A Subset of TAFIIs Are Integral Components of the SAGA Complex Required for Nucleosome Acetylation and Transcriptional Stimulation

Grant, Patrick A.; Schieltz, David; Pray-Grant, Marilyn G.; Steger, David J.; Reese, Joseph C.; Yates, John R.; Workman, Jerry L.

doi:10.1016/s0092-8674(00)81220-9

Cited by 404 publications

(365 citation statements)

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“…The SPT genes encode many proteins important in transcription, including subunits of the SAGA histone-modifying complex (Grant et al 1998), TBP itself, and histones (Clark-Adams et al 1988;Winston and Sudarsanam 1998;Yamaguchi et al 2001). SPT10 is not an essential gene, but the null allele is associated with very slow growth and defects in gene regulation (Denis and Malvar 1990;Natsoulis et al 1991;Prelich and Winston 1993;Yamashita 1993;Dollard et al 1994;Natsoulis et al 1994).…”

Section: Cell-cycle-dependent Activation Of the Histone Genesmentioning

confidence: 99%

Regulation of Histone Gene Expression in Budding Yeast

Eriksson¹,

Ganguli²,

Nagarajavel³

et al. 2012

Genetics

116

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We discuss the regulation of the histone genes of the budding yeast Saccharomyces cerevisiae. These include genes encoding the major core histones (H3, H4, H2A, and H2B), histone H1 (HHO1), H2AZ (HTZ1), and centromeric H3 (CSE4). Histone production is regulated during the cell cycle because the cell must replicate both its DNA during S phase and its chromatin. Consequently, the histone genes are activated in late G1 to provide sufficient core histones to assemble the replicated genome into chromatin. The major core histone genes are subject to both positive and negative regulation. The primary control system is positive, mediated by the histone gene-specific transcription activator, Spt10, through the histone upstream activating sequences (UAS) elements, with help from the major G1/S-phase activators, SBF (Swi4 cell cycle box binding factor) and perhaps MBF (MluI cell cycle box binding factor). Spt10 binds specifically to the histone UAS elements and contains a putative histone acetyltransferase domain. The negative system involves negative regulatory elements in the histone promoters, the RSC chromatin-remodeling complex, various histone chaperones [the histone regulatory (HIR) complex, Asf1, and Rtt106], and putative sequence-specific factors. The SWI/SNF chromatin-remodeling complex links the positive and negative systems. We propose that the negative system is a damping system that modulates the amount of transcription activated by Spt10 and SBF. We hypothesize that the negative system mediates negative feedback on the histone genes by histone proteins through the level of saturation of histone chaperones with histone. Thus, the negative system could communicate the degree of nucleosome assembly during DNA replication and the need to shut down the activating system under replication-stress conditions. We also discuss post-transcriptional regulation and dosage compensation of the histone genes.

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Section: Cell-cycle-dependent Activation Of the Histone Genesmentioning

confidence: 99%

Regulation of Histone Gene Expression in Budding Yeast

Eriksson¹,

Ganguli²,

Nagarajavel³

et al. 2012

Genetics

116

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“…In contrast, genetic analysis of other TFIID subunits that have sequence similarities to the core histones has shown that they are required for the transcription of a larger number of genes (Apone et al, 1998;Holstege et al, 1998;Michel et al, 1998;Moqtaderi et al, 1998;Natajaran et al, 1998;Sanders et al, 1999;Reese et al, 2000). The interpretation of these results is complicated by the presence of certain TAF II s in the SAGA histone acetyltransferase complex (Grant et al, 1998), and their function in multiple complexes may partially explain the expanded requirement for these TAF II s in transcription (Lee et al, 2000). However, while Yeast Yeast 2001; 18: 1197-1205.…”

Section: Introductionmentioning

confidence: 99%

Genetic analysis of TAF68/61 reveals links to cell cycle regulators

Reese

Green

2001

Yeast

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In yeast, inactivation of certain TBP-associated factors (TAF II s) results in arrest at specific stages of the cell cycle. In some cases, cell cycle arrest is not observed because overlapping defects in other cellular processes precludes the manifestation of an arrest phenotype. In the latter situation, genetic analysis has the potential to reveal the involvement of TAF II s in cell cycle regulation. In this report, a temperature-sensitive mutant of TAF68/61 was used to screen for high-copy dosage suppressors of its growth defect. Ten genes were isolated: TAF suppressor genes, TSGs 1-10. Remarkably, most TSGs have either a genetic or a direct link to control of the G 2 /M transition. Moreover, eight of the 10 TSGs can suppress a CDC28 mutant specifically defective for mitosis (cdc28-1N) but not an allele defective for passage through start. The identification of these genes as suppressors of cdc28-1N has identified four unreported suppressors of this allele. Moreover, synthetic lethality is observed between taf68-9 and cdc28-1N. The isolation of multiple genes involved in the control of a specific phase of the cell cycle argue that the arrest phenotypes of certain TAF II mutants reflect their role in specifically regulating cell cycle functions.

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“…The yeast SAGA complex is composed of several distinct classes of factors including alteration/deficiency in activation (ADAs), suppressor of Ty (SPTs), TATAbinding protein-associated factors (TAFs), general control non-repressed 5 (GCN5) and TRA1, and acts as a transcriptional coactivator/adapter required at specific promoters (Grant et al, 1998;Hampsey, 1998). Recently, novel SAGA components such as UBP8, SGF11, SGF29, SGF73 and SUS1 have been identified (Sanders et al, 2002;Rodriguez-Navarro et al, 2004).…”

Section: Introductionmentioning

confidence: 99%