Methylation of lysine 36 on histone H3 is required to control transposon activities in somatic cells.
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Lindehell H, Schwartz YB, Larsson J
Life Sci. Alliance 6 (8) - [2023-08-00; online 2023-05-11]
Transposable elements constitute a substantial portion of most eukaryotic genomes and their activity can lead to developmental and neuronal defects. In the germline, transposon activity is antagonized by the PIWI-interacting RNA pathway tasked with repression of transposon transcription and degrading transcripts that have already been produced. However, most of the genes required for transposon control are not expressed outside the germline, prompting the question: what causes deleterious transposons activity in the soma and how is it managed? Here, we show that disruptions of the Histone 3 lysine 36 methylation machinery led to increased transposon transcription in Drosophila melanogaster brains and that there is division of labour for the repression of transposable elements between the different methyltransferases Set2, NSD, and Ash1. Furthermore, we show that disruption of methylation leads to somatic activation of key genes in the PIWI-interacting RNA pathway and the preferential production of RNA from dual-strand piRNA clusters.
Bioinformatics Support for Computational Resources [Service]
NGI Stockholm (Genomics Production) [Service]
National Genomics Infrastructure [Service]
PubMed 37169594
DOI 10.26508/lsa.202201832
Crossref 10.26508/lsa.202201832
pmc: PMC10176111
pii: 6/8/e202201832