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

Reese, Joseph C.; Green, Michael R.

doi:10.1002/yea.761

Cited by 10 publications

(5 citation statements)

References 62 publications

(89 reference statements)

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“…In fact, previous studies supported the involvement of specific TAFs in cell cycle control (Apone et al 1996;Walker et al 1997;Reese and Green 2001), including the fact that TAF9 interacts with SWI6 genetically and biochemically (Figure 1; Macpherson et al 2000;Sanders et al 2002). Identification in our SGA screen of MSN5, encoding a karyopherin required for proper nucleocytoplasmic transport of Swi6 (Queralt and Igual 2003), provides additional support for this notion, further linking TAF9 to control of the G 1 /S transition via Swi6 localization.…”

Section: Caf40 Cdc40 Loc1supporting

confidence: 78%

TFIID and Spt-Ada-Gcn5-Acetyltransferase Functions Probed by Genome-wide Synthetic Genetic Array Analysis Using a Saccharomyces cerevisiae taf9-ts Allele

Milgröm¹,

West²,

Gao³

et al. 2005

Genetics

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TAF9 is a TATA-binding protein associated factor (TAF) conserved from yeast to humans and shared by two transcription coactivator complexes, TFIID and SAGA. The essentiality of the TAFs has made it difficult to ascertain their roles in TFIID and SAGA function. Here we performed a genomic synthetic genetic array analysis using a temperature-sensitive allele of TAF9 as a query. Results from this experiment showed that TAF9 interacts genetically with: (1) genes for multiple transcription factor complexes predominantly involving Mediator, chromatin modification/remodeling complexes, and regulators of transcription elongation; (2) virtually all nonessential genes encoding subunits of the SWR-C chromatin-remodeling complex and both TAF9 and SWR-C required for expressing the essential housekeeping gene RPS5; and (3) key genes for cell cycle control at the G 1 /S transition, as well as genes involved in cell polarity, cell integrity, and protein synthesis, suggesting a link between TAF9 function and cell growth control. We also showed that disruption of SAGA by deletion of SPT20 alters histone-DNA contacts and phosphorylated forms of RNA polymerase II at coding sequences. Our results raise the possibility of an unappreciated role for TAF9 in transcription elongation, perhaps in the context of SAGA, and provide further support for TAF9 involvement in cell cycle progression and growth control.

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Section: Caf40 Cdc40 Loc1supporting

confidence: 78%

TFIID and Spt-Ada-Gcn5-Acetyltransferase Functions Probed by Genome-wide Synthetic Genetic Array Analysis Using a Saccharomyces cerevisiae taf9-ts Allele

Milgröm¹,

West²,

Gao³

et al. 2005

Genetics

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“…Subunits of the Ccr4-Not complex show both genetic and physical interactions with TFIID, the SAGA histone acetyltransferase complex, TATA-binding protein (TBP) and SRB/Mediator complex (Badarinarayana et al, 2000, Benson et al, 1998, Deluen et al, 2002, Lemaire and Collart, 2000, Liu et al, 2001, Reese and Green, 2001, Sanders et al, 2002), supporting a role in transcription initiation. Physical interactions between Not2 and Not5 and TBP and TFIID-specific TAF II s have been described in the literature (Sanders et al, 2002, Lemaire and Collart, 2000, Deluen et al, 2002).…”

Section: Ccr4-not and Transcriptionmentioning

confidence: 99%

Ccr4-Not complex: the control freak of eukaryotic cells

Miller

Reese

2012

Critical Reviews in Biochemistry and Molecular Biology

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161

191

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The purpose of this review is to provide an analysis of the latest developments on the functions of the Ccr4-Not complex in regulating eukaryotic gene expression. Ccr4-Not is a nine-subunit protein complex that is conserved in sequence and function throughout the eukaryotic kingdom. Although Ccr4-Not has been studied since the 1980s, our understanding of what it does is constantly evolving. Once thought to solely regulate transcription, it is now clear that it has much broader roles in gene regulation, such as in mRNA decay and quality control, RNA export, translational repression and protein ubiquitylation. The mechanism of actions for each of its functions is still being debated. Some of the difficulty in drawing a clear picture is that it has been implicated in so many processes that regulate mRNAs and proteins in both the cytoplasm and the nucleus. We will describe what is known about the Ccr4-Not complex in yeast and other eukaryotes in an effort to synthesize a unified model for how this complex coordinates multiple steps in gene regulation and provide insights into what questions will be most exciting to answer in the future.

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“…Importantly, the identity of the factors generated in the #2 strain and their relationship to the promoter reprograming factor(s) generated in the #3 strain are unclear. In any case, these observations raised an intriguing possibility that the altered gene expression profiles obtained at restrictive temperatures for the taf1-N568Δ mutant (#2 strain) as well as for many other previously reported taf mutants [24,[57][58][59][60][61][62][63][64][65][66][67][68][69][70][71][72] could be achieved by the combined effects not only of impaired TFIID function but also of other prion (s) or condensate(s) ectopically generated in taf mutant strains.…”

Section: Plos Onementioning

confidence: 99%

TFIID dependency of steady-state mRNA transcription altered epigenetically by simultaneous functional loss of Taf1 and Spt3 is Hsp104-dependent

et al. 2023

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In Saccharomyces cerevisiae, class II gene promoters have been divided into two subclasses, TFIID- and SAGA-dominated promoters or TFIID-dependent and coactivator-redundant promoters, depending on the experimental methods used to measure mRNA levels. A prior study demonstrated that Spt3, a TBP-delivering subunit of SAGA, functionally regulates the PGK1 promoter via two mechanisms: by stimulating TATA box-dependent transcriptional activity and conferring Taf1/TFIID independence. However, only the former could be restored by plasmid-borne SPT3. In the present study, we sought to determine why ectopically expressed SPT3 is unable to restore Taf1/TFIID independence to the PGK1 promoter, identifying that this function was dependent on the construction protocol for the SPT3 taf1 strain. Specifically, simultaneous functional loss of Spt3 and Taf1 during strain construction was a prerequisite to render the PGK1 promoter Taf1/TFIID-dependent in this strain. Intriguingly, genetic approaches revealed that an as-yet unidentified trans-acting factor reprogrammed the transcriptional mode of the PGK1 promoter from the Taf1/TFIID-independent state to the Taf1/TFIID-dependent state. This factor was generated in the haploid SPT3 taf1 strain in an Hsp104-dependent manner and inherited meiotically in a non-Mendelian fashion. Furthermore, RNA-seq analyses demonstrated that this factor likely affects the transcription mode of not only the PGK1 promoter, but also of many other class II gene promoters. Collectively, these findings suggest that a prion or biomolecular condensate is generated in a Hsp104-dependent manner upon simultaneous functional loss of TFIID and SAGA, and could alter the roles of these transcription complexes on a wide variety of class II gene promoters without altering their primary sequences. Therefore, these findings could provide the first evidence that TFIID dependence of class II gene transcription can be altered epigenetically, at least in Saccharomyces cerevisiae.

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

Cited by 10 publications

References 62 publications

TFIID and Spt-Ada-Gcn5-Acetyltransferase Functions Probed by Genome-wide Synthetic Genetic Array Analysis Using a Saccharomyces cerevisiae taf9-ts Allele

TFIID and Spt-Ada-Gcn5-Acetyltransferase Functions Probed by Genome-wide Synthetic Genetic Array Analysis Using a Saccharomyces cerevisiae taf9-ts Allele

Ccr4-Not complex: the control freak of eukaryotic cells

TFIID dependency of steady-state mRNA transcription altered epigenetically by simultaneous functional loss of Taf1 and Spt3 is Hsp104-dependent

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