Daughter-Specific Transcription Factors Regulate Cell Size Control in Budding Yeast

Talia, Stefano Di; Wang, Hongyin; Rosebrock, Adam P.; Futcher, Bruce; Cross, Frederick R.

doi:10.1371/journal.pbio.1000221

Cited by 111 publications

(143 citation statements)

References 71 publications

(173 reference statements)

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“…Ash1 shows similarity to the GATA family of DNA-binding proteins and has been suggested to target Rpd3(L) to some promoters (16). In addition to repressing HO expression, Ash1 is required for efficient activation of the FLO11 gene required for pseudohyphal growth (20,21) and may regulate CLN3 expression in daughter cells (22). Ash1 is therefore another regulator of HO transcription that acts by altering the structure of chromatin, in this case by assisting the recruitment of the Rpd3(L) histone deacetylase complex.…”

mentioning

confidence: 99%

Repressive Chromatin Affects Factor Binding at Yeast HO (Homothallic Switching) Promoter

Takahata¹,

Stillman

2011

Journal of Biological Chemistry

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Background: Expression of the yeast HO gene is tightly regulated, with a large complex promoter. Results: The Rpd3(L) histone deacetylase is recruited twice by distinct factors to different promoter regions. Conclusion: Chromatin represses the HO promoter, making multiple coactivators required for gene expression. Significance: Multiple factors contribute to the establishment of a tightly repressed, cell cycle-regulated promoter.

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confidence: 99%

Repressive Chromatin Affects Factor Binding at Yeast HO (Homothallic Switching) Promoter

Takahata¹,

Stillman

2011

Journal of Biological Chemistry

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“…This asymmetric localization of the transcript results in the specific sorting of the Ash1 protein to the nucleus of the daughter cell, where it controls mating type switching and cell size (Jansen et al 1996;Sil and Herskowitz 1996;Di Talia et al 2009). During its transport to the bud tip, translation of the ASH1 mRNA is repressed by the RNAbinding proteins Khd1p (Irie et al 2002;Paquin et al 2007) and Puf6p (Gu et al 2004).…”

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confidence: 99%

Cotranscriptional recruitment of She2p by RNA pol II elongation factor Spt4–Spt5/DSIF promotes mRNA localization to the yeast bud

St‐Denis¹,

Chartrand²

2010

Genes Dev.

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Pre-mRNA processing is coupled with transcription. It is still unclear if the transcription machinery can also directly affect the cytoplasmic fate of a transcript, such as its intracellular localization. In yeast, the RNA-binding protein She2p binds several mRNAs and targets them for localization at the bud. Here we report that She2p is recruited cotranscriptionally to the nascent bud-localized ASH1, IST2, and EAR1 mRNA. She2p interacts in vivo with the elongating forms of RNA polymerase II (pol II) via the transcription elongation factor Spt4-Spt5. Mutations in either SPT4 or SPT5 reduce the cotranscriptional recruitment of She2p on the ASH1 gene, disrupt the proper localization of ASH1 mRNA at the bud tip, and affect Ash1p sorting to the daughter cell nucleus. We propose that She2p is recruited by the RNA pol II machinery prior to its transfer to nascent bud-localized mRNAs. Indeed, She2p is present with RNA pol II on genes coding for localized or nonlocalized transcripts, but is associated with nascent mRNA only on genes coding for bud-localized transcripts. Moreover, a She2p mutant defective in RNA binding still associates with RNA pol II transcribed genes. This study uncovers a novel mechanism for the cotranscriptional assembly of mRNP complexes primed for localization in the cytoplasm.[Keywords: mRNA; localization; yeast; She2p; Spt4p; Spt5p; cotranscriptional] Supplemental material is available at http://www.genesdev.org.

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“…Furthermore, our analysis of DR genes as regulatory targets allowed the establishment of a set of ranked transcription factors (DR regulators) orchestrating the cellular response to nitrogen restriction. Strikingly, most high‐ranked DR regulators were transcription factors involved in mitotic cell cycle transitions, either by repression of Cln3 specifically in yeast daughter cells (Ace2 and Ash1) (Di Talia et al., 2009; Laabs et al., 2003), activation of ribosomal‐protein genes (Sfp1) (Marion et al., 2004), or cell differentiation in response to nutrients or pheromone (Tec1 and Ste12) (Madhani, Galitski, Lander & Fink, 1999). Top‐hit transcription factors also included, Msn2 and Msn4, two positive regulators of stress response and lifespan extension downstream of the Tor/Ras‐PKA pathways that converge on Rim15, the main protein kinase involved in cell survivorship in response to nutrients (Wei et al., 2008).…”

Section: Discussionmentioning

confidence: 99%

Genomewide mechanisms of chronological longevity by dietary restriction in budding yeast

et al. 2018

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SummaryDietary restriction is arguably the most promising nonpharmacological intervention to extend human life and health span. Yet, only few genetic regulators mediating the cellular response to dietary restriction are known, and the question remains which other regulatory factors are involved. Here, we measured at the genomewide level the chronological lifespan of Saccharomyces cerevisiae gene deletion strains under two nitrogen source regimens, glutamine (nonrestricted) and γ‐aminobutyric acid (restricted). We identified 473 mutants with diminished or enhanced extension of lifespan. Functional analysis of such dietary restriction genes revealed novel processes underlying longevity by the nitrogen source quality, which also allowed us to generate a prioritized catalogue of transcription factors orchestrating the dietary restriction response. Importantly, deletions of transcription factors Msn2, Msn4, Snf6, Tec1, and Ste12 resulted in diminished lifespan extension and defects in cell cycle arrest upon nutrient starvation, suggesting that regulation of the cell cycle is a major mechanism of chronological longevity. We further show that STE12 overexpression is enough to extend lifespan, linking the pheromone/invasive growth pathway with cell survivorship. Our global picture of the genetic players of longevity by dietary restriction highlights intricate regulatory cross‐talks in aging cells.

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Daughter-Specific Transcription Factors Regulate Cell Size Control in Budding Yeast

Abstract: The asymmetric localization of cell fate determinants results in asymmetric cell cycle control in budding yeast.

Cited by 111 publications

References 71 publications

Repressive Chromatin Affects Factor Binding at Yeast HO (Homothallic Switching) Promoter

Repressive Chromatin Affects Factor Binding at Yeast HO (Homothallic Switching) Promoter

Cotranscriptional recruitment of She2p by RNA pol II elongation factor Spt4–Spt5/DSIF promotes mRNA localization to the yeast bud

Genomewide mechanisms of chronological longevity by dietary restriction in budding yeast

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