ArticlePLoS genetics2020
DOT-1.1-dependent H3K79 methylation promotes normal meiotic progression and meiotic checkpoint function in C. elegans.
Article in PLoS genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Distinct cellular and reproductive consequences of meiotic chromosome synapsis defects in syce2 and sycp1 mutant zebrafish.PLoS genetics · 2025Article
- Repeat sequence corresponding to the nucleosome length at the opposite end of the pairing center on autosomes inmicroPublication biology · 2024Article
- The CRTC-1 transcriptional domain is required for COMPASS complex-mediated longevity in C. elegans.Nature aging · 2023Article
- The DOT1L-MLLT10 complex regulates male fertility and promotes histone removal during spermiogenesis.Development (Cambridge, England) · 2023Article
- The transcription factor TCFL5 responds to A-MYB to elaborate the male meiotic program in mice.Reproduction (Cambridge, England) · 2023Article
- ATM/ATR kinases link the synaptonemal complex and DNA double-strand break repair pathway choice.Current biology : CB · 2022Article
- DNA repair, recombination, and damage signaling.Genetics · 2022Review
- Epigenetic Dysregulation of Mammalian Male Meiosis Caused by Interference of Recombination and Synapsis.Cells · 2021Article
- Getting there: understanding the chromosomal recruitment of the AAA+ ATPase Pch2/TRIP13 during meiosis.Current genetics · 2021Review
- Pch2 orchestrates the meiotic recombination checkpoint from the cytoplasm.PLoS genetics · 2021Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Epigenetic modifiers are emerging as important regulators of the genome. However, how they regulate specific processes during meiosis is not well understood. Methylation of H3K79 by the histone methyltransferase Dot1 has been shown to be involved in the maintenance of genomic stability in various organisms. In S. cerevisiae, Dot1 modulates the meiotic checkpoint response triggered by synapsis and/or recombination defects by promoting Hop1-dependent Mek1 activation and Hop1 distribution along unsynapsed meiotic chromosomes, at least in part, by regulating Pch2 localization. However, how this protein regulates meiosis in metazoans is unknown. Here, we describe the effects of H3K79me depletion via analysis of dot-1.1 or zfp-1 mutants during meiosis in Caenorhabditis elegans. We observed decreased fertility and increased embryonic lethality in dot-1.1 mutants suggesting meiotic dysfunction. We show that DOT-1.1 plays a role in the regulation of pairing, synapsis and recombination in the worm. Furthermore, we demonstrate that DOT-1.1 is an important regulator of mechanisms surveilling chromosome synapsis during meiosis. In sum, our results reveal that regulation of H3K79me plays an important role in coordinating events during meiosis in C. elegans.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.