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      The Fate of Transposable Elements in Asexual Populations

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      Genetics
      Genetics Society of America

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          Abstract

          Sexual reproduction and recombination are important for maintaining a stable copy number of transposable elements (TEs). In sexual populations, elements can be contained by purifying selection against host carriers with higher element copy numbers; however, in the absence of sex and recombination, asexual populations could be driven to extinction by an unchecked proliferation of TEs. Here we provide a theoretical framework for analyzing TE dynamics under asexual reproduction. Analytic results show that, in an infinite asexual population, an equilibrium in copy number is achieved if no element excision is possible, but that all TEs are eliminated if there is some excision. In a finite population, computer simulations demonstrate that small populations are driven to extinction by a Muller's ratchet-like process of element accumulation, but that large populations can be cured of vertically transmitted TEs, even with excision rates well below transposition rates. These results may have important consequences for newly arisen asexual lineages and may account for the lack of deleterious retrotransposons in the putatively ancient asexual bdelloid rotifers.

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          Most cited references36

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          Selfish genes, the phenotype paradigm and genome evolution.

          Natural selection operating within genomes will inevitably result in the appearance of DNAs with no phenotypic expression whose only 'function' is survival within genomes. Prokaryotic transposable elements and eukaryotic middle-repetitive sequences can be seen as such DNA's and thus no phenotypic or evolutionary function need be assigned to them.
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            The evolutionary dynamics of repetitive DNA in eukaryotes.

            Repetitive DNA sequences form a large portion of the genomes of eukaryotes. The 'selfish DNA' hypothesis proposes that they are maintained by their ability to replicate within the genome. The behaviour of repetitive sequences can result in mutations that cause genetic diseases, and confer significant fitness losses on the organism. Features of the organization of repetitive sequences in eukaryotic genomes, and their distribution in natural populations, reflect the evolutionary forces acting on selfish DNA.
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              The age and evolution of non-LTR retrotransposable elements.

              A comprehensive phylogenetic analysis was conducted of non-long-terminal-repeat (non-LTR) retrotransposons based on an extended sequence alignment of their reverse transcriptase (RT) domain. The 440 amino acid positions used included a region proposed to be similar to the "thumb" of the right-handed RT structure found in retroviruses. All identified non-LTR elements could be grouped into 11 distinct clades. Using the rates of sequence change derived from studies of the vertical inheritance of R1 and R2 elements in arthropods as a comparison, we found no evidence for the horizontal transmission of non-LTR elements. Assuming vertical descent, the phylogeny suggested that non-LTR elements are as old as eukaryotes, with each of the 11 clades dating back to the Precambrian era. The analysis enabled us to propose a simple chronology for the acquisition of different enzymatic domains in the evolution of the non-LTR class of retrotransposons. The first non-LTR elements were sequence specific by virtue of a restriction-enzyme-like endonuclease located downstream of the RT domain. Evolving from this original group were elements (eight clades) that acquired an apurinic-apyrimidic endonuclease-like domain upstream of the RT domain. Finally, four of these clades have inherited an RNase H domain downstream of the RT domain. The phylogenies of the AP endonuclease and RNase H domains were also determined for this report and are consistent with the monophyletic acquisition of these domains. These studies represent the most comprehensive effort to date to trace the evolution of a major class of transposable elements.
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                Author and article information

                Journal
                Genetics
                Genetics
                Genetics Society of America
                0016-6731
                1943-2631
                October 26 2006
                October 2006
                October 2006
                August 03 2006
                : 174
                : 2
                : 817-827
                Article
                10.1534/genetics.106.060434
                1602064
                16888330
                f8c9a3cf-16b8-4ace-8e26-662f6aa9ad42
                © 2006
                History

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