Abstract
Paternal epigenetic inheritance is gaining attention for its growing medical relevance. However, the form in which paternal epigenetic information is transmitted to offspring and how it influences offspring development remain poorly understood. Here we show that in C. elegans, sperm-inherited chromatin states transmitted to the primordial germ cells in offspring influence germline transcription and development. We show that sperm chromosomes inherited lacking the repressive histone modification H3K27me3 are maintained in that state by H3K36me3 antagonism. Inheritance of H3K27me3-lacking sperm chromosomes results in derepression in the germline of somatic genes, especially neuronal genes, predominantly from sperm-inherited alleles. This results in germ cells primed for losing their germ cell identity and adopting a neuronal fate. These data demonstrate that histone modifications are one mechanism through which epigenetic information from a father can shape offspring gene expression and development.
Highlights
Paternal epigenetic inheritance is gaining attention for its growing medical relevance
We previously showed that C. elegans sperm retain nucleosomes and histone marking genome-wide[11] and that C. elegans Polycomb Repressive Complex 2 (PRC2) maintains inherited states of H3K27me[3] during embryogenesis[12]
We show that inheriting a sperm genome lacking the repressive mark H3K27me[3] results in derepression of many genes for somatic development, especially neuronal genes, in offspring germlines
Summary
Paternal epigenetic inheritance is gaining attention for its growing medical relevance. Inheritance of H3K27me3-lacking sperm chromosomes results in derepression in the germline of somatic genes, especially neuronal genes, predominantly from sperm-inherited alleles This results in germ cells primed for losing their germ cell identity and adopting a neuronal fate. We show that inheriting a sperm genome lacking the repressive mark H3K27me[3] results in derepression of many genes for somatic development, especially neuronal genes, in offspring germlines This results in germ cells that in a sensitized genetic background lose their germ cell identity and adopt a neuronal fate. Taken together, these findings establish a cause–effect relationship between sperm-inherited histone marks and offspring transcription and development in C. elegans
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