ArticleGenetics1998
The phenotype of mes-2, mes-3, mes-4 and mes-6, maternal-effect genes required for survival of the germline in Caenorhabditis elegans, is sensitive to chromosome dosage.
Article in Genetics, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
37 citing papers in PubMed, 96 citations in OpenAlex.
- Dual genomic localizations and gene regulatory functions of MBD-2 with and without NuRD in Caenorhabditis elegans which lacks DNA methylation.Nature communications · 2026Article
- Sterility in the offspring ofmicroPublication biology · 2024Article
- Developmentally programmed histone H3 expression regulates cellular plasticity at the parental-to-early embryo transition.Science advances · 2023Article
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- Wnt Signaling Drives Ectopic Gene Expression and Larval Arrest in the Absence of theG3 (Bethesda, Md.) · 2020Article
- Transgenerational epigenetic inheritance: from phenomena to molecular mechanisms.Current opinion in neurobiology · 2019Review
- Distinct Roles of Two Histone Methyltransferases in Transmitting H3K36me3-Based Epigenetic Memory Across Generations inGenetics · 2018Article
- Highly efficient RNAi and Cas9-based auto-cloning systems for C. elegans research.Nucleic acids research · 2018Article
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- EZH2 protects glioma stem cells from radiation-induced cell death in a MELK/FOXM1-dependent manner.Stem cell reports · 2015Article
- Gene repression. H3K27me and PRC2 transmit a memory of repression across generations and during development.Science (New York, N.Y.) · 2014Article
- Regulation of the X chromosomes in Caenorhabditis elegans.Cold Spring Harbor perspectives in biology · 2014Review
- The onset of C. elegans dosage compensation is linked to the loss of developmental plasticity.Developmental biology · 2014Article
- Opposing activities of DRM and MES-4 tune gene expression and X-chromosome repression in Caenorhabditis elegans germ cells.G3 (Bethesda, Md.) · 2014Article
- Phosphorylation of RNA polymerase II is independent of P-TEFb in the C. elegans germline.Development (Cambridge, England) · 2013Article
- Genetic regulators of a pluripotent adult stem cell system in planarians identified by RNAi and clonal analysis.Cell stem cell · 2012Article
- Histone methyltransferases MES-4 and MET-1 promote meiotic checkpoint activation in Caenorhabditis elegans.PLoS genetics · 2012Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Mutations in mes-2, mes-3, mes-4, and mes-6 result in maternal-effect sterility: hermaphrodite offspring of mes/mes mothers are sterile because of underproliferation and death of the germ cells, as well as an absence of gametes. Mutant germ cells do not undergo programmed cell death, but instead undergo a necrotic-type death, and their general poor health apparently prevents surviving germ cells from forming gametes. Male offspring of mes mothers display a significantly less severe germline phenotype than their hermaphrodite siblings, and males are often fertile. This differential response of hermaphrodite and male offspring to the absence of mes+ product is a result of their different X chromosome compositions; regardless of their sexual phenotype, XX worms display a more severe germline phenotype than XO worms, and XXX worms display the most severe phenotype. The sensitivity of the mutant phenotype to chromosome dosage, along with the similarity of two MES proteins to chromatin-associated regulators of gene expression in Drosophila, suggest that the essential role of the mes genes is in control of gene expression in the germline. An additional, nonessential role of the mes genes in the soma is suggested by the surprising finding that mutations in the mes genes, like mutations in dosage compensation genes, feminize animals whose male sexual identity is somewhat ambiguous. We hypothesize that the mes genes encode maternally supplied regulators of chromatin structure and gene expression in the germline and perhaps in somatic cells of the early embryo, and that at least some of their targets are on the X chromosomes.
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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.