Article

Retroviruses and Primate Genome Evolution

Institute of Molecular Genetics RAS, Kurchatov Sq., 123182 Moscow, Russia.
BioEssays (Impact Factor: 4.73). 02/2000; 22(2):161-71. DOI: 10.1002/(SICI)1521-1878(200002)22:2<161::AID-BIES7>3.0.CO;2-X
Source: PubMed

ABSTRACT

Human endogenous retroviruses (HERVs), probably representing footprints of ancient germ-cell retroviral infections, occupy about 1% of the human genome. HERVs can influence genome regulation through expression of retroviral genes, either via genomic rearrangements following HERV integrations or through the involvement of HERV LTRs in the regulation of gene expression. Some HERVs emerged in the genome over 30 MYr ago, while others have appeared rather recently, at about the time of hominid and ape lineages divergence. HERVs might have conferred antiviral resistance on early human ancestors, thus helping them to survive. Furthermore, newly integrated HERVs could have changed the pattern of gene expression and therefore played a significant role in the evolution and divergence of Hominoidea superfamily. Comparative analysis of HERVs, HERV LTRs, neighboring genes, and their regulatory interplay in the human and ape genomes will help us to understand the possible impact of HERVs on evolution and genome regulation in the primates. BioEssays 22:161-171, 2000.

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    • "For example, a DNA transposon named " Tigger " gave rise to 308 numerous, miniature inverted repeat transposable element sequences in the genome of 309 ancestral primates (Smit and Riggs, 1996). Next, ERVs comprise nearly 1% of the human 310 genome (Sverdlov, 2000) and are the remnants of ancient germline retroviral infections (Fig. 3114). The integration of ERVs into the germline allows them to be inherited in a Mendelian 312 fashion. "
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    ABSTRACT: The Human Genome Project revealed that almost half of the human genome consists of transposable elements (TEs), which are also abundant in non-human primates. Various studies have confirmed the roles of different TE families in primate evolution. TEs such as endogenous retroviruses (ERVs), long terminal repeats (LTRs), long interspersed nuclear elements (LINEs) and short interspersed nuclear elements (SINEs) all have numerous effects on the primate genome, including genomic rearrangement, regulatory functions and epigenetic mechanisms. This review offers an overview of research on TEs, including our current understanding of their presence in modern primate lineages, their evolutionary origins, and their regulatory and modifying effects on primate as well as human genomes. The information provided here should be useful for the study of primate genomics.
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    • "Despite their similar propagation mechanisms, retroviruses synthesize a glycoprotein " ENVELOPE " which provides cell-to-cell transfer of retrovirus. However, retrotransposons lack a functional envelope domain (Sverdlov 2000). Class II elements are characterized by terminal inverted repeats (TIRs) and they use DNA as a direct-transposition intermediate. "
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    ABSTRACT: Molecular marker is a nucleotide sequence associated with a trait of interest. Molecular marker techniques are based on either hybridization or Polymerase Chain Reaction (PCR) and rely on DNA polymorphisms between samples. Various PCR-based markers are widely used for diverse purposes and their technical properties have been widely explored. New and improved techniques have been developed by a combination of different strategies e.g. cDNAs, enzyme digestion or the utilization of specific sequences e.g. expressed sequence tags (ESTs), microsatellites, retrotransposons. Retrotransposons are a class (Class I) of transposable elements (TE) and constitute a major portion of the genome in plants with large genomes. They are important for chromatin modifications and epigenetic reprogramming. Retrotransposons are also an ideal target for developing molecular marker techniques because of their amplification mechanism and sequence characteristics. There are different types of transposon based marker techniques. Some of them are; Inter-Retrotransposon Amplified Polymorphism (IRAP), Retrotransposon-Microsatellite Amplified Polymorphism (REMAP), inter Primer Binding Site
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    • "Similarly, as the ERVs in a genome are only derived from a relatively small number of ERV lineages, any replication affinity of particular lineages could, in principle, bias the result. For example, in humans one-third of all ERVs are descended from thirty-one to forty distinct colonizations [3,25]. "
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    ABSTRACT: We wish to understand how sex and recombination affect endogenous retroviral insertion and deletion. While theory suggests that the risk of ectopic recombination will limit the accumulation of repetitive DNA in areas of high meiotic recombination, the experimental evidence so far has been inconsistent. Under the assumption of neutrality, we examine the genomes of eighteen species of animal in order to compute the ratio of solo-LTRs that derive from insertions occurring down the male germ line as opposed to the female one (male bias). We also extend the simple idea of comparing autosome to allosome in order to predict the ratio of full-length proviruses we would expect to see under conditions of recombination linked deletion or otherwise. Using our model, we predict the ratio of allosomal to autosomal full-length proviruses to lie between 3/2 and 2/3 under increasing male bias in mammals and between 1 and 2 under increasing male bias in birds. In contrast to our expectations, we find that a pattern of male bias is not universal across species and that there is a frequent overabundance of full-length proviruses on the allosome beyond the ratios predicted by our model. We use our data as a whole to argue that full-length proviruses should be treated as deleterious mutations or as effectively neutral mutations whose persistence in a full-length state is linked to the rate of meiotic recombination and whose origin is not universally male biased. These conclusions suggest that retroviral insertions on the allosome may be more prolific and that it might be possible to identify mechanisms of replication that are enhanced in the female sex.
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