ArticleCell2015
Product binding enforces the genomic specificity of a yeast polycomb repressive complex.
Article in Cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 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
92 citing papers in PubMed, 155 citations in OpenAlex.
- Mammalian-evolved strains of the fungal pathogen Cryptococcus neoformans show adaptation via heritable transcript level differences specific to mouse MHC haplotype.BMC genomics · 2026Article
- Variable ectopic heterochromatin islands provide an alternative route to antifungal heteroresistance inbioRxiv : the preprint server for biology · 2026Article
- Neofunctionalization of H1 linker histones drives divergent gene expression and histone methylation in Cryptococcus neoformans.Communications biology · 2026Article
- Structural landscape of H3K27me3 recognition by protein domains and their potential for inhibition.The Journal of biological chemistry · 2026Review
- A H3K27me3 reader complex couples H3K27me3 accumulation to nascent transcription of transposable elements in Paramecium.Genome biology · 2026Article
- Temperature and genetic background drive mobilization of diverse transposable elements in a global human fungal pathogen.PLoS genetics · 2026Article
- Organization principles of dynamic three-dimensional genome architecture associated with centromere clustering states.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- CRISPR/Cas9-compatible plasmids enabling seven dominant genetic selection methods for the human fungal pathogenMicrobiology spectrum · 2025Article
- Chromatin profiling identifies putative dual roles for H3K27me3 in regulating cell type-specific genes and transposable elements in choanoflagellates.Nature communications · 2025Article
- Epigenetic regulation of pathogenicity in fungi.Current genetics · 2025Review
- HISTONE DEACETYLASE-1 is required for epigenome stability inProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Fungi as models of centromere innovation: from DNA sequence to 3-dimensional arrangement.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2025Review
- Article
- Is a Fungal Apocalypse Inevitable or Just a Hallucination? An Overview of the Antifungal Armamentarium Used in the Fight against Pathogenic Fungi.ACS medicinal chemistry letters · 2025Review
- Article
- Transposon load and RNAi loss synergize to drive intraspecies diversity inProceedings of the National Academy of Sciences of the United States of America · 2024Article
- The PRC2.1 Subcomplex Opposes G1 Progression through Regulation of CCND1 and CCND2.bioRxiv : the preprint server for biology · 2024Article
- Comparative genomics of the closely related fungal genera Cryptococcus and Kwoniella reveals karyotype dynamics and suggests evolutionary mechanisms of pathogenesis.PLoS biology · 2024Article
- Comparative genomics ofbioRxiv : the preprint server for biology · 2024Article
- Uncoupled evolution of the Polycomb system and deep origin of non-canonical PRC1.Communications biology · 2023Article
32 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
10 authors at 3 institutions in 1 country.
Funding
Abstract
We characterize the Polycomb system that assembles repressive subtelomeric domains of H3K27 methylation (H3K27me) in the yeast Cryptococcus neoformans. Purification of this PRC2-like protein complex reveals orthologs of animal PRC2 components as well as a chromodomain-containing subunit, Ccc1, which recognizes H3K27me. Whereas removal of either the EZH or EED ortholog eliminates H3K27me, disruption of mark recognition by Ccc1 causes H3K27me to redistribute. Strikingly, the resulting pattern of H3K27me coincides with domains of heterochromatin marked by H3K9me. Indeed, additional removal of the C. neoformans H3K9 methyltransferase Clr4 results in loss of both H3K9me and the redistributed H3K27me marks. These findings indicate that the anchoring of a chromatin-modifying complex to its product suppresses its attraction to a different chromatin type, explaining how enzymes that act on histones, which often harbor product recognition modules, may deposit distinct chromatin domains despite sharing a highly abundant and largely identical substrate-the nucleosome.
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What OpenQuestion holds
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.