Histone H3 lysine 4 methylation is mediated by Set1 and required for cell growth and rDNA silencing in Saccharomyces cerevisiae.
By S. Briggs, M. Bryk, Brian D. Strahl, Wang L. Cheung, J. Davie, Sharon Y. R. Dent, F. Winston, C. D. Allis. Genes & Development, 2001
664 citations recorded by the source corpus.
Histone methylation is known to be associated with both transcriptionally active and repressive chromatin states. Recent studies have identified SET domain-containing proteins such as SUV39H1 and Clr4 as mediators of H3 lysine 9 (Lys9) methylation and heterochromatin formation. Interestingly, H3 Lys9 methylation is not observed from bulk histones isolated from asynchronous populations of Saccharomyces cerevisiae or Tetrahymena thermophila. In contrast, H3 lysine 4 (Lys4) methylation is a predominant modification in these smaller eukaryotes. To identify the responsible methyltransferase(s) and to gain insight into the function of H3 Lys4 methylation, we have developed a histone H3 Lys4 methyl-specific antiserum. With this antiserum, we show that deletion of SET1, but not of other putative SET domain-containing genes, in S. cerevisiae, results in the complete abolishment of H3 Lys4 methylation in vivo. Furthermore, loss of H3 Lys4 methylation in a set1 Delta strain can be rescued by SET1. Analysis of histone H3 mutations at Lys4 revealed a slow-growth defect similar to a set1 Delta strain. Chromatin immunoprecipitation assays show that H3 Lys4 methylation is present at the rDNA locus and that Set1-mediated H3 Lys4 methylation is required for repression of RNA polymerase II transcription within rDNA. Taken together, these data suggest that Set1-mediated H3 Lys4 methylation is required for normal cell growth and transcriptional silencing.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/caf1907fbfff0caca28e41a4a20330cbf8e3cc01
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In Molecular Biology
- D. Reinberg
- Yi Zhang
- C. D. Allis
- A. Shilatifard
- T. Jenuwein
- Paul Tempst
- Tony Kouzarides
- H. Erdjument‐Bromage
Citations in the corpus
- Targeted recruitment of Set1 histone methylase by elongating Pol II provides a localized mark and memory of recent transcriptional activity. (2003, background): “K4 hypermethylation provides a molecular memory of In Saccharomyces cerevisiae, Set1 and H3-K4 methyl-recent transcriptional activity. ation are important for ribosomal DNA (Briggs et al., 2001; Bryk et al., 2002) and telomeric silencing (NislowIntroduction et al., 1997; Krogan et al., 2002a).”
- Cotranscriptional set2 methylation of histone H3 lysine 36 recruits a repressive Rpd3 complex. (2005, neutral): “For Figure 4E, whole-cell extracts (WCEs) from 100 ml cultures f wild-type H2B-Flag and set2 H2B-Flag strains were prepared s previously described (Briggs et al., 2001).”
- An epigenetic road map for histone lysine methylation (2003, background): “H3-K9 methylation, by contrast, is present mainly in silenced chromatin domains (Noma et al., 2001; Litt et al., 2001), and the ‘activated genome’ of S. cerevisiae exhibits abundant H3-K4 methylation but lacks apparent H3-K9 di-methylation (Briggs et al., 2001).”
- SETDB1: a novel KAP-1-associated histone H3, lysine 9-specific methyltransferase that contributes to HP1-mediated silencing of euchromatic genes by KRAB zinc-finger proteins. (2002, methodology): “Previously described PHD finger and bromodomain mutations in KAP-1 were subcloned into the SmaI site of pBTM116 (Capili et al. 2001; Schultz et al. 2001).”
- The diverse functions of histone lysine methylation (2005, background): “cerevisiae , a lysine methyltransferase named Set1 is responsible for all three H3-K4 methylation states, implying that these states and their distinct spatial patterns must result from the regulation of the enzymatic activity and/or targeting of Set1 (Ref”
- Genome-wide map of nucleosome acetylation and methylation in yeast. (2005, neutral): “The histone methyltransferase Set1 has previously been shown to be recruited to the 5# end of actively transcribed genes where it is responsible for histone H3K4 methylation (Bernstein et al., 2002; Briggs et al., 2001; Krogan et al., 2003a; Ng et al., 2003b; SantosRosa et al., 2002).”