ArticlePLoS genetics2012
RNA methylation by the MIS complex regulates a cell fate decision in yeast.
Article in PLoS genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 161 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
161 citing papers in PubMed, 281 citations in OpenAlex.
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- METTL3 promotes vascular stability in intracranial aneurysm via m6A-AMPK axis.Scientific reports · 2025Article
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- Why does the m6A writer complex require so many proteins?PLoS biology · 2025Review
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- Regulatory mechanism of Haa1p and Hap4p in Saccharomyces cerevisiae to mixed acetic acid and formic acid when fermenting mixed glucose and xylose.Microbial cell factories · 2025Article
- An Investigation of the RNA Modification mInternational journal of molecular sciences · 2025Article
- Selective Translation Under Heat Shock: Integrating HSP70 mRNA Regulation with Cellular Stress Responses in Yeast and Mammals.Molecular biology of the cell · 2025Review
- Regulation of meiotic gene expression is functional in the human fungal pathogen Candida glabrata.FEMS yeast research · 2025Article
- The mFrontiers in oncology · 2025Article
- Role of N6-Methyladenosine (m6A) epitranscriptomic mark in regulating viral infections and target for antiviral development.Frontiers in pharmacology · 2025Review
- TTC7B triggers the PI4KA-AKT1-RXRA-FTO axis and inhibits colon cancer cell proliferation by increasing RNA methylation.International journal of biological sciences · 2025Article
- The role of RNA modifications in disease-associated macrophages.Molecular therapy. Nucleic acids · 2024Review
- Role of circular RNAs in preeclampsia (Review).Experimental and therapeutic medicine · 2024Review
101 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
For the yeast Saccharomyces cerevisiae, nutrient limitation is a key developmental signal causing diploid cells to switch from yeast-form budding to either foraging pseudohyphal (PH) growth or meiosis and sporulation. Prolonged starvation leads to lineage restriction, such that cells exiting meiotic prophase are committed to complete sporulation even if nutrients are restored. Here, we have identified an earlier commitment point in the starvation program. After this point, cells, returned to nutrient-rich medium, entered a form of synchronous PH development that was morphologically and genetically indistinguishable from starvation-induced PH growth. We show that lineage restriction during this time was, in part, dependent on the mRNA methyltransferase activity of Ime4, which played separable roles in meiotic induction and suppression of the PH program. Normal levels of meiotic mRNA methylation required the catalytic domain of Ime4, as well as two meiotic proteins, Mum2 and Slz1, which interacted and co-immunoprecipitated with Ime4. This MIS complex (Mum2, Ime4, and Slz1) functioned in both starvation pathways. Together, our results support the notion that the yeast starvation response is an extended process that progressively restricts cell fate and reveal a broad role of post-transcriptional RNA methylation in these decisions.
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Registered trials
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.