Abstract
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.
Highlights
Spt10 is a putative acetyltransferase of Saccharomyces cerevisiae that directly activates the transcription of histone genes
To study the basis of the spt10D slow growth phenotype, we screened for mutations that enhance or suppress the growth defect by using both transposon insertion mutagenesis (Burns et al 1994) and the S
We have identified a broad spectrum of mutations that either cause lethality when combined with spt10D or that suppress the slow growth phenotype caused by spt10D
Summary
Spt is a putative acetyltransferase of Saccharomyces cerevisiae that directly activates the transcription of histone genes. Partial suppressors of the spt10D growth defect include mutations that perturb cell-cycle progression through the. Consistent with these results, slowing of cell-cycle progression by treatment with hydroxyurea or growth on medium containing glycerol as the carbon source partially suppresses the spt10D slow-growth defect. Mutations that impair the Lsm1-72Pat complex, which regulates decapping of polyadenylated mRNAs, partially suppress the spt10D growth defect. Suppression of the spt10D growth defect is not accompanied by a restoration of normal histone mRNA levels. These findings suggest that Spt has multiple roles during cell division. Mutations in the SPT10 gene have been identified in many different ways, including as suppressors of the transcriptional defects caused by Ty and Ty LTR insertion mutations (Fassler and Winston 1988; Natsoulis et al 1991), suppressors of glucose repression of ADH2 (Denis and Malvar 1990), and suppressors of loss of an upstream activation sequence
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