Rog Ofer, Smolikov Sarit, Krauskopf Anat, Kupiec Martin
Department of Molecular Microbiology and Biotechnology, Tel Aviv University, Ramat Aviv, 69978, Israel.
Curr Genet. 2005 Jan;47(1):18-28. doi: 10.1007/s00294-004-0548-y. Epub 2004 Nov 18.
Eukaryotic cells invest a large proportion of their genome in maintaining telomere length homeostasis. Among the 173 non-essential yeast genes found to affect telomere length, a large proportion is involved in vacuolar traffic. When mutated, these vacuolar protein-sorting (VPS) genes lead to telomeres shorter than those observed in the wild type. Using genetic analysis, we characterized the pathway by which VPS15, VPS34, VPS22, VPS23 and VPS28 affect the telomeres. Our results indicate that these VPS genes affect telomere length through a single pathway and that this effect requires the activity of telomerase and the Ku heterodimer, but not the activity of Tel1p or Rif2p. We present models to explain the link between vacuolar traffic and telomere length homeostasis.
真核细胞在维持端粒长度稳态方面投入了其基因组的很大一部分。在发现的173个影响端粒长度的非必需酵母基因中,很大一部分参与液泡运输。这些液泡蛋白分选(VPS)基因发生突变时,会导致端粒比野生型中观察到的更短。通过遗传分析,我们对VPS15、VPS34、VPS22、VPS23和VPS28影响端粒的途径进行了表征。我们的结果表明,这些VPS基因通过单一途径影响端粒长度,并且这种影响需要端粒酶和Ku异源二聚体的活性,但不需要Tel1p或Rif2p的活性。我们提出了模型来解释液泡运输与端粒长度稳态之间的联系。