SGS1 gene resulted in very poor sporulat'/> Sgs1 Helicase Activity Is Required for Mitotic but Apparently Not for Meiotic Functions
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Sgs1 Helicase Activity Is Required for Mitotic but Apparently Not for Meiotic Functions

机译：Sgs1解旋酶活性是有丝分裂所必需的，但显然对减数分裂功能不是必需的

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The SGS1 gene of Saccharomyces cerevisiaeis a homologue for the Bloom's syndrome and Werner's syndrome genes. The disruption of the SGS1 gene resulted in very poor sporulation, and the majority of the cells were arrested at the mononucleated stage. The recombination frequency measured by a return-to-growth assay was reduced considerably in sgs1disruptants. However, double-strand break formation, which is a key event in the initiation of meiotic DNA recombination, occurred; crossover and noncrossover products were observed in the disruptants, although the amounts of these products were slightly decreased compared with those in wild-type cells. The spores produced by sgs1disruptants showed relatively high viability. The sgs1 spo13 double disruptants sporulated poorly, like thesgs1 disruptants, but spore viability was reduced much more than with either sgs1 or spo13 single disruptants. Disruption of the RED1 or RAD17gene partially alleviated the poor-sporulation phenotype ofsgs1 disruptants, indicating that portions of the population of sgs1 disruptants are blocked by the meiotic checkpoint. The poor sporulation of sgs1 disruptants was complemented with a mutated SGS1 gene encoding a protein lacking DNA helicase activity; however, the mutated gene could suppress neither the sensitivity of sgs1 disruptants to methyl methanesulfonate and hydroxyurea nor the mitotic hyperrecombination phenotype of sgs1 disruptants.
机译：酿酒酵母的 SGS1 基因是布鲁姆氏综合症和沃纳氏综合症基因的同源物。 SGS1 基因的破坏导致孢子形成非常差，并且大多数细胞在单核阶段被阻滞。在 sgs1 分散剂中，通过生长恢复法测定的重组频率显着降低。然而，发生了双链断裂的形成，这是减数分裂DNA重组起始的关键事件。在破坏物中观察到了交叉和非交叉产物，尽管与野生型细胞相比，这些产物的量略有减少。由 sgs1 破坏剂产生的孢子显示出较高的生存能力。 sgs1 spo13 双重破坏者的孢子形成较差，与 sgs1 破坏者一样，但孢子活力的下降幅度远大于 sgs1 或 spo13 单个破坏者。破坏 RED1 或 RAD17 基因部分缓解了 sgs1 破坏者的弱孢子表型，表明 sgs1的部分人口破坏剂被减数分裂检查点阻止。 sgs1 破坏株的孢子形成较差，辅以突变的 SGS1 基因，该基因编码的蛋白质缺乏DNA解旋酶活性。然而，该突变基因既不能抑制 sgs1 破坏者对甲磺酸甲酯和羟基脲的敏感性，也不能抑制 sgs1 破坏者的有丝分裂超重组表型。

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