An update on post-transcriptional regulation of retrotransposons

被引:11
|
作者
Warkocki, Zbigniew [1 ,2 ]
机构
[1] Polish Acad Sci, Inst Bioorgan Chem, Dept RNA Metab, Poznan, Poland
[2] Polish Acad Sci, Inst Bioorgan Chem, Dept RNA Metab, Ul Noskowskiego 12-14, PL-61704 Poznan, Poland
关键词
autophagy; DNA repair; innate immunity; LINE-1; m(6)A; mobile genome; polyadenylation and uridylation; retrotransposition; retrotransposon; RNA decay; SOMATIC L1 RETROTRANSPOSITION; LONG INTERSPERSED ELEMENT-1; EXOSOME TARGETING COMPLEX; HUMAN LINE-1 PROTEIN; SMALL NUCLEAR-RNA; MESSENGER-RNA; ORF1; PROTEIN; REVERSE-TRANSCRIPTASE; TRANSPOSABLE ELEMENTS; DIFFERENTIAL INHIBITION;
D O I
10.1002/1873-3468.14551
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Retrotransposons, including LINE-1, Alu, SVA, and endogenous retroviruses, are one of the major constituents of human genomic repetitive sequences. Through the process of retrotransposition, some of them occasionally insert into new genomic locations by a copy-paste mechanism involving RNA intermediates. Irrespective of de novo genomic insertions, retrotransposon expression can lead to DNA double-strand breaks and stimulate cellular innate immunity through endogenous patterns. As a result, retrotransposons are tightly regulated by multi-layered regulatory processes to prevent the dangerous effects of their expression. In recent years, significant progress was made in revealing how retrotransposon biology intertwines with general post-transcriptional RNA metabolism. Here, I summarize current knowledge on the involvement of post-transcriptional factors in the biology of retrotransposons, focusing on LINE-1. I emphasize general RNA metabolisms such as methylation of adenine (m(6)A), RNA 3 '-end polyadenylation and uridylation, RNA decay and translation regulation. I discuss the effects of retrotransposon RNP sequestration in cytoplasmic bodies and autophagy. Finally, I summarize how innate immunity restricts retrotransposons and how retrotransposons make use of cellular enzymes, including the DNA repair machinery, to complete their replication cycles.
引用
收藏
页码:380 / 406
页数:27
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