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Targeted reprogramming of H3K27me3 resets epigenetic memory in plant paternal chromatin [sperm - third party reanalysis]

ABSTRACT: Epigenetic marks are reprogrammed in the gametes to reset genomic potential in the next generation. In mammals, paternal chromatin is extensively reprogrammed through the global erasure of DNA methylation and the exchange of histones with protamines1,2. Precisely how the paternal epigenome is reprogrammed in flowering plants remains unclear since DNA is not demethylated in sperm and histones are retained3,4. Here, we describe a multi-layered mechanism by which H3K27me3 is globally lost from histone-based sperm chromatin in Arabidopsis. This mechanism involves silencing of H3K27me3 ‘writers’, the activity of H3K27me3 ‘erasers’ and deposition of a sperm-specific histone, H3.105, which we show is immune to lysine 27 methylation. The loss of H3K27me3 facilitates transcription of genes essential for spermatogenesis and pre-configures sperm with a chromatin state that forecasts gene expression in the next generation. Thus, plants have evolved a specific mechanism to simultaneously differentiate male gametes and reprogram the paternal epigenome.

ORGANISM(S): Arabidopsis thaliana Homo sapiens

PROVIDER: GSE144900 | GEO | 2020/03/17

REPOSITORIES: GEO

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Targeted reprogramming of H3K27me3 resets epigenetic memory in plant paternal chromatin [sperm]

Project description:Epigenetic marks are reprogrammed in the gametes to reset genomic potential in the next generation. In mammals, paternal chromatin is extensively reprogrammed through the global erasure of DNA methylation and the exchange of histones with protamines1,2. Precisely how the paternal epigenome is reprogrammed in flowering plants remains unclear since DNA is not demethylated in sperm and histones are retained3,4. Here, we describe a multi-layered mechanism by which H3K27me3 is globally lost from histone-based sperm chromatin in Arabidopsis. This mechanism involves silencing of H3K27me3 ‘writers’, the activity of H3K27me3 ‘erasers’ and deposition of a sperm-specific histone, H3.105, which we show is immune to lysine 27 methylation. The loss of H3K27me3 facilitates transcription of genes essential for spermatogenesis and pre-configures sperm with a chromatin state that forecasts gene expression in the next generation. Thus, plants have evolved a specific mechanism to simultaneously differentiate male gametes and reprogram the paternal epigenome.

2020-03-17 | GSE144899 | GEO

Targeted reprogramming of H3K27me3 resets epigenetic memory in plant paternal chromatin [mature pollen]

Project description:Epigenetic marks are reprogrammed in the gametes to reset genomic potential in the next generation. In most animal species, paternal chromatin is extensively reprogrammed through the global erasure of DNA methylation and the exchange of histones with protamine. Precisely how the paternal epigenome is reprogrammed in flowering plants remains unclear since sperm chromatin is not demethylated and histones are retained. Here, we show that the sperm-specific histone, H3.10, is immune to lysine 27 methylation and that its deposition in sperm contributes to the global and specific resetting of the epigenetic mark H3K27me3 by uncoupling its inheritance during DNA replication. The loss of H3K27me3 facilitates transcription of genes essential for spermatogenesis and pre-configures sperm with a chromatin state that forecasts gene expression in the next generation, revealing a global wave of epigenetic resetting that coordinates with early plant life. Thus, in contrast to the indiscriminate removal of epigenetic marks in animal sperm, plants have evolved a specific mechanism to simultaneously differentiate male gametes and reprogram the paternal epigenome.

2020-03-17 | GSE137887 | GEO

Targeted reprogramming of H3K27me3 resets epigenetic memory in plant paternal chromatin

2020-03-17 | GSE120668 | GEO

Targeted reprogramming of H3K27me3 resets epigenetic memory in plant paternal chromatin

2020-03-17 | GSE120664 | GEO

Polycomb protein SCML2 mediates paternal epigenetic inheritance through sperm chromatin

Project description:Sperm chromatin retains small amounts of histones, and the chromatin states of sperm mirror gene expression programs of the next generation. It remains largely unknown how paternal epigenetic information is transmitted through sperm chromatin. Here we developed a novel mouse model of paternal epigenetic inheritance in which deposition of Polycomb repressive complex 2 (PRC2) mediated-repressive H3K27me3 is attenuated in the paternal germline. By applying modified methods of assisted reproductive technology, we rescued infertility of mice absent of Polycomb protein SCML2, which is the regulator of germline gene expression through the establishment of H3K27me3 on bivalent promoters with other active marks H3K4me2/3. In F1 males of Scml2-knockout mice, which has wild-type genotype, gene expression is dysregulated in the male germline during spermiogenesis. These dysregulated genes are targets of SCML2-mediated H3K27me3 in mature sperm. Thus, SCML2 mediates intergenerational inheritance of paternal epigenetic information through the regulation of sperm chromatin.

2023-05-06 | GSE183994 | GEO

Initiation of Parental Genome Reprogramming in Fertilized Oocyte by Splicing Kinase SRPK1-Catalyzed Protamine Phosphorylation

Project description:We performed ATAC-seq in mouse sperms and fertilized eggs with wild-type or P1 mutation (phosphorylation sites by SRPK1) to capture early genome reprogramming events ~5 hours post insemination. Surprisingly, we detected broadly distributed ATAC-seq reads across the mouse genome to paternal and maternal gametes formed with wild-type and single mutant sperm, and in contrast, we saw individual peaks with zygotes formed with the double mutant sperm. After assigning to paternal and maternal genomes, we found that the reads assignable to paternal genome was decreased with single and double mutants, compare with wild-type. Furthermore, we found the paternal genome in eggs fertilized with the double mutant sperm essentially retained all sperm-specific ATAC-seq peaks, which were also overlapped with the published H3.3 ChIP-seq signals on wild-type sperm, mostly corresponding to TSSs. Strikingly, the ATAC-seq signals on the maternal genome from eggs fertilized with the double mutant P1 sperm were literally identical to those in MII oocyte. Based on these data, we draw two important conclusions: (i) dramatic chromatin remodeling takes place in a highly coordinated fashion in both paternal and maternal pronuclei before they merge, and (ii) SRPK1-catalyzed protamine phosphorylation initiates such synchronized genome reprogramming in both gametes.

2020-03-16 | GSE136403 | GEO

Sperm histone H3 lysine 4 trimethylation is altered in a genetic mouse model of transgenerational epigenetic inheritance

Project description:Advancing the molecular knowledge surrounding fertility and inheritance has become critical given the halving of sperm counts in the last 40 years, and the rise in complex disease which cannot be explained by genetics alone. The connection between both these trends may lie in alterations to the sperm epigenome and occur through environmental exposures. Changes to the sperm epigenome are also associated with health risks across generations such as metabolic disorders and cancer. Thus it is imperative to identify the epigenetic modifications that escape reprogramming during spermatogenesis. Here, we aimed to identify the chromatin signature(s) associated with transgenerational phenotypes in our genetic mouse model of epigenetic inheritance that overexpresses the histone demethylase KDM1A in their germ cells. We used sperm-specific chromatin immunoprecipitation followed by in depth sequencing (ChIP-seq), and computational analysis to identify whether differential enrichment of histone H3 lysine 4 trimethylation (H3K4me3), and histone H3 lysine 27 trimethylation (H3K27me3) serve as mechanisms for transgenerational epigenetic inheritance through the paternal germline. Our analysis on the sperm of KDM1A transgenic males revealed specific changes in H3K4me3 enrichment that occurred independently from non-bivalent H3K4me3/H3K27me3 regions. Many regions with altered H3K4me3 enrichment in sperm were identified on the paternal allele of the pre-implantation embryo. These findings suggest that sperm H3K4me3 functions in the transmission of non-genetic phenotypes transgenerationally.

2020-10-15 | GSE145679 | GEO

Sperm but not oocyte DNA methylome is inherited by zebrafish early embyros

Project description:5-methylcytosine is a major epigenetic modification sometimes called "the fifth nucleotide". However, our knowledge of how offspring inherit the DNA methylome from parents is limited. We generated nine single-base resolution DNA methylomes including zebrafish gametes and early embryos. The oocyte methylome is significantly hypo-methylated compared to sperm. Strikingly, the paternal DNA methylation pattern is maintained throughout early embryogenesis. The maternal DNA methylation pattern is maintained until the 16-cell stage. Then, the oocyte methylome is gradually discarded through cell division, and progressively reprogrammed to a pattern similar to that of the sperm methylome. The passive demethylation rate and the de novo methylation rate are similar in the maternal DNA. By the midblastula stage, the embryo?s methylome is virtually identical to the sperm methylome. Moreover, inheritance of the sperm methylome facilitates the epigenetic regulation of embryogenesis. Therefore, besides DNA sequences, sperm DNA methylome is also inherited in zebrafish early embryos.

2013-05-20 | GSE44075 | GEO

Sperm but not oocyte DNA methylome is inherited by zebrafish early embyros

2013-05-20 | E-GEOD-44075 | biostudies-arrayexpress

The reproductive toxicant acrylamide modulates the mouse epididymal proteome to drive alterations to the sperm epigenome and dysregulate embryo development

Project description:Paternal exposure to a range of environmental and lifestyle factors elicits distinct changes to the sperm sncRNA profile; modifications that have significant post-fertilization consequences. Despite this knowledge, there remains limited mechanistic understanding of how paternal exposures effect the sperm sncRNA landscape. Here, we report the acute sensitivity of the sperm sncRNA profile to the potent reproductive toxicant, acrylamide. Further, we traced the differential accumulation of acrylamide responsive sncRNAs to coincide with sperm transit of the proximal (caput) segment of the epididymis, wherein acrylamide exposure altered the expression of several transcription factors implicated in the expression of acrylamide-sensitive sncRNAs. We also identified extracellular vesicles secreted from the caput epithelium in relaying altered sncRNA profiles to maturing spermatozoa, the implications of which manifest in the form of dysregulated gene expression during early embryonic development. These data provide a causative mechanistic link to account for how environmental insults can alter the sperm epigenome and compromise the transcriptomic profile of early embryos

2021-10-07 | PXD022865 | Pride

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