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G9a regulates temporal preimplantation developmental program and lineage segregation in blastocyst

ABSTRACT: Early mouse development is regulated and accompanied by dynamic changes in chromatin modifications, including G9a-mediated histone H3 lysine 9 dimethylation (H3K9me2). Previously, we provided insights into its role in post-implantation development (Zylicz et al., 2015). Here we explore the impact of depleting the maternally inherited G9a in oocytes on development shortly after fertilisation. We show that H3K9me2 normally accumulates at 8- cell stage to promote timely repression of a subset of 4-cell stage specific genes. Loss of maternal inheritance of G9a disrupts the gene regulatory network resulting in developmental delay and destabilisation of inner cell mass lineages by the late blastocyst stage. Our results indicate a vital role of this maternally inherited epigenetic regulator in creating conductive conditions for developmental progression and on cell fate choices.

ORGANISM(S): Mus musculus

PROVIDER: GSE106790 | GEO | 2018/05/15

REPOSITORIES: GEO

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Chromatin dynamics and the role of G9a in gene regulation and enhancer silencing during early mouse development

Project description:Early mouse development is accompanied by dynamic changes in chromatin modifications, including G9a-mediated histone H3 lysine 9 dimethylation (H3K9me2), which is essential for embryogenesis. Here we show that H3K9me2 directs repression of 2-cell stage specific genes in nascent embryos to facilitate preimplantation development. Thereafter, genome-wide accumulation of H3K9me2 is crucial for postimplantation development, and coincides with redistribution of EZH2-dependent histone H3 lysine 27 trimethylation (H3K27me3). Loss of G9a or EZH2 results in upregulation of distinct gene sets involved in processes such as cell cycle regulation as well as germline and embryonic development. Accumulation of H3K9me2 not only occurs at promoters and gene bodies, but also extends to active enhancer elements to promote their developmentally-linked silencing. This epigenetic mechanism is important for priming gene regulatory networks in epiblast cells undergoing rapid cell proliferation in preparation for critical cell fate decisions. Examination of 2 histone modification in 3 cell types and transcriptional analysis of G9a and Ezh2 KO epiblasts and Whole genome bisulfite sequencing in two cell types

2015-11-09 | E-GEOD-70355 | biostudies-arrayexpress

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2016-03-16 | PXD003466 | Pride

Regulation of mammalian 3D genome organization and histone H3K9 dimethylation by H3K9 methyltransferases

Project description:Histone H3 lysine 9 dimethylation (H3K9me2) is a highly conserved silencing epigenetic mark. Chromatin marked with H3K9me2 forms large domains in mammalian cells and overlaps well with lamina-associated domains and the B compartment defined by Hi-C. However, the role of H3K9me2 in 3-dimensional (3D) genome organization remains unclear. We investigated genome-wide H3K9me2 distribution, transcriptome, and 3D genome organization in mouse embryonic stem cells following the inhibition or depletion of five H3K9 methyltransferases (MTases): G9a, GLP, SETDB1, SUV39H1, and SUV39H2. H3K9me2 was regulated by all five MTases; however, H3K9me2 and transcription in the A and B compartments were regulated by different MTases. H3K9me2 in A compartments was primarily regulated by G9a/GLP and SETDB1, while H3K9me2 in the B compartments was regulated by all five MTases. Furthermore, decreased H3K9me2 correlated with changes to the more active compartmental state that accompanied transcriptional activation.

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2013-03-13 | E-GEOD-45105 | biostudies-arrayexpress

GLP is critical for oogenesis exhibiting a G9A-independent role in transcriptional repression

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2013-02-01 | E-GEOD-41456 | biostudies-arrayexpress

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