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Fission yeast Whi5 represses MBF-dependent transcription in quiescent cells II

ABSTRACT: When cells arrest the cell cycle in G1 to enter the non-dividing quiescent state, the transcriptional machinery that promotes G1/S transition must be inactivated. Central to this regulation is Whi5, in budding yeast, and the Retinoblastoma (Rb) protein, in mammalian cells, acting as repressors of the transcription factors SBF, and E2F, respectively. In fission yeast, the MBF complex is the functional homologue of E2F in metazoans. Fission yeast Whi5/Mug54 is an uncharacterized protein predicted to function as a cell cycle transcriptional repressor at the G1/S transition. In this work, we show that after induction of quiescence by nitrogen starvation, fission yeast Whi5 is localised to the nucleus, and it is required for the repression of MBF-dependent genes. Mass spectrometry and bimolecular fluorescence complementation (BiFC) analyses revealed that Whi5 physically interacts with components of both the MBF and the histone deacetylase Clr6-I complexes. Moreover, Whi5 is required for the interaction of the MBF complex with Clr6-I, suggesting a role for Whi5 in maintaining transcriptional repression of MBF-dependent genes in quiescent cells by the recruitment of HDACs to gene promoters.

ORGANISM(S): Schizosaccharomyces pombe

PROVIDER: GSE285763 | GEO | 2025/12/20

REPOSITORIES: GEO

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Fission yeast Whi5 represses MBF-dependent transcription in quiescent cells

Project description:When cells arrest the cell cycle in G1 to enter the non-dividing quiescent state, the transcriptional machinery that promotes G1/S transition must be inactivated. Central to this regulation is Whi5, in budding yeast, and the Retinoblastoma (Rb) protein, in mammalian cells, acting as repressors of the transcription factors SBF, and E2F, respectively. In fission yeast, the MBF complex is the functional homologue of E2F in metazoans. Fission yeast Whi5/Mug54 is an uncharacterized protein predicted to function as a cell cycle transcriptional repressor at the G1/S transition. In this work, we show that after induction of quiescence by nitrogen starvation, fission yeast Whi5 is localised to the nucleus, and it is required for the repression of MBF-dependent genes. Mass spectrometry and bimolecular fluorescence complementation (BiFC) analyses revealed that Whi5 physically interacts with components of both the MBF and the histone deacetylase Clr6-I complexes. Moreover, Whi5 is required for the interaction of the MBF complex with Clr6-I, suggesting a role for Whi5 in maintaining transcriptional repression of MBF-dependent genes in quiescent cells by the recruitment of HDACs to gene promoters.

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Fission yeast Whi5 represses MBF-dependent transcription in quiescent cells

Project description:Fission yeast Whi5 represses MBF-dependent transcription in quiescent cells

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Fission yeast Whi5 represses MBF-dependent transcription in quiescent cells II

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Role of a Candida albicans Whi5/Nrm1 homolog in cell cycle and hyphal-specific gene expression

Project description:Candida albicans is an opportunistic pathogenic fungus that is able to assume several morphologies, including yeast and hyphal growth forms. The hyphal morphology can be induced by various environmental stimuli and is accompanied by expression of a large set of hyphal-specific genes (HSGs). Cell cycle and morphogenetic programs are interconnected: notably, inhibition of cell cycle progression often causes a switch to filamentous growth. Here we identify and characterize CaNrm1, a C. albicans homolog of the S. cerevisiae Whi5 and Nrm1 transcription inhibitors that, analogous to mammalian Rb, regulate the cell cycle transcription program in the G1 phase and at the G1/S transition. CaNRM1 is able to complement the phenotypes of both whi5 and nrm1 mutants in S. cerevisiae. Deletion of CaNRM1 causes a reduction in cell size and results in increased resistance to hydroxyurea (HU), an inhibitor of DNA replication; analysis of the expression of ribonucleotide reductase, the target of HU, suggests that its transcriptional induction in response to HU is mainly dependent upon CaNrm1. Genetic epistasis analysis suggests that CaNrm1 interacts with the SBF and MBF transcription factors in S. cerevisiae and with the MBF functional homolog in C. albicans. At the transcription level, deletion of CaNRM1 causes an induction of many G1 and G1/S-specific genes. Induction of the HSGs is dampened under certain conditions in the Canrm1-/- mutant, suggesting that the cell cycle transcription program influences the morphogenetic transcription program of C. albicans. One aspect of the characterization of the C. albicans Whi5/Nrm1 gene was to examine how this molecule influences global gene expression. To that end, we isolated total RNA from log-phase nrm1-/nrm1- (as well as parent/background strain) cells in two independent replicate experiments. These samples were processed, labeled, and subsequently used for hybridization of custom C. albicans Affymetrix arrays.

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Differential regulation of SBF and MBF target genes by genotoxic stress occurs via Rad53-dependent inactivation of the MBF correpressor Nrm1

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Deconvolution of ChIP-chip MBF occupancies reveals the temporal recruitment of Rep2 at the MBF-target genes

Project description:Deconvolution analysis using Rpb1 ChIP-chip results distinguishes the Cdc10 bindings at the Rpb1-poor loci (promoters) from those at the Rpb1-rich loci (intragenic sequences). Importantly, Res1 binding at the Rpb1-poor loci, but not at the Rpb1-rich loci, are dependent on the Cdc10 function, suggesting a distinct binding mechanism. Most Cdc10 promoter bindings at the Rpb1-poor loci are associated with the G1/S-phase genes. While Res1 or Res2 is found at both the Cdc10 promoter and intragenic binding sites, Rep2 appears to be absent at the Cdc10 promoter binding sites but present at the intragenic sites. Time-course ChIP-chip analysis demonstrates that Rep2 is temporally accumulated at the coding region of the MBF-target genes, resembling the RNAP-II occupancies. We analyzed MBF binding sites using Nimblegen arrays.

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Nrm1 is a bistable switch connecting cell cycle progression to transcriptional control

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