2021
DOI: 10.1242/dev.196600
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Caenorhabditis elegans establishes germline versus soma by balancing inherited histone methylation

Abstract: Formation of a zygote is coupled with extensive epigenetic reprogramming to enable appropriate inheritance of histone methylation and prevent developmental delays. In C. elegans, this reprogramming is mediated by the H3K4me2 demethylase, SPR-5, and the H3K9 methyltransferase, MET-2. In contrast, the H3K36 methyltransferase, MES-4, maintains H3K36me2/3 at germline genes between generations to facilitate re-establishment of the germline. To determine whether the MES-4 germline inheritance pathway antagonizes spr… Show more

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Cited by 13 publications
(20 citation statements)
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“…Furthermore, our genetic findings show that mes-4 mutants can develop a full-sized germline if they inherit X chromosomes that have a history of repression, demonstrating that MES-4 is not required for PGCs to launch a germline program. Interestingly, MES-4 is required for the mis-expression of germline genes in somatic tissues of several mutants, such as spr-5; met-2 , lin-15B , and mutants of DREAM complex components (Wang et al, 2005; Petrella et al, 2011; Carpenter et al, 2021). This suggests that maternal MES-4 has tissue-dependent roles in gene regulation.…”
Section: Discussionmentioning
confidence: 99%
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“…Furthermore, our genetic findings show that mes-4 mutants can develop a full-sized germline if they inherit X chromosomes that have a history of repression, demonstrating that MES-4 is not required for PGCs to launch a germline program. Interestingly, MES-4 is required for the mis-expression of germline genes in somatic tissues of several mutants, such as spr-5; met-2 , lin-15B , and mutants of DREAM complex components (Wang et al, 2005; Petrella et al, 2011; Carpenter et al, 2021). This suggests that maternal MES-4 has tissue-dependent roles in gene regulation.…”
Section: Discussionmentioning
confidence: 99%
“…mep-1, lin-15B, lin-35, and spr-5; met-2 mutants), and as a result, have developmental defects (Unhavaithaya et al, 2002; Wang et al, 2005; Cui et al, 2006; Petrella et al, 2011; Wu et al, 2012; Carpenter et al, 2021). Concomitant loss of MES-4 from these mutants prevents ectopic expression of germline genes and restores worm health (Wang et al, 2005; Cui et al, 2006; Petrella et al, 2011; Wu et al, 2012; Carpenter et al, 2021). In wild-type early embryos, MES-4 and methylated H3K36 associate with genes that were transcribed in the maternal germline, regardless of whether they are transcribed in embryos (Furuhashi et al, 2010; Rechtsteiner et al, 2010).…”
Section: Introductionmentioning
confidence: 99%
“…This question is underscored because, during normal development in all animals, chromatin modifications acquired during germline transcriptional activity are removed at fertilization to epigenetically reprogram the embryo (D'Urso and Brickner, 2017;Guo et al, 2017;Kaneshiro et al, 2019). These reprograming mechanisms remove marks of active gene expression that are added during normal germline transcription and, in some cases, also increase repressive marks at germline active genes to prevent their ectopic expression in subsequent generations (Andersen and Horvitz, 2007;Bessler et al, 2010;Carpenter et al, 2021;Rechtsteiner et al, 2019). Nevertheless, in many organisms, the memory of early-life stress exposure persists through meiosis and cycles of mitosis to alter later-life cellular programs through still poorly understood mechanisms (Brunet and Berger, 2014;D'Urso and Brickner, 2017;Leimar and McNamara, 2015;Sen et al, 2016).…”
Section: Introductionmentioning
confidence: 99%
“…As in many organisms, in the nematode Caenorhabditis elegans, environmental stressors that affect the parent also affect the unfertilized gametes. In C. elegans, epigenetic mechanisms that affect chromatin in one generation have been found to alter offspring lifespan and behavior in subsequent generations (Baugh and Day, 2020;Baugh and Hu, 2020;Camacho et al, 2018;Carpenter et al, 2021;Furuhashi et al, 2010;Greer et al, 2011Greer et al, , 2014Houri-Ze'evi et al, 2016;Jobson et al, 2015;Kaneshiro et al, 2019;Katz et al, 2009;Kerr et al, 2014;Kreher et al, 2018;Lev et al, 2017;Lim and Brunet, 2013;Minkina and Hunter, 2018;Moore et al, 2019;Posner et al, 2019;Rechavi et al, 2014;Tabuchi et al, 2018;Wan et al, 2021). In the parent, stress activates the heat shock transcription factor HSF1 (HSF-1 in C. elegans), which increases expression of protective heat-shock protein (hsp) genes to counteract stressinduced damage (Gomez-Pastor et al, 2018;Vihervaara et al, 2018).…”
Section: Introductionmentioning
confidence: 99%
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