The ubiquitin-conjugating enzyme Rad6 (Ubc2) is required for silencing in Saccharomyces cerevisiae

Hanhua Huang, Alon Kahana, Daniel E. Gottschling, Louise Prakash, Susan W. Liebman

Research output: Contribution to journalArticle

108 Scopus citations


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-Δ 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 Ubr1 is the recognition component of the N-end rule-dependent protein degradation pathway, this suggests that N-end role-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.

Original languageEnglish (US)
Pages (from-to)6693-6699
Number of pages7
JournalMolecular and Cellular Biology
Issue number11
StatePublished - Nov 1997


ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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