Shields up: the Tup1–Cyc8 repressor complex blocks coactivator recruitment: Figure 1.

Parnell, Emily J.; Stillman, David J.

doi:10.1101/gad.181768.111

Cited by 18 publications

(18 citation statements)

References 47 publications

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“…However, we speculate that several repressive mechanisms work cooperatively to regulate genes involved in mannitol metabolism. Tup1-Cyc8 represses transcription via multiple mechanisms (16,19,38): modifying chromatin structure via recruitment of HDACs, directing the positioning of nucleosomes, inhibiting the general transcription machinery via direct interactions, and masking the activation domains of DNA-binding proteins to prevent the recruitment of coactivators. When the CYC8 allele from MK4416 was overexpressed in BY4742, the overexpressing cells did not grow in SM medium (see Fig.…”

Section: Discussionmentioning

confidence: 99%

Acquisition of the Ability To Assimilate Mannitol by Saccharomyces cerevisiae through Dysfunction of the General Corepressor Tup1-Cyc8

Chujo

Yoshida

Ota

et al. 2015

Appl Environ Microbiol

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Saccharomyces cerevisiae normally cannot assimilate mannitol, a promising brown macroalgal carbon source for bioethanol production. The molecular basis of this inability remains unknown. We found that cells capable of assimilating mannitol arose spontaneously from wild-type S. cerevisiae during prolonged culture in mannitol-containing medium. Based on microarray data, complementation analysis, and cell growth data, we demonstrated that acquisition of mannitol-assimilating ability was due to spontaneous mutations in the genes encoding Tup1 or Cyc8, which constitute a general corepressor complex that regulates many kinds of genes. We also showed that an S. cerevisiae strain carrying a mutant allele of CYC8 exhibited superior salt tolerance relative to other ethanologenic microorganisms; this characteristic would be highly beneficial for the production of bioethanol from marine biomass. Thus, we succeeded in conferring the ability to assimilate mannitol on S. cerevisiae through dysfunction of Tup1-Cyc8, facilitating production of ethanol from mannitol. Macroalgae, consisting of green, red, and brown algae, are promising sources of biofuels for several reasons: (i) macroalgae are more productive than land crops; (ii) arable land is not required for algal cultivation, obviating the necessity for irrigation, fertilizer, etc.; and (iii) macroalgae contain no lignin (1-4). Both red and brown algae contain high levels of carbohydrates, and a method for producing biofuel from these carbohydrates would be of tremendous economic and environmental benefit.Brown macroalgae contain up to 33% (wt/wt [dry weight]) mannitol, which is the sugar alcohol corresponding to mannose and a promising carbon source for bioethanol production (1, 5, 6). Although some bacteria, such as Escherichia coli and Zymobacter palmae, can assimilate mannitol, i.e., utilize mannitol and produce ethanol (6, 7), bacteria are generally sensitive to ethanol, as well as, several other growth-inhibitory compounds. Z. palmae and E. coli KO11 can produce ca. 1.3% (wt/vol) and 2.6% (wt/vol) ethanol from 3.8% (wt/vol) and 9.0% (wt/vol) mannitol, respectively; however, both strains are sensitive to 5% (wt/vol) ethanol (8,9). Yeast is currently considered to have several advantages over ethanologenic bacteria, including high tolerance to ethanol and inhibitory compounds (10). Several yeast strains, such as Pichia angophorae and Saccharomyces paradoxus NBRC0259-3, can produce ethanol from mannitol (8, 11). However, compared to the well-characterized model organism Saccharomyces cerevisiae, the host-vector systems of these yeasts are not well equipped, and their genetics and physiologies are poorly defined.Mannitol dehydrogenase is the key enzyme that catalyzes the pyridine nucleotide-dependent oxidation of D-mannitol to Dfructose (12). Despite the existence of genes encoding putative homologs of mannitol dehydrogenase (YEL070W and YNR073C), S. cerevisiae strains, including the S288C reference strain, are unable to assimilate mannitol for growth; a few exceptions exi...

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Section: Discussionmentioning

confidence: 99%

Acquisition of the Ability To Assimilate Mannitol by Saccharomyces cerevisiae through Dysfunction of the General Corepressor Tup1-Cyc8

Chujo

Yoshida

Ota

et al. 2015

Appl Environ Microbiol

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“…This complex is especially well studied in the yeast Saccharomyces cerevisiae , and mutational and genome-wide expression studies have shown that Tup1 is responsible for the repression of over 180 genes, including gene sets regulated by glucose, DNA damage, mating type, and oxygen availability, and gene sets involved in osmotic stress responses, flocculation, and dimorphism [25]–[28]. Recent studies have shown that the repressor function of Tup1-Cyc8 is caused by the interaction of the complex with a specific DNA-binding domain, thereby preventing the recruitment of transcriptional co-activators [29], [30]. The important role of Tup1/TupA in pathogenic fungi has received further attention because of its important role in dimorphism and pathogenicity.…”

Section: Introductionmentioning

confidence: 99%

The Transcriptional Repressor TupA in Aspergillus niger Is Involved in Controlling Gene Expression Related to Cell Wall Biosynthesis, Development, and Nitrogen Source Availability

Schachtschabel

Arentshorst²,

Nitsche³

et al. 2013

PLoS ONE

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The Tup1-Cyc8 (Ssn6) complex is a well characterized and conserved general transcriptional repressor complex in eukaryotic cells. Here, we report the identification of the Tup1 (TupA) homolog in the filamentous fungus Aspergillus niger in a genetic screen for mutants with a constitutive expression of the agsA gene. The agsA gene encodes a putative alpha-glucan synthase, which is induced in response to cell wall stress in A. niger. Apart from the constitutive expression of agsA, the selected mutant was also found to produce an unknown pigment at high temperatures. Complementation analysis with a genomic library showed that the tupA gene could complement the phenotypes of the mutant. Screening of a collection of 240 mutants with constitutive expression of agsA identified sixteen additional pigment-secreting mutants, which were all mutated in the tupA gene. The phenotypes of the tupA mutants were very similar to the phenotypes of a tupA deletion strain. Further analysis of the tupA-17 mutant and the ΔtupA mutant revealed that TupA is also required for normal growth and morphogenesis. The production of the pigment at 37°C is nitrogen source-dependent and repressed by ammonium. Genome-wide expression analysis of the tupA mutant during exponential growth revealed derepression of a large group of diverse genes, including genes related to development and cell wall biosynthesis, and also protease-encoding genes that are normally repressed by ammonium. Comparison of the transcriptome of up-regulated genes in the tupA mutant showed limited overlap with the transcriptome of caspofungin-induced cell wall stress-related genes, suggesting that TupA is not a general suppressor of cell wall stress-induced genes. We propose that TupA is an important repressor of genes related to development and nitrogen metabolism.

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“…Various models for Tup1-Cyc8 mediated repression of target gene promoters have been described 21,23,24 . It has been proposed that Tup1-Cyc8 primarily regulates promoters by masking transcription factors from recruiting co-activators 25 .…”

Section: Resultsmentioning

confidence: 99%

“…The Tup1-Cyc8 regulates transcription of a subset of promoters in yeast 18,46 . Several mechanisms have been described for Tup1-Cyc8 mediated gene repression 21,23,24 . For example, Tup1-Cyc8 interacts with HDACs, which in turn facilitate repression of promoters by deacetylating nucleosomes.…”

Section: Remarkably There Was Little or No Delay Between Depletion Omentioning

confidence: 99%

Regulated repression, and not activation, governs the cell fate promoter controlling yeast meiosis

Tam

Werven

2020

Preprint

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Intrinsic signals and cues from the external environment drive cell fate decisions.In budding yeast, the decision to enter meiosis is controlled by nutrient and matingtype signals that regulate expression of the master transcription factor for meiotic entry, IME1. How nutrient signals control IME1 expression remains poorly understood. Here we show that IME1 transcription is regulated by multiple sequence-specific transcription factors that mediate association of Tup1-Cyc8 corepressor to its promoter. We find that at least eight transcription factors bind the IME1 promoter when nutrients are ample. Remarkably, association of these transcription factors is highly regulated by different nutrient cues. Mutant cells lacking three transcription factors (Sok2/Phd1/Yap6) displayed reduced Tup1-Cyc8 association, increased IME1 expression and earlier onset of meiosis. Our data demonstrate that the promoter of a master regulator is primed for rapid activation while repression by multiple transcription factors mediating Tup1-Cyc8 recruitment dictates the fate decision to enter meiosis.

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Shields up: the Tup1–Cyc8 repressor complex blocks coactivator recruitment: Figure 1.

Cited by 18 publications

References 47 publications

Acquisition of the Ability To Assimilate Mannitol by Saccharomyces cerevisiae through Dysfunction of the General Corepressor Tup1-Cyc8

Acquisition of the Ability To Assimilate Mannitol by Saccharomyces cerevisiae through Dysfunction of the General Corepressor Tup1-Cyc8

The Transcriptional Repressor TupA in Aspergillus niger Is Involved in Controlling Gene Expression Related to Cell Wall Biosynthesis, Development, and Nitrogen Source Availability

Regulated repression, and not activation, governs the cell fate promoter controlling yeast meiosis

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