Cell-cycle perturbations suppress the slow-growth defect of spt10Δ mutants in Saccharomyces cerevisiae.
Cell-cycle perturbations suppress the slow-growth defect of spt10Δ mutants in Saccharomyces cerevisiae.
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DOI：
10.1534/g3.112.005389
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发表时间：
2013-03
期刊：
影响因子：
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通讯作者：
Winston F
中科院分区：
文献类型：
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作者：
Chang JS;Winston F
Spt10 是一种假定的酿酒酵母乙酰转移酶，可直接激活组蛋白基因的转录。 SPT10 的缺失会导致严重的生长缓慢表型，表明 Spt10 对于正常细胞分裂至关重要。为了深入了解 Spt10 的功能，我们鉴定了损害或促进 spt10 null (spt10Δ) 突变体生长的突变。与 spt10Δ 结合导致致死性的突变包括 SAGA 复合体的特定成分以及 asf1Δ 和 hir1Δ。 spt10Δ生长缺陷的部分抑制因子包括扰乱细胞周期通过G1/S转变、S期和G2/M的突变。与这些结果一致，通过用羟基脲处理或在含有甘油作为碳源的培养基上生长来减缓细胞周期进程也部分抑制了 spt10Δ 缓慢生长缺陷。此外，损害调节聚腺苷酸化 mRNA 脱帽的 Lsm1-7−Pat1 复合体的突变也会部分抑制 spt10Δ 生长缺陷。有趣的是，抑制 spt10Δ 生长缺陷并不伴随着正常组蛋白 mRNA 水平的恢复。这些发现表明 Spt10 在细胞分裂过程中发挥多种作用。
Spt10 is a putative acetyltransferase of Saccharomyces cerevisiae that directly activates the transcription of histone genes. Deletion of SPT10 causes a severe slow growth phenotype, showing that Spt10 is critical for normal cell division. To gain insight into the function of Spt10, we identified mutations that impair or improve the growth of spt10 null (spt10Δ) mutants. Mutations that cause lethality in combination with spt10Δ include particular components of the SAGA complex as well as asf1Δ and hir1Δ. Partial suppressors of the spt10Δ growth defect include mutations that perturb cell-cycle progression through the G1/S transition, S phase, and G2/M. Consistent with these results, slowing of cell-cycle progression by treatment with hydroxyurea or growth on medium containing glycerol as the carbon source also partially suppresses the spt10Δ slow-growth defect. In addition, mutations that impair the Lsm1-7−Pat1 complex, which regulates decapping of polyadenylated mRNAs, also partially suppress the spt10Δ growth defect. Interestingly, suppression of the spt10Δ growth defect is not accompanied by a restoration of normal histone mRNA levels. These findings suggest that Spt10 has multiple roles during cell division.