Chromatin Modifiers SET-25 and SET-32 Are Required for Establishment but Not Long-Term Maintenance of Transgenerational Epigenetic Inheritance

Woodhouse, Rachel M.; Buchmann, Gabriele; Hoe, Matthew; Harney, Dylan; Low, Jason K. K.; Larance, Mark; Boag, Peter R.; Ashe, Alyson

doi:10.1016/j.celrep.2018.10.085

Cited by 54 publications

(65 citation statements)

References 50 publications

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“…We did not detected methylation at any of the other lysine residues of H3 (data not shown). These results agree with published histone mass spectrometry analysis of set-32 mutant animals 21 . Our data indicate that SET-32 has H3K23 methyltransferase activity in vitro .…”

Section: Resultssupporting

confidence: 92%

“…SET-25 and SET-32, but not MET-2, are required for the silencing of a piRNA-targeted reporter gene 10 . In addition, while MET-2, SET-25, and SET-32 were all dispensable for silencing maintenance in nuclear RNAi, SET-32 and, to a lesser extent, SET-25 are required for the silencing establishment 15,21 . Given SET-32’s unique role in nuclear RNAi, we hypothesized that its biochemical activity may differ from MET-2 and SET-25.…”

Section: Introductionmentioning

confidence: 98%

“…While the enzymes responsible for H3K9me3 have been studied, the function of this histone modification in nuclear RNAi remains unknown. In nuclear RNAi, it was assumed that heterochromatin was required for transcriptional silencing, surprisingly, H3K9me3 is not essential for silencing maintenance if HRDE-1 is present 7,10,19-21 . By uncovering the histone methyltransferases (HMTs) responsible for each histone modification we can better understand their function in nuclear RNAi.…”

Section: Introductionmentioning

confidence: 99%

“…The SET-domain containing EZL3 in Tetrahymena is required for H3K23me3 in vivo 29 . In C. elegans , loss of SET-32 causes reduced levels of H3K23me1 or H3K23me2, however, H3K23me3 was not tested 21 . No H3K23 HMT has been biochemically validated at the time of this manuscript.…”

Section: Introductionmentioning

confidence: 99%

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C. elegansnuclear RNAi factor SET-32 deposits the transgenerational heritable histone modification, H3K23me3

Schwartz-Orbach

Zhang

Amin

et al. 2020

Preprint

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Nuclear RNAi provides a highly tractable system to study RNA-mediated chromatin changes and epigenetic inheritance. Recent studies have indicated that the regulation and function of nuclear RNAi-mediated heterochromatin are highly complex. Our knowledge of histone modifications and the corresponding histone modifying enzymes involved in the system remains limited. In this study, we show that the heterochromatin mark, H3K23me3, is induced by nuclear RNAi at both exogenous and endogenous targets in C. elegans. In addition, dsRNA-induced H3K23me3 can be inherited for four generations. We demonstrate that the histone methyltransferase SET-32, methylates H3K23 in vitro. Both set-32 and the germline nuclear RNAi Argonaute, hrde-1, are required for nuclear RNAi-induced H3K23me3 in vivo. Our data poise H3K23me3 as an additional chromatin modification in the nuclear RNAi pathway and provides the field with a new target for uncovering the role of heterochromatin in transgenerational epigenetic silencing.

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Section: Resultssupporting

confidence: 92%

Section: Introductionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

C. elegansnuclear RNAi factor SET-32 deposits the transgenerational heritable histone modification, H3K23me3

Schwartz-Orbach

Zhang

Amin

et al. 2020

Preprint

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“…2h). Some studies have documented the deposition of chromatin modifications that extend to several kilobases surrounding the RNAi-targeted genomic sequence 10 and others have suggested that chromatin modifiers are required in P0 animals 11 for the establishment of transgenerational silencing. The transgenerational silencing of gfp with low mCherry silencing for a few generations ( Fig.…”

mentioning

confidence: 99%

Recovery from transgenerational RNA silencing is driven by gene-specific homeostasis

Devanapally

Raman

Allgood

et al. 2017

Preprint

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Gene silencing is a significant obstacle to genome engineering and has been proposed to be a non-self response against foreign DNA 1,2,3,4 . Yet, some foreign genes remain expressed for many generations 1,3,4 and some native genes remain silenced for many generations 1,5,6 . How organisms determine whether a sequence is expressed or silenced is unclear. Here we show that a stably expressed foreign DNA sequence in C. elegans is converted into a stably silenced sequence when males with the foreign DNA mate with wild-type hermaphrodites. This conversion does not occur when the hermaphrodite also has exonic sequences from the foreign DNA. Once initiated, silencing persists for many generations independent of mating and is associated with a DNA-independent signal that can silence other homologous loci in every generation. This mating-induced silencing resembles piRNA- generations. Thus, our results reveal the existence of a mechanism that maintains gene silencing initiated upon ancestral mating. By allowing retention of potentially detrimental sequences acquired through mating, this mechanism could create a reservoir of sequences that contribute to novelty when activated during evolution. ResultsMating is routinely used to introduce genes, including fluorescent reporters, into different genetic backgrounds and it is generally assumed that gene expression is unaffected by this manipulation. While

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A Review on Epigenetic Inheritance of Experiences in Humans

Ghai

Kader

2021

Biochem Genet

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Chromatin Modifiers SET-25 and SET-32 Are Required for Establishment but Not Long-Term Maintenance of Transgenerational Epigenetic Inheritance

Cited by 54 publications

References 50 publications

C. elegansnuclear RNAi factor SET-32 deposits the transgenerational heritable histone modification, H3K23me3

C. elegansnuclear RNAi factor SET-32 deposits the transgenerational heritable histone modification, H3K23me3

Recovery from transgenerational RNA silencing is driven by gene-specific homeostasis

A Review on Epigenetic Inheritance of Experiences in Humans

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