PT  - JOURNAL ARTICLE
AU  - Brandon S. Carpenter
AU  - Teresa W. Lee
AU  - Caroline F. Plott
AU  - Jovan S. Brockett
AU  - Dexter A. Myrick
AU  - David J. Katz
TI  - Failure to maternally reprogram histone methylation causes developmental delay due to germline transcription in somatic tissues
AID  - 10.1101/2020.01.22.914580
DP  - 2020 Jan 01
TA  - bioRxiv
PG  - 2020.01.22.914580
4099  - http://biorxiv.org/content/early/2020/01/23/2020.01.22.914580.short
4100  - http://biorxiv.org/content/early/2020/01/23/2020.01.22.914580.full
AB  - In C. elegans, the H3K36 methyltransferase, MES-4, helps establish germ cell fate by maintaining H3K36me2/3 at germline genes between generations. Previously, we showed that the H3K4me2 demethylase, SPR-5, and the H3K9 methyltransferase, MET-2, reprogram histone methylation at fertilization to prevent the ectopic expression of germline genes in somatic tissues. Together, this indicates that SPR-5 and MET-2 maternal reprogramming may antagonize MES-4 to establish germline versus soma. Here, we show that spr-5; met-2 mutant progeny have a severe developmental delay that is associated with the ectopic maintenance of H3K36me2/3 at MES-4 targeted germline genes in somatic tissues, and the ectopic expression of these genes. We further show that the developmental delay and the ectopic expression are dependent upon MES-4. Thus, we propose that SPR-5, MET-2, and MES-4 balance inherited histone methylation to establish germline versus soma. Without this balance, the inappropriate transcription of germline genes in somatic tissues causes developmental delay.