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      Tracing the history of LINE and SINE extinction in sigmodontine rodents

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      1 , 2 , 1 , 2 , 1 , 2 ,
      Mobile DNA
      BioMed Central

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          Abstract

          Background

          L1 retrotransposons have co-evolved with their mammalian hosts for the entire history of mammals and currently compose ~ 20% of a mammalian genome. B1 retrotransposons are dependent on L1 for retrotransposition and span the evolutionary history of rodents since their radiation. L1s were found to have lost their activity in a group of South American rodents, the Sigmodontinae, and B1 inactivation preceded the extinction of L1 in the same group. Consequently, a basal group of sigmodontines have active L1s but inactive B1s and a derived clade have both inactive L1s and B1s. It has been suggested that B1s became extinct during a long period of L1 quiescence and that L1s subsequently reemerged in the basal group.

          Results

          Here we investigate the evolutionary histories of L1 and B1 in the sigmodontine rodents and show that L1 activity continued until after the L1-extinct clade and the basal group diverged. After the split, L1 had a small burst of activity in the former group, followed by extinction. In the basal group, activity was initially low but was followed by a dramatic increase in L1 activity. We found the last wave of B1 retrotransposition was large and probably preceded the split between the two rodent clades.

          Conclusions

          Given that L1s had been steadily retrotransposing during the time corresponding to B1 extinction and that the burst of B1 activity preceding B1 extinction was large, we conclude that B1 extinction was not a result of L1 quiescence. Rather, the burst of B1 activity may have contributed to L1 extinction both by competition with L1 and by putting strong selective pressure on the host to control retrotransposition.

          Electronic supplementary material

          The online version of this article (10.1186/s13100-019-0164-5) contains supplementary material, which is available to authorized users.

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          Most cited references53

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          FLASH: fast length adjustment of short reads to improve genome assemblies.

          Next-generation sequencing technologies generate very large numbers of short reads. Even with very deep genome coverage, short read lengths cause problems in de novo assemblies. The use of paired-end libraries with a fragment size shorter than twice the read length provides an opportunity to generate much longer reads by overlapping and merging read pairs before assembling a genome. We present FLASH, a fast computational tool to extend the length of short reads by overlapping paired-end reads from fragment libraries that are sufficiently short. We tested the correctness of the tool on one million simulated read pairs, and we then applied it as a pre-processor for genome assemblies of Illumina reads from the bacterium Staphylococcus aureus and human chromosome 14. FLASH correctly extended and merged reads >99% of the time on simulated reads with an error rate of <1%. With adequately set parameters, FLASH correctly merged reads over 90% of the time even when the reads contained up to 5% errors. When FLASH was used to extend reads prior to assembly, the resulting assemblies had substantially greater N50 lengths for both contigs and scaffolds. The FLASH system is implemented in C and is freely available as open-source code at http://www.cbcb.umd.edu/software/flash. t.magoc@gmail.com.
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            L1 retrotransposition in human neural progenitor cells.

            Long interspersed element 1 (LINE-1 or L1) retrotransposons have markedly affected the human genome. L1s must retrotranspose in the germ line or during early development to ensure their evolutionary success, yet the extent to which this process affects somatic cells is poorly understood. We previously demonstrated that engineered human L1s can retrotranspose in adult rat hippocampus progenitor cells in vitro and in the mouse brain in vivo. Here we demonstrate that neural progenitor cells isolated from human fetal brain and derived from human embryonic stem cells support the retrotransposition of engineered human L1s in vitro. Furthermore, we developed a quantitative multiplex polymerase chain reaction that detected an increase in the copy number of endogenous L1s in the hippocampus, and in several regions of adult human brains, when compared to the copy number of endogenous L1s in heart or liver genomic DNAs from the same donor. These data suggest that de novo L1 retrotransposition events may occur in the human brain and, in principle, have the potential to contribute to individual somatic mosaicism.
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              DNA methylation and the frequency of CpG in animal DNA.

              A Bird (1980)
              An analysis of nearest neighbour dinucleotide frequencies and the level of DNA methylation in animals strongly supports the suggestion that 5-methylcytosine (5mC) tends to mutate abnormally frequently to T. This tendency is the likely cause of the CpG deficiency in heavily methylated genomes.
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                Author and article information

                Contributors
                leiyangly@gmail.com
                lscott@uidaho.edu
                +1(208)885-7805 , hwichman@uidaho.edu
                Journal
                Mob DNA
                Mob DNA
                Mobile DNA
                BioMed Central (London )
                1759-8753
                21 May 2019
                21 May 2019
                2019
                : 10
                : 22
                Affiliations
                [1 ]ISNI 0000 0001 2284 9900, GRID grid.266456.5, Department of Biological Sciences, University of Idaho, ; Moscow, ID USA
                [2 ]ISNI 0000 0001 2284 9900, GRID grid.266456.5, Institute for Bioinformatics and Evolutionary Studies, , University of Idaho, ; Moscow, ID USA
                Article
                164
                10.1186/s13100-019-0164-5
                6530004
                31139266
                4f597ece-9e15-4d7a-a532-cd61c025d289
                © The Author(s). 2019

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 24 January 2019
                : 30 April 2019
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/100000057, National Institute of General Medical Sciences;
                Award ID: R01-GM38737
                Award ID: P20GM103408
                Award ID: P30GM103324
                Award ID: P20GM102420
                Funded by: FundRef http://dx.doi.org/10.13039/100000076, Directorate for Biological Sciences;
                Award ID: DDIG-1210694
                Award Recipient :
                Categories
                Research
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                © The Author(s) 2019

                Genetics
                Genetics

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