Different Species With The Same Junk DNA don-lindsay-archive.org/creation/dna_virus.html Four reasons the patterns arent random. First, the patterns are too large to randomly occur several times. Second, they were not found anywhere in the computer databases of previously known DNA patterns, meaning that they arent particularly probable. Third, randomness should have caused creatures that had one pattern but not the other. Fourth, they are found in the identical places on the chromosomes of different species. Random things should occur in random places. As the editors of Nature pointed out, the chance of two such events happening at the same location is virtually nil. Yet the patterns are found, not at one matching location, but at seven matching locations. The overall coincidence is virtually nil to the seventh power. Reasons that retroviruses didnt just infect multiple species. Cross-infection does happen. For example, AIDS is thought to have jumped from monkeys to humans. However, cross-infection is quite rare, and it only happens when the two target species share an environment. Cows and humpback whales do not share an environment, yet both have both patterns. Hippos and elephants do share some environments, but one has both patterns and the other has neither pattern. Cows and mice share some environments, but one has both patterns and the other has neither. Also, it is improbable that one virus could attack so many species and yet be the same: it should have had to mutate into several variants, as AIDS has. It is improbable that two viruses would both succeed in spreading widely. It is improbable that both would attack the identical set of targets. But more importantly, if a retrovirus had infected multiple species, it should have left itself in a different place in each species. After all, leaving a pattern in junk DNA is an accident: a virus dies as a result. In fact, in cows, one of the patterns has been copied to five different places. Clearly, there is no single place in the junk DNA where the pattern should be, or tries to be. So, finding a pattern in the exact same place (at the same genetic locus) in two species implies that the two species inherited the pattern. Finding one pattern at the same place in five different whales, a dolphin and a porpoise settles the matter. That locus must have been affected once, in their common ancestor. Arguments obsolete, because: 1) There is no such thing as junk DNA. 2) Transposons they are in the regulation of expression of genes. Transposons Integrates into the genome at specific sites (sticky ends of; classconnection.s3.amazonaws/55/flashcards/1122055/jpg/picture161330370511072.jpg), and Therefore in some species Integrates identical areas,; This the same pattern of regulation of expression of genes.; detectingdesign/pseudogenes.html Transposons, or Jumping Genes: Not Junk DNA? nature/scitable/topicpage/transposons-or-jumping-genes-not-junk-dna-1211 For decades, scientists dismissed transposable elements, also known as transposons or “jumping genes”, as useless “junk DNA”. But are they really? Transposable elements (TEs), also known as jumping genes or transposons, are sequences of DNA that move (or jump) from one location in the genome to another. Maize geneticist Barbara McClintock discovered TEs in the 1940s, and for decades thereafter, most scientists dismissed transposons as useless or junk DNA. McClintock, however, was among the first researchers to suggest that these mysterious mobile elements of the genome might play some kind of regulatory role, determining which genes are turned on and when this activation takes place (McClintock, 1965). At about the same time that McClintock performed her groundbreaking research, scientists Roy Britten and Eric Davidson further speculated that TEs not only play a role in regulating gene expression, but also in generating different cell types and different biological structures, based on where in the genome they insert themselves (Britten & Davidson, 1969). Britten and Davidson hypothesized that this might partially explain why a multicellular organism has many different types of cells, tissues, and organs, even though all of its cells share the same genome. Consider your own body as an example: You have dozens of different cell types, even though the majority of cells in your body have exactly the same DNA. If every single gene was expressed in every single one of your cells all the time, you would be one huge undifferentiated blob of matter! The early speculations of both McClintock and Britten and Davidson were largely dismissed by the scientific community. Only recently have biologists begun to entertain the possibility that this so-called junk DNA might not be junk after all. In fact, scientists now believe that TEs make up more than 40% of the human genome (Smit, 1999). It is also widely believed that TEs might carry out some biological function, most likely a regulatory one—just as McClintock and Britten and Davidson speculated. Like all scientific hypotheses, however, data from multiple experiments were required to convince the scientific community of this possibility. The same applies to endogenous retroviruses, which are found in the same locations in the genomes of various species. These retroviruses potentially useful functions in organisms; Genetic defects are Caused by damage to the genetic sequences. In endogenous viruses too. Only useful sequences can cause disease if they are damaged; ncbi.nlm.nih.gov/pubmed/17199106 [....] They also block exogenous retrovirus replication by receptor interference or antisense mRNA. Their presence is considered to be connected with a number of autoimmunological diseases (multiple sclerosis, insulin-dependent diabetes mellitus, systemic lupus erythematosus), cancer, or even psychiatric disorders (schizophrenia). There are also other problems connected with the potential role of ERVs in genomic therapy (with retroviruses vectors) and transplantology (xenotransplantation). Neo-darwinist once again succumbed to the illusion.
Posted on: Sat, 01 Feb 2014 01:16:45 +0000