Cln3 Activates G1-Specific Transcription via Phosphorylation of the SBF Bound Repressor Whi5

Bruin, Robertus A.M. de; McDonald, W. Hayes; Kalashnikova, Tatyana I.; Yates, John R.; Wittenberg, Curt

doi:10.1016/j.cell.2004.05.025

Cited by 387 publications

(598 citation statements)

References 54 publications

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“…Early studies showed that cells lacking Swi6 produced an intermediate constitutive level of transcripts for other Swi6 target genes (Dirick et al 1992;Lowndes et al 1992), suggesting that Swi6 performs a regulatory function that is both positive and negative within the cell cycle. This hypothesis is supported by the recent discovery of Whi5, which associates with Swi4/Swi6 complexes during early G 1 and dissociates when the complex is activated ( Jorgensen et al 2002;Costanzo et al 2004;de Bruin et al 2004). Activation of Swi4/Swi6 complexes requires the Cln3 cyclin and the Cdc28 cyclindependent kinase, which phosphorylates Whi5 and promotes its dissociation.…”

supporting

confidence: 53%

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Genetic Interactions Between Mediator and the Late G1-Specific Transcription Factor Swi6 in Saccharomyces cerevisiae

Quinton²,

Miles

et al. 2005

Genetics

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Swi6 associates with Swi4 to activate HO and many other late G 1 -specific transcripts in budding yeast. Genetic screens for suppressors of SWI6 mutants have been carried out. A total of 112 of these mutants have been identified and most fall into seven complementation groups. Six of these genes have been cloned and identified and they all encode subunits of the mediator complex. These mutants restore transcription to the HO-lacZ reporter in the absence of Swi6 and have variable effects on other Swi6 target genes. Deletions of other nonessential mediator components have been tested directly for suppression of, or genetic interaction with, swi6. Mutations in half of the known subunits of mediator show suppression and/or growth defects in combination with swi6. These phenotypes are highly variable and do not correlate with a specific module of the mediator. Mutations in tail module components sin4 and pgd1 showed both growth defects and suppression when combined with swi6, but a third tail component, gal11, showed neither. A truncated form of the essential Srb7 mediator subunit also suppresses swi6 mutations and shows a defect in recruitment of the tail module components Sin4, Pgd1, and Gal11 to the mediator complex.

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supporting

confidence: 53%

“…Once bound to SCB elements, Swi4/Swi6/ Whi5 recruits mediator, but this takes place well before the complex is activated by Cln3/Cdk. Whi5 dissociates and transcription ensues (Costanzo et al 2004;de Bruin et al 2004), with the further recruitment of PolII, TFIIB, and TFIIH (Cosma et al 2001).…”

mentioning

confidence: 99%

Genetic Interactions Between Mediator and the Late G1-Specific Transcription Factor Swi6 in Saccharomyces cerevisiae

Quinton²,

Miles

et al. 2005

Genetics

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“…As protein synthesis seems to increase exponentially during the cell (a) scheme of the start network with components and interactions. Briefly, the Cdk-cyclin complex formed by Cln3 [16][17][18][19][20] and Cdc28 21 phosphorylates the transcriptional repressor Whi5 22,23 and activates sBF (swi6/swi4) and mBF (swi6/mbp1) transcription factors 14 to induce the G1/s regulon 15 and trigger cell cycle entry. Whi3 and Ydj1 act as negative and positive regulators, respectively, of release of cyclin Cln3 from the ER [31][32][33] to allow its accumulation in the nucleus.…”

Section: Discussionmentioning

confidence: 99%

“…Whi5 22,23 binds G1/S transcription factors 14 to inhibit their activity in the nucleus during G1. Thus, we analysed cells deficient for Whi3 (Fig.…”

Section: Cell Size At Start Is Dictated By Volume Growth Rate In G1mentioning

confidence: 99%

The critical size is set at a single-cell level by growth rate to attain homeostasis and adaptation

et al. 2012

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Budding yeast cells are assumed to trigger start and enter the cell cycle only after they attain a critical size set by external conditions. However, arguing against deterministic models of cell size control, cell volume at start displays great individual variability even under constant conditions. Here we show that cell size at start is robustly set at a single-cell level by the volume growth rate in G1, which explains the observed variability. We find that this growth-rate-dependent sizer is intimately hardwired into the start network and the Ydj1 chaperone is key for setting cell size as a function of the individual growth rate. mathematical modelling and experimental data indicate that a growth-rate-dependent sizer is sufficient to ensure size homeostasis and, as a remarkable advantage over a rigid sizer mechanism, it reduces noise in G1 length and provides an immediate solution for size adaptation to external conditions at a population level.

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“…In the case of SBF, this is probably due to Whi5-mediated inactivation (Costanzo et al 2004;De Bruin et al 2004), which involves recruitment of the Rpd3L histone deacetylase (Takahata et al 2009). SBF is subsequently activated through phosphorylation of Whi5 by the Cln3-Cdc28 kinase (Costanzo et al 2004;De Bruin et al 2004).…”

Section: Mechanism Of Histone Gene Regulation During the Cell Cyclementioning

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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Cln3 Activates G1-Specific Transcription via Phosphorylation of the SBF Bound Repressor Whi5

Cited by 387 publications

References 54 publications

Genetic Interactions Between Mediator and the Late G1-Specific Transcription Factor Swi6 in Saccharomyces cerevisiae

Genetic Interactions Between Mediator and the Late G1-Specific Transcription Factor Swi6 in Saccharomyces cerevisiae

The critical size is set at a single-cell level by growth rate to attain homeostasis and adaptation

Regulation of Histone Gene Expression in Budding Yeast

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