of (morpho)genetic algorithms present in the baranome can readily be modulated by variation-inducing genetic elements (VIGEs). VIGEs are frontloaded genetic elements normally referred to as endogenous retroviruses, insertion sequences, LINEs, SINEs, microsatellites, transposons, insertion sequences, and the like. In the present report, these transposable and repetitive DNA sequences are redefined as VIGEs, which solves the RNA virus paradox. The (morpho)genetic algorithms were designed in such way that VIGEs easily integrated into it and became a part of it, hence making the program explicit.. [pdf]

4. Peter Borge, The design of life: part 4—variation inducing genetic elements and their function. TIRIO, Germany. email: peterborger at hotmail dot com

• Abstract Endogenous retroviruses (ERVs) are believed to be the selfish remnants of ancient RNA viruses that invaded the cells of organisms millions of years ago and now merely free-ride the genome in order to be replicated. This selfish gene thinking still dominates the public scene, but well-informed biologists know that the view among researchers is rapidly changing. Increasingly, ancient RNA viruses and their remnants are being thought of as having played (and still do) a significant role in protein evolution, gene structure, and transcriptional regulation. As argued in part 3 of this series of articles, ERVs may be the executors of genetic variation, and qualify as specifically designed variation-inducing genetic elements (VIGEs) responsible for variation in higher organisms. VIGEs induce variation by duplication, transposition, and may even rearrange chromosomes. This extraordinary claim requires extraordinary scientific support, which is present throughout this paper. In addition, the VIGE hypothesis may be a framework to understand the origin of diseases and explain rapid speciation events through facilitated chromosome swapping. [pdf]