ArticleMolecular and cellular biology1997
The ubiquitin-conjugating enzyme Rad6 (Ubc2) is required for silencing in Saccharomyces cerevisiae.
Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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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
51 citing papers in PubMed.
- Article
- Essential roles of Rad6 in conidial property, stress tolerance, and pathogenicity ofVirulence · 2024Article
- Paf1 complex subunit Rtf1 stimulates H2B ubiquitylation by interacting with the highly conserved N-terminal helix of Rad6.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Epigenetic modulations of immune cells: from normal development to tumor progression.International journal of biological sciences · 2023Review
- More Than Just Cleaning: Ubiquitin-Mediated Proteolysis in Fungal Pathogenesis.Frontiers in cellular and infection microbiology · 2021Review
- The Epigenetic Pathways to Ribosomal DNA Silencing.Microbiology and molecular biology reviews : MMBR · 2016Review
- The SCFDia2 ubiquitin E3 ligase ubiquitylates Sir4 and functions in transcriptional silencing.PLoS genetics · 2012Article
- The Paf1 complex represses ARG1 transcription in Saccharomyces cerevisiae by promoting histone modifications.Eukaryotic cell · 2011Article
- The specificity and topology of chromatin interaction pathways in yeast.Molecular cell · 2011Article
- The Roles of the Paf1 Complex and Associated Histone Modifications in Regulating Gene Expression.Genetics research international · 2011Article
- Yin and Yang of histone H2B roles in silencing and longevity: a tale of two arginines.Genetics · 2010Article
- Novel trans-tail regulation of H2B ubiquitylation and H3K4 methylation by the N terminus of histone H2A.Molecular and cellular biology · 2010Article
- Reconstitution of heterochromatin-dependent transcriptional gene silencing.Molecular cell · 2009Article
- Interaction of APC/C-E3 ligase with Swi6/HP1 and Clr4/Suv39 in heterochromatin assembly in fission yeast.The Journal of biological chemistry · 2009Article
- HST3/HST4-dependent deacetylation of lysine 56 of histone H3 in silent chromatin.Molecular biology of the cell · 2008Article
- The histone H2B-specific ubiquitin ligase RNF20/hBRE1 acts as a putative tumor suppressor through selective regulation of gene expression.Genes & development · 2008Article
- Controlling histone methylation via trans-histone pathways.Epigenetics · 2008Review
- Article
- Sir3 C-terminal domain involvement in the initiation and spreading of heterochromatin.Molecular and cellular biology · 2006Article
- Dot1a-AF9 complex mediates histone H3 Lys-79 hypermethylation and repression of ENaCalpha in an aldosterone-sensitive manner.The Journal of biological chemistry · 2006Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
It has been previously shown that genes transcribed by RNA polymerase II (RNAP II) are subject to position effect variegation when located near yeast telomeres. This telomere position effect requires a number of gene products that are also required for silencing at the HML and HMR loci. Here, we show that a null mutation of the DNA repair gene RAD6 reduces silencing of the HM loci and lowers the mating efficiency of MATa strains. Likewise, rad6-delta reduces silencing of the telomere-located RNAP II-transcribed genes URA3 and ADE2. We also show that the RNAP III-transcribed tyrosyl tRNA gene, SUP4-o, is subject to position effect variegation when located near a telomere and that this silencing requires the RAD6 and SIR genes. Neither of the two known Rad6 binding factors, Rad18 and Ubr1, is required for telomeric silencing. Since Ubrl is the recognition component of the N-end rule-dependent protein degradation pathway, this suggests that N-end rule-dependent protein degradation is not involved in telomeric silencing. Telomeric silencing requires the amino terminus of Rad6. Two rad6 point mutations, rad6(C88A) and rad6(C88S), which are defective in ubiquitin-conjugating activity fail to complement the silencing defect, indicating that the ubiquitin-conjugating activity of RAD6 is essential for full telomeric silencing.
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