Abstract
Here I review the properties of the mouse retroelement VL30-1, which apparently derived from retrotranspostions of a founder VL30 retrovirus that infected the mouse germline after the mouse–human speciation. The VL30-1 gene is transcribed as a long noncoding RNA (lncRNA) with an essential host function in an epigenetic transcription switch (ETS) that regulates transcription of multiple genes, including proto-oncogenes that control cell proliferation and oncogenesis. The ETS involves the tumor suppressor protein PSF that has a DNA-binding domain (DBD) and two RNA-binding domains (RBDs). The DBD binds to promoters that have a DBD-binding sequence and switches off transcription, and the RBDs bind lncRNAs that have a RBD-binding sequence, releasing PSF and switching on transcription. VL30-1 lncRNA has two RBD-binding sequences, apparently acquired by mutations during retrotranspositions of the founder retrovirus, which drive proto-oncogene transcription and oncogenesis via the ETS. VL30-1 lncRNA is a seminal example of the key role of endogenous retroviruses (ERVs) and their retroelements in the evolution of transcription regulatory systems.
Highlights
I review the properties of the mouse retroelement VL30-1, which apparently derived from retrotranspostions of a founder VL30 retrovirus that infected the mouse germline after the mouse–human speciation
An endogenous retroviruses (ERVs) initially functions as a selfish DNA that integrates at multiple genomic sites via successive cycles of duplicative retrotansposition (DRT), involving integration, transcription, reverse transcription and integration at another genomic site, which must eventually be suppressed in order for the host to survive, while the ERV must acquire a beneficial host function to survive as a component of the host genome
In the full-length VL30 genes sequenced so far, including VL30-1, the internal DNA flanked by the long terminal repeats (LTRs) contains multiple mutations, including stop codons in all three reading frames, which block translation of the retroviral proteins required for further DRT cycles
Summary
I review the properties of the mouse retroelement VL30-1, which apparently derived from retrotranspostions of a founder VL30 retrovirus that infected the mouse germline after the mouse–human speciation.
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