Transcriptional control of nonfermentative metabolism in the yeast Saccharomyces cerevisiae

Schüller, Hans‐Joachim

doi:10.1007/s00294-003-0381-8

Cited by 401 publications

(289 citation statements)

References 311 publications

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“…In yeast, Δsnf1 is unable to survive on media with non-fermentable carbon as sole carbon source [5]. To determine whether M. oryzae SNF1 pathway contributes to non-fermentable carbon metabolism, mycelial agar plugs of the SNF1 pathway mutants were incubated on minimal media supplemented with various non-fermentable carbons as sole carbon source.…”

Section: Resultsmentioning

confidence: 99%

“…In fungi, where non-fermentable compounds like fatty acids and acetate can serve as sole source of carbon and energy, the acetyl-CoA must be converted to C4 compounds via the glyoxylate cycle, allowing gluconeogenesis [5], [47]. Peroxisome plays an essential role in this process, as it could serve as the location where fatty acid beta-oxidation occurs to generate acetyl-CoA [48], meanwhile many glyoxylate cycle enzymes are also peroxisomal [49].…”

Section: Discussionmentioning

confidence: 99%

“…The yeast SNF1 kinase is a heterotrimer, composed of a catalytic α-subunit Snf1, a regulatory γ-subunit Snf4, and one of the three β-subunit isoforms, Sip1, Sip2, or Gal83, which tethers Snf1 and Snf4 together to form the functional kinase complex [4]. The best documented function of SNF1 kinase is to respond to glucose limitation and enable yeast cells to utilize non-preferred carbon sources when glucose is deprived [3], [5]. The kinase activity of SNF1 is activated by its upstream kinases, Sak1, Tos3, and Elm1 in yeast, which phosphorylate the activation-loop residue Thr210 of the Snf1/α subunit [6], [7].…”

Section: Introductionmentioning

confidence: 99%

“…Meanwhile, recent transcriptomic analysis independently confirms the pivotal role of peroxisomal acetyl-CoA production during appressorial development [37]. In yeast, both lipid metabolism and peroxisomal proliferation are under the regulation of SNF1 pathway [5], [38]. As opposed to the wealthy information in yeast, the function of SNF1 in these critical processes has not yet been studied in filamentous fungi.…”

Section: Introductionmentioning

confidence: 99%

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Crosstalk between SNF1 Pathway and the Peroxisome-Mediated Lipid Metabolism in Magnaporthe oryzae

et al. 2014

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The SNF1/AMPK pathway has a central role in response to nutrient stress in yeast and mammals. Previous studies on SNF1 function in phytopathogenic fungi mostly focused on the catalytic subunit Snf1 and its contribution to the derepression of cell wall degrading enzymes (CWDEs). However, the MoSnf1 in Magnaporthe oryzae was reported not to be involved in CWDEs regulation. The mechanism how MoSnf1 functions as a virulence determinant remains unclear. In this report, we demonstrate that MoSnf1 retains the ability to respond to nutrient-free environment via its participation in peroxisomal maintenance and lipid metabolism. Observation of GFP-tagged peroxisomal targeting signal-1 (PTS1) revealed that the peroxisomes of ΔMosnf1 were enlarged in mycelia and tended to be degraded before conidial germination, leading to the sharp decline of peroxisomal amount during appressorial development, which might impart the mutant great retard in lipid droplets mobilization and degradation. Consequently, ΔMosnf1 exhibited inability to maintain normal appressorial cell wall porosity and turgor pressure, which are key players in epidermal infection process. Exogenous glucose could partially restore the appressorial function and virulence of ΔMosnf1. Toward a further understanding of SNF1 pathway, the β-subunit MoSip2, γ-subunit MoSnf4, and two putative Snf1-activating kinases, MoSak1 and MoTos3, were additionally identified and characterized. Here we show the null mutants ΔMosip2 and ΔMosnf4 performed multiple disorders as ΔMosnf1 did, suggesting the complex integrity is essential for M. oryzae SNF1 kinase function. And the upstream kinases, MoSak1 and MoTos3, play unequal roles in SNF1 activation with a clear preference to MoSak1 over MoTos3. Meanwhile, the mutant lacking both of them exhibited a severe phenotype comparable to ΔMosnf1, uncovering a cooperative relationship between MoSak1 and MoTos3. Taken together, our data indicate that the SNF1 pathway is required for fungal development and facilitates pathogenicity by its contribution to peroxisomal maintenance and lipid metabolism in M. oryzae.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Crosstalk between SNF1 Pathway and the Peroxisome-Mediated Lipid Metabolism in Magnaporthe oryzae

et al. 2014

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“…Therefore, a strong correlation among MIG1 , TUP1 and SSN6 for glucose repression was observed. Previous studies have shown that the maltose metabolism of baker’s yeast could be partly glucose derepressed by MIG1 single-gene mutant through enhancing the transcription of the MAL gene [[17]–[19]]. However, the effect of relieving glucose repression on maltose metabolism of baker’s yeast by silencing TUP1 and/or SSN6 remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Effects of MIG1, TUP1 and SSN6 deletion on maltose metabolism and leavening ability of baker’s yeast in lean dough

et al. 2014

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BackgroundGlucose repression is a global regulatory system in baker’s yeast. Maltose metabolism in baker’s yeast strains is negatively influenced by glucose, thereby affecting metabolite productivity (leavening ability in lean dough). Even if the general repression system constituted by MIG1, TUP1 and SSN6 factors has already been reported, the functions of these three genes in maltose metabolism remain unclear. In this work, we explored the effects of MIG1 and/or TUP1 and/or SSN6 deletion on the alleviation of glucose-repression to promote maltose metabolism and leavening ability of baker’s yeast.ResultsResults strongly suggest that the deletion of MIG1 and/or TUP1 and/or SSN6 can exert various effects on glucose repression for maltose metabolism. The deletion of TUP1 was negative for glucose derepression to facilitate the maltose metabolism. By contrast, the deletion of MIG1 and/or SSN6, rather than other double-gene or triple-gene mutations could partly relieve glucose repression, thereby promoting maltose metabolism and the leavening ability of baker’s yeast in lean dough.ConclusionsThe mutants of industrial baker’s yeast with enhanced maltose metabolism and leavening ability in lean dough were developed by genetic engineering. These baker’s yeast strains had excellent potential industrial applications.

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Signaling between the Organelles and the Nucleus

Fernández

Strand

2018

Annual Plant Reviews Online

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The function of the eukaryotic cell depends on regulated and reciprocal communication between its different compartments. This includes the exchange of metabolic intermediates and energy equivalents but also exchange of information. The presence of genes encoding organellar proteins in both the nucleus and the organelle necessitates tight coordination of expression by the different genomes, and this has led to the evolution of retrograde control. Retrograde (organelle‐to‐nucleus) signaling coordinates the expression of nuclear genes encoding organellar proteins with the metabolic and developmental state of the organelle. Complex networks of retrograde signals coordinate cellular activities and assist the cell during plant development and stress response.

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Transcriptional control of nonfermentative metabolism in the yeast Saccharomyces cerevisiae

Cited by 401 publications

References 311 publications

Crosstalk between SNF1 Pathway and the Peroxisome-Mediated Lipid Metabolism in Magnaporthe oryzae

Crosstalk between SNF1 Pathway and the Peroxisome-Mediated Lipid Metabolism in Magnaporthe oryzae

Effects of MIG1, TUP1 and SSN6 deletion on maltose metabolism and leavening ability of baker’s yeast in lean dough

Signaling between the Organelles and the Nucleus

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