Distinct functions and temporal regulation of methylated histone H3 during early embryogenesis

0303 health sciences Embryo, Nonmammalian Time Factors Transcription, Genetic Gastrulation Embryonic Development Cell Count Methylation S Phase Histones 03 medical and health sciences Heterochromatin Animals RNA Polymerase II Caenorhabditis elegans Caenorhabditis elegans Proteins Interphase
DOI: 10.1242/dev.174516 Publication Date: 2019-09-20T14:05:13Z
ABSTRACT
ABSTRACT During the first hours of embryogenesis, formation higher-order heterochromatin coincides with loss developmental potential. Here, we examine relationship between these two events, and probe processes that contribute to timing their onset. Mutations disrupt histone H3 lysine 9 (H3K9) methyltransferases reveal methyltransferase MET-2 helps terminate plasticity, through mono- di-methylation H3K9 (me1/me2), promotes formation, H3K9me3. Although H3K9me3 perturbs heterochromatin, embryos are still able indicating can be uncoupled. Methylated appears gradually in developing C. elegans depends on nuclear localization MET-2. We find H3K9me2 is sensitive rapid cell cycles, but not zygotic genome activation or counting. These data distinct roles for different methylation states generation plasticity by MET-2, identify cycle as a crucial parameter regulation.
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