ArticlePLoS genetics2014
Loss of histone H3 methylation at lysine 4 triggers apoptosis in Saccharomyces cerevisiae.
Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 48 citations in OpenAlex.
- A systematic interactome ofeLife · 2026Article
- Set1 promotes Notch-induced transcriptional activation.Cellular and molecular life sciences : CMLS · 2026Article
- PKA plays a conserved role in regulating gene expression and metabolic adaptation by phosphorylating Rpd3/HDAC1.Nature communications · 2025Article
- Functional Roles of H3K4 Methylation in Transcriptional Regulation.Molecular and cellular biology · 2024Review
- Regulation of telomere silencing by the core histones-autophagy-Sir2 axis.Life science alliance · 2023Article
- Mechanisms of gene regulation by histone degradation in adaptation of yeast: an overview of recent advances.Archives of microbiology · 2022Review
- Loss of SET1/COMPASS methyltransferase activity reduces lifespan and fertility inLife science alliance · 2022Article
- Distinct structural groups of histone H3 and H4 residues have divergent effects on chronological lifespan in Saccharomyces cerevisiae.PloS one · 2022Article
- Histone Methylation Is Required for Virulence, Conidiation, and Multi-Stress Resistance ofFrontiers in microbiology · 2022Article
- Ready, SET, Go: Post-translational regulation of the histone lysine methylation network in budding yeast.The Journal of biological chemistry · 2021Review
- H3K4 Methylation in Aging and Metabolism.Epigenomes · 2021Review
- Is There a Histone Code for Cellular Quiescence?Frontiers in cell and developmental biology · 2021Review
- Genetic interaction profiles of regulatory kinases differ between environmental conditions and cellular states.Molecular systems biology · 2020Article
- Review
- Novel compounds protect auditory hair cells against gentamycin-induced apoptosis by maintaining the expression level of H3K4me2.Drug delivery · 2018Article
- Article
- Choose Your Own Adventure: The Role of Histone Modifications in Yeast Cell Fate.Journal of molecular biology · 2017Review
- Distinct histone methylation and transcription profiles are established during the development of cellular quiescence in yeast.BMC genomics · 2017Article
- Assessing histone demethylase inhibitors in cells: lessons learned.Epigenetics & chromatin · 2017Article
- The Epigenetic Pathways to Ribosomal DNA Silencing.Microbiology and molecular biology reviews : MMBR · 2016Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Monoubiquitination of histone H2B lysine 123 regulates methylation of histone H3 lysine 4 (H3K4) and 79 (H3K79) and the lack of H2B ubiquitination in Saccharomyces cerevisiae coincides with metacaspase-dependent apoptosis. Here, we discovered that loss of H3K4 methylation due to depletion of the methyltransferase Set1p (or the two COMPASS subunits Spp1p and Bre2p, respectively) leads to enhanced cell death during chronological aging and increased sensitivity to apoptosis induction. In contrast, loss of H3K79 methylation due to DOT1 disruption only slightly affects yeast survival. SET1 depleted cells accumulate DNA damage and co-disruption of Dot1p, the DNA damage adaptor protein Rad9p, the endonuclease Nuc1p, and the metacaspase Yca1p, respectively, impedes their early death. Furthermore, aged and dying wild-type cells lose H3K4 methylation, whereas depletion of the H3K4 demethylase Jhd2p improves survival, indicating that loss of H3K4 methylation is an important trigger for cell death in S. cerevisiae. Given the evolutionary conservation of H3K4 methylation this likely plays a role in apoptosis regulation in a wide range of organisms.
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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 OpenQuestion graph.