KTI11 and KTI13, Saccharomyces cerevisiae genes controlling sensitivity to G1 arrest induced by Kluyveromyces lactis zymocin
KTI11 and KTI13, Saccharomyces cerevisiae genes controlling sensitivity to G1 arrest induced by Kluyveromyces lactis zymocin
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DOI：
10.1046/j.1365-2958.2002.02928.x
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发表时间：
2002-05-01
影响因子：
3.6
通讯作者：
Schaffrath, R
中科院分区：
文献类型：
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作者：
Fichtner, L;Schaffrath, R
乳酸克鲁维酵母发酵素及其γ-毒素亚基抑制酿酒酵母细胞周期进程。鉴定S.酿酒酵母基因赋予酵母敏感性，我们补充了未分类的酵母耐药的意志和kti 13突变，使用单拷贝酵母文库。因此，我们将酵母开放阅读框（ORF）YBL 071 w-A和YAL 020 c/ATS 1分别鉴定为KTI 11和KTI 13。KTI 11和KTI 13的破坏导致在γ-毒素靶位点突变体tot 1 -7中观察到的复杂tot表型，并且包括酶霉素抗性、热敏性、对药物的超敏性和缓慢生长。这两个位点，KTI 11和KTI 13，是积极转录的蛋白质编码基因，通过逆转录酶-聚合酶链反应（RT-PCR）和体内HA表位标记确定。Kti 11 p是从酵母到人高度保守的，Kti 13 p/Ats 1 p与酵母Prp 20 p和哺乳动物RCC 1相关，它们是Ran-GTP/GDP循环的组分。将KTI 11或KTI 13中的破坏与编码RNA聚合酶II（RNAPII）延伸子组蛋白乙酰转移酶（HAT）的TOT 3/ELP 3中的缺失相结合，对缓慢生长表型表达产生了合成效应。这表明遗传相互作用，并可能将KTI 11和KTI 13与延长子功能联系起来。
The Kluyveromyces lactis zymocin and its gamma-toxin subunit inhibit cell cycle progression of Saccharomyces cerevisiae. To identify S. cerevisiae genes conferring zymocin sensitivity, we complemented the unclassified zymocin-resistant Will and kti13 mutations using a single-copy yeast library. Thus, we identified yeast open reading frames (ORFs) YBL071w-A and YAL020c/ATS1 as KTI11 and KTI13 respectively. Disruption of KTI11 and KTI13 results in the complex tot phenotype observed for the gamma-toxin target site mutants, tot1-7, and includes zymocin resistance, thermosensitivity, hypersensitivity to drugs and slow growth. Both loci, KTI11 and KTI13, are actively transcribed protein-encoding genes as determined by reverse transcriptase-polymerase chain reaction (RT-PCR) and in vivo HA epitope tagging. Kti11p is highly conserved from yeast to man, and Kti13p/Ats1p is related to yeast Prp20p and mammalian RCC1, components of the Ran-GTP/GDP cycle. Combining disruptions in KTI11 or KTI13 with a deletion in TOT3/ELP3 coding for the RNA polymerase II (RNAPII) Elongator histone acetyltransferase (HAT) yielded synthetic effects on slow growth phenotype expression. This suggests genetic interaction and possibly links KTI11 and KTI13 to Elongator function.