The Zinc Cluster Protein Sut1 Contributes to Filamentation in Saccharomyces cerevisiae

Foster, Helen A.; Cui, Mingfei; Naveenathayalan, Angel; Unden, Heike; Schwanbeck, Ralf; Höfken, Thomas

doi:10.1128/ec.00214-12

Cited by 20 publications

(49 citation statements)

References 54 publications

(67 reference statements)

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“…Early Northern blotting experiments suggested that SUT1 is not expressed under aerobic conditions [8]. However, later real-time PCR and immunoblotting experiments showed that mRNA and protein are aerobically expressed and induced under anaerobic conditions, as suggested earlier [8,34,53]. Rox1 partially represses SUT1 in the presence of oxygen [8] (Figure 5).…”

Section: Regulatory Mechanismsmentioning

confidence: 72%

From Lipid Homeostasis to Differentiation: Old and New Functions of the Zinc Cluster Proteins Ecm22, Upc2, Sut1 and Sut2

Joshua

Höfken

2017

IJMS

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Zinc cluster proteins are a large family of transcriptional regulators with a wide range of biological functions. The zinc cluster proteins Ecm22, Upc2, Sut1 and Sut2 have initially been identified as regulators of sterol import in the budding yeast Saccharomyces cerevisiae. These proteins also control adaptations to anaerobic growth, sterol biosynthesis as well as filamentation and mating. Orthologs of these zinc cluster proteins have been identified in several species of Candida. Upc2 plays a critical role in antifungal resistance in these important human fungal pathogens. Upc2 is therefore an interesting potential target for novel antifungals. In this review we discuss the functions, mode of actions and regulation of Ecm22, Upc2, Sut1 and Sut2 in budding yeast and Candida.

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Section: Regulatory Mechanismsmentioning

confidence: 72%

From Lipid Homeostasis to Differentiation: Old and New Functions of the Zinc Cluster Proteins Ecm22, Upc2, Sut1 and Sut2

Joshua

Höfken

2017

IJMS

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“…The transcription factor Sut1 regulates filamentation through its targets GAT2 , HAP4 , MGA1 , MSN4 , NCE102 , PRR2 , RHO3 and RHO5 (Foster et al ., ). Under optimal growth conditions, Sut1 represses the expression of these genes, whereas under filamentation‐inducing conditions, this repression is lifted.…”

Section: Resultsmentioning

confidence: 97%

“…Next, we examined whether the newly identified targets of Ecm22 and Upc2 ( PRR2 , NPR1 and FHN1 ) play a role in filamentation. As shown before, PRR2 expression is strongly upregulated during haploid and diploid filamentation (Foster et al ., ). Furthermore, PRR2 expression correlates with filamentation phenotypes.…”

Section: Resultsmentioning

confidence: 97%

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The zinc cluster proteins Upc2 and Ecm22 promote filamentation in Saccharomyces cerevisiae by sterol biosynthesis‐dependent and ‐independent pathways

Woods

Höfken

2015

Molecular Microbiology

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SummaryThe transition between a unicellular yeast form to multicellular filaments is crucial for budding yeast foraging and the pathogenesis of many fungal pathogens such as Candida albicans. Here, we examine the role of the related transcription factors Ecm22 and Upc2 in Saccharomyces cerevisiae filamentation. Overexpression of either ECM22 or UPC2 leads to increased filamentation, whereas cells lacking both ECM22 and UPC2 do not exhibit filamentous growth. Ecm22 and Upc2 positively control the expression of FHN1, NPR1, PRR2 and sterol biosynthesis genes. These genes all play a positive role in filamentous growth, and their expression is upregulated during filamentation in an Ecm22/Upc2-dependent manner. Furthermore, ergosterol content increases during filamentous growth. UPC2 expression also increases during filamentation and is inhibited by the transcription factors Sut1 and Sut2. The expression of SUT1 and SUT2 in turn is under negative control of the transcription factor Ste12. We suggest that during filamentation Ste12 becomes activated and reduces SUT1/SUT2 expression levels. This would result in increased UPC2 levels and as a consequence to transcriptional activation of FHN1, NPR1, PRR2 and sterol biosynthesis genes. Higher ergosterol levels in combination with the proteins Fhn1, Npr1 and Prr2 would then mediate the transition to filamentous growth.

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“…SUT1, which improved anaerobic cellobiose fermentation when overexpressed, is an activator of sterol uptake and hypoxic genes [75], but its regulatory role in central carbon metabolism is not known. Constitutive overexpression of SUT1 has been shown to slow growth on glucose in aerobic cultures by downregulating genes important for respiratory metabolism [76], and it was also shown to block filamentous growth [77]. HAP4, deletion of which improved anaerobic cellobiose fermentation is a regulatory subunit of the Hap2/3/4/5 complex that positively regulates respiratory gene expression, and is a hotspot of genetic variation in cell physiology between yeast strains [27].…”

Section: Discussionmentioning

confidence: 99%

Leveraging transcription factors to speed cellobiose fermentation by

Lin

Chomvong

Acosta-Sampson

et al. 2014

Biotechnol Biofuels

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Background: Saccharomyces cerevisiae, a key organism used for the manufacture of renewable fuels and chemicals, has been engineered to utilize non-native sugars derived from plant cell walls, such as cellobiose and xylose. However, the rates and efficiencies of these non-native sugar fermentations pale in comparison with those of glucose. Systems biology methods, used to understand biological networks, hold promise for rational microbial strain development in metabolic engineering. Here, we present a systematic strategy for optimizing non-native sugar fermentation by recombinant S. cerevisiae, using cellobiose as a model. Results: Differences in gene expression between cellobiose and glucose metabolism revealed by RNA deep sequencing indicated that cellobiose metabolism induces mitochondrial activation and reduces amino acid biosynthesis under fermentation conditions. Furthermore, glucose-sensing and signaling pathways and their target genes, including the cAMP-dependent protein kinase A pathway controlling the majority of glucose-induced changes, the Snf3-Rgt2-Rgt1 pathway regulating hexose transport, and the Snf1-Mig1 glucose repression pathway, were at most only partially activated under cellobiose conditions. To separate correlations from causative effects, the expression levels of 19 transcription factors perturbed under cellobiose conditions were modulated, and the three strongest promoters under cellobiose conditions were applied to fine-tune expression of the heterologous cellobiose-utilizing pathway. Of the changes in these 19 transcription factors, only overexpression of SUT1 or deletion of HAP4 consistently improved cellobiose fermentation. SUT1 overexpression and HAP4 deletion were not synergistic, suggesting that SUT1 and HAP4 may regulate overlapping genes important for improved cellobiose fermentation. Transcription factor modulation coupled with rational tuning of the cellobiose consumption pathway significantly improved cellobiose fermentation.

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The Zinc Cluster Protein Sut1 Contributes to Filamentation in Saccharomyces cerevisiae

Cited by 20 publications

References 54 publications

From Lipid Homeostasis to Differentiation: Old and New Functions of the Zinc Cluster Proteins Ecm22, Upc2, Sut1 and Sut2

From Lipid Homeostasis to Differentiation: Old and New Functions of the Zinc Cluster Proteins Ecm22, Upc2, Sut1 and Sut2

The zinc cluster proteins Upc2 and Ecm22 promote filamentation in Saccharomyces cerevisiae by sterol biosynthesis‐dependent and ‐independent pathways

Leveraging transcription factors to speed cellobiose fermentation by

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