Transposable elements and the epigenetic regulation of the genome

Abstract

Overlapping epigenetic mechanisms have evolved in eukaryotic cells to silence the expression and mobility of transposable elements (TEs). Owing to their ability to recruit the silencing machinery, TEs have served as building blocks for epigenetic phenomena, both at the level of single genes and across larger chromosomal regions. Important progress has been made recently in understanding these silencing mechanisms. In addition, new insights have been gained into how this silencing has been co-opted to serve essential functions in 'host' cells, highlighting the importance of TEs in the epigenetic regulation of the genome.

Improved maize reference genome with single-molecule technologies

“…Transposable elements were first reported in maize 19 and have since been shown to have important roles in shaping genome evolution and gene regulatory networks of many species 20 . Most of the maize Letter reSeArCH genome is derived from transposable elements 3, 21 , and careful study of a few regions has revealed a characteristic structure of sequentially nested retrotransposons 21,22 and the effect of deletions and recombina tion on retrotransposon evolution 23 .…”

Regulation of mammalian gene expression by retroelements and non‐coding tandem repeats

“…(60) It is not known how cells recognize newly transposed elements and induce chromatin and DNA methylation but, in some eukaryotic organisms (S.pombe, C.elegans, D.melanogaster, A.thaliana), duplex RNA formed by transcripts from both strands of RT is cleaved with specific RNase III (DICER) and the resulting small RNAs (<30 nt) are captured by complexes containing an ARGONAUTE (Ago) protein, which either induce cleavage of RT transcripts (RISC complexes) or induce histone H3 methylation at lysine-9 in chromatin and de novo DNA methylation of RT genomic sequences (RITS complexes) (reviewed in Ref. 23). Although this RNA interference (RNAi)-mediated RT silencing is not yet established in mammalian cells, LINE1-encoded RNA-binding protein ORF1p colocalizes at cytoplasmic stress granules in human cells with components of the RISC complex (Ago2, FMRP) suggesting that mammalian retrotransposition can be also controlled by RNAi.…”

“…Epigenetic silencing of non-mutated retrotransposons (''genome defense'') in many non-mammalian animals and plants can be also achieved without their methylation through the mechanism of RNA interference. (23) The vast majority of genomic copies of retroelements is already mutated and retropositionally inactive, so their continuous methylation is not required for repression of retroposition. A protein that binds to methyl-CpG (MeCP2) and that can mediate effects of DNA methylation has been identified.…”

“…This is likely in view of the growing evidence for the roles of transcripts from non-coding DNAs in eukaryotes. (23,36) Exchange of GFP-HP1 in heterochromatin is also inhibited by ActD but is stimulated by alpha-amanitin. (97) In interphase nuclei, ITS do not colocalize with transcription foci (''hubs'') detected by analysis of incorporation of 5-bromouridine monophosphate into RNA in vivo (96) indicating that ITS are not associated with extensively transcribed genome compartments.…”

“…(17)(18)(19)(20) Furthermore, retroelements are heavily methylated in somatic and germ-line cells (21) and inherited epigenetic patterns of their methylation can effect expression of adjacent genes. (22,23) Since SINEs and LINEs are very abundant, they may also facilitate compartmentalization in the nucleus of transcribed and non-transcribed domains. (24) The positioning of heterochromatin in the nucleus is affected by intrachromosomal distribution of G-dark bands (25) which are enriched in LINE1 sequences.…”