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Comment
. 2021 Aug;31(8):829-831.
doi: 10.1038/s41422-021-00518-5.

Nascent RNA m6A modification at the heart of the gene-retrotransposon conflict

Victor Billon  1 , Gael Cristofari  2
Affiliations
Comment

Nascent RNA m6A modification at the heart of the gene-retrotransposon conflict

Victor Billon et al. Cell Res. 2021 Aug.
No abstract available

PubMed Disclaimer

Conflict of interest statement

G.C. is an unpaid associate editor of the journal Mobile DNA (Springer-Nature) and an unpaid review editor of the Genetics, Genomics and Epigenomics of Aging section within the Frontiers in Aging journal (Frontiers).

Figures

Fig. 1
Fig. 1. A dual role for SAFB/SAFB2 in protecting the genome against L1 retrotransposons.
a SAFB limits transcriptional attenuation caused by intronic L1s. RNA polymerase II (Pol II) transcribes a gene containing a sense-oriented intronic L1 (red). The nascent RNA segment containing the L1 sequence is m6A-modified (black circles) by METTL3/14 (blue) and bound by SAFB/SAFB2 (grey). The intronic L1 causes a transcription roadblock (dark line). Deletion (KO, green dashed line) or inversion of the L1 sequence prevents attenuation while depletion of SAFB increases it (KD, red dashed line). b A model for the influence of m6A on L1 mobilization. When transcribed from its own promoter, L1 RNA can also be N6A-methylated by METTL3/14 (1). SAFB/SAFB2 proteins preferentially bind m6A-modified L1 RNA (2). Unmodified L1 RNAs and SAFB-bound L1 RNAs are destabilized (3). In the cytoplasm, m6A-modified L1 RNA can hijack the translation initiation factor eIF3 (green), enhancing L1 translation (4). L1 ribonucleoprotein particles (RNPs) formed by L1 proteins and RNA (5) drive reverse transcription and genomic integration (6). Inset, m6A pathway effectors regulating L1 mobilization.
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Comment on

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