SINEs

Abstract

Short interspersed elements (SINEs) are mobile genetic elements that invade the genomes of many eukaryotes. Since their discovery about 30 years ago, many gaps in our understanding of the biology and function of SINEs have been filled. This review summarizes the past and recent advances in the studies of SINEs. The structure and origin of SINEs as well as the processes involved in their amplification, transcription, RNA processing, reverse transcription, and integration of a SINE copy into the genome are considered. Then we focus on the significance of SINEs for the host genomes. While these genomic parasites can be deleterious to the cell, the long-term being in the genome has made SINEs a valuable source of genetic variation providing regulatory elements for gene expression, alternative splice sites, polyadenylation signals, and even functional RNA genes.

Control of myogenesis by rodent SINE-containing lncRNAs

“…The integration of SINEs into mouse and other mammalian genomes can affect nuclear RNA metabolism by creating positive or negative regulators of transcription, splicing, or polyadenylation (Kramerov and Vassetzky 2011;Hancks and Kazazian 2012;Roy-Engel 2012). Here we provide the first report that the integration of B1, B2, B4, and ID SINEs into the mouse genome can also influence cytoplasmic RNA metabolism: Imperfect base-pairing between a SINE within a largely cytoplasmic and polyadenylated lncRNA, which we call an m 1 ⁄ 2 -sbsRNA, and a SINE from the same family within the 39 UTR of an mRNA can generate an SBS and target the mRNA for degradation by SMD.…”

“…These families consist of B1, B2, B4, identifier (ID), and mammalian-wide interspersed repeat (MIR) SINEs that are present at, respectively, ;564,000, ;348,000, ;391,000, ;79,000, and ;115,000 copies per genome (Kass and Jamison 2007 and references therein). While all of the ;1.4 million Alu SINEs in the human genome derive from 7SL RNA (Batzer and Deininger 2002), mouse SINEs derive from a broader range of RNA polymerase III (pol III) transcripts that include not only 7SL RNA, but also tRNAs and 5S rRNA (Kramerov and Vassetzky 2011).…”

Transcriptional interference by RNA polymerase III affects expression of the Polr3e gene

“…Although most SINEs are epigenetically repressed, some are actively transcribed by Pol III as independent transcription units (Roberts et al 2003;Barski et al 2010;Canella et al 2010Canella et al , 2012Moqtaderi et al 2010;Oler et al 2010;Raha et al 2010;Renaud et al 2014). SINEs have long been considered as junk DNA, but it is now clear that they can profoundly impact genome functions both in cis (for example, by constituting new enhancers or splice sites) and in trans (for example, by producing RNAs that affect Pol II transcription) (Kramerov and Vassetzky 2011). Here we examined the role of a member of the mammalian interspersed repeat (MIR) family, an ancient family of tRNA-derived SINEs that were amplified before the mammalian radiation (Smit and Riggs 1995).…”

Host Noncoding Retrotransposons Induced by DNA Viruses: a SINE of Infection?

“…SINEs are unique in that they are transcribed by RNA polymerase III (pol III), a polymerase responsible for the expression of essential housekeeping genes such as transfer RNAs (tRNAs) and the 5S rRNA. Like other pol III genes, SINEs produce short noncoding RNAs (ncRNAs) (typically Ͻ500 bp) and therefore do not encode the protein machinery to assist with their retrotransposition (4). Proteins with reverse transcriptase and integrase activities required for replication of SINEs are provided by pol II-dependent retrotransposons called long interspersed nuclear elements (LINEs) (5,6).…”

“…The B1 elements, like Alu elements, are derived from 7SL, while B2 elements most closely resemble a tRNA gene (9,10). B1 and B2 are both monomeric in structure and are ϳ135 bases long and ϳ200 bases long, respectively (4).…”