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

The ubiquitin-conjugating enzyme Rad6 (Ubc2) is required for silencing in Saccharomyces cerevisiae
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DOI:
10.1128/mcb.17.11.6693
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发表时间:
1997-11-01
影响因子:
5.3
通讯作者:
Liebman, SW
Liebman, SW
中科院分区:
生物学2区
文献类型:
--
作者:
Huang, HH;Kahana, A;Liebman, SW

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先前已经表明,由RNA聚合酶II(RNAP II)转录的基因在位于酵母端粒附近时受到位置效应杂色。这种端粒位置效应需要许多基因产物,这些基因产物也是在HML和HMR基因座处沉默所需的。在此,黑麦表明DNA修复基因RAD 6的无效突变减少HM基因座的沉默并降低MATa菌株的交配效率,同样地,rad 6-Delta减少了位于端粒的RNAP II转录的基因URA 3和ADE 2的沉默。我们还表明,RNAP III转录的酪氨酰tRNA基因,SUP 4-o,当位于端粒附近时受到位置效应杂色的影响,并且这种沉默需要RAD 6和SIR基因。两种已知的Rad 6结合因子Rad 18和Ubr 1都不是端粒沉默所必需的,由于Ubr 1是N端规则依赖性蛋白降解途径的识别组分,这表明N端规则依赖性蛋白降解不参与端粒沉默,端粒沉默需要Rad 6的氨基末端。两个rad 6点突变,rad 6(C88 A)和rad 6(C88 S),这是缺陷的泛素缀合活性不能弥补沉默缺陷,表明泛素缀合活性的RAD 6是必不可少的完整的端粒沉默。
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, rye 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 Ubr1 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.