Gln3–Gcn4 hybrid transcriptional activator determines catabolic and biosynthetic gene expression in the yeast Saccharomyces cerevisiae

Hernández-Barrios, Hugo; Aranda, Cristina; Riego, Lina; González, Alicia

doi:10.1016/j.bbrc.2010.12.075

Cited by 12 publications

(12 citation statements)

References 32 publications

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“…On the other hand, there are many instances where Gln3 and Gat1 regulate NCR-sensitive transcription independently of Gcn4 (3-6). Sometimes, both Gcn4 and these GATA factors cooperatively regulate expression of a nitrogen-catabolic gene (61). Also consistent with this explanation, Sch9 is required for the proper regulation of ribosome biogenesis, translation initiation, and entry into G 0 phase but not for NCR-sensitive gene expression (45).…”

Section: Discussionsupporting

confidence: 51%

Five Conditions Commonly Used to Down-regulate Tor Complex 1 Generate Different Physiological Situations Exhibiting Distinct Requirements and Outcomes

Tate

Cooper

2013

Journal of Biological Chemistry

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Background: Five different conditions have been employed interchangeably to down-regulate TorC1. Results: Four of the five conditions exhibit different, hierarchially related phosphatase requirements. Gln3 responses to longterm nitrogen starvation and Msx treatment exhibit the same phosphatase requirements. Conclusion: Previous conditions for down-regulating TorC1 are not physiologically equivalent. Significance: The cellular responses to varying nitrogen supplies occur via multiple, distinguishable regulatory pathways.

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Section: Discussionsupporting

confidence: 51%

Five Conditions Commonly Used to Down-regulate Tor Complex 1 Generate Different Physiological Situations Exhibiting Distinct Requirements and Outcomes

Tate

Cooper

2013

Journal of Biological Chemistry

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“…How could Gcn4, a highly characterized transcription activator, influence intracellular Gln3 localization? It is true that Gcn4 collaborates with Gln3 in upregulating the expression of a limited number of NCR-sensitive genes containing binding sites for both transcription factors in their promoters, as well as those encoding GLN3 and GAT1 (Mitchell and Magasanik 1984;Natarajan, et al 2001;Valenzuela et al 2001, data set URL is no longer active; Riego et al 2002;Staschke et al 2010;Hernández et al 2011). Such collaboration of Gln3 and Gcn4 coactivating transcription might conceptually shift the Gln3 localization balance toward greater dwell times in the nucleus.…”

Section: Participation Of Bmh1/2 In Gln3 Localization and Functionmentioning

confidence: 99%

“…Gcn4 is the transcription factor responsible for stimulating expression of .500 genes, including those of amino acid biosynthesis (Garcia-Barrio et al 2000;Krishnamurthy et al 2001;Hinnebusch 2005;Natarajan et al 2001Staschke et al 2010. Gcn4 additionally participates in combination with Gln3 to coactivate transcription of a small number of specific NCR-sensitive genes whose promoters contain Gcn4 binding sites (Mitchell and Magasanik 1984;Natarajan et al 2001;Valenzuela et al 2001, data set URL is no longer active; Riego et al 2002;Sosa et al 2003;Staschke et al 2010;Hernández et al 2011). On the other hand, when charged tRNAs are in excess, Gcn2-mediated regulatory outcomes are reversed.…”

Section: Candidates To Join Mtorc1 In Cumulative Gln3 Regulationmentioning

confidence: 99%

General Amino Acid Control and 14-3-3 Proteins Bmh1/2 Are Required for Nitrogen Catabolite Repression-Sensitive Regulation of Gln3 and Gat1 Localization

Tate¹,

Buford²,

Rai³

et al. 2017

Genetics

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Nitrogen catabolite repression (NCR), the ability of Saccharomyces cerevisiae to use good nitrogen sources in preference to poor ones, derives from nitrogen-responsive regulation of the GATA family transcription activators Gln3 and Gat1. In nitrogen-replete conditions, the GATA factors are cytoplasmic and NCR-sensitive transcription minimal. When only poor nitrogen sources are available, Gln3 is nuclear, dramatically increasing GATA factor-mediated transcription. This regulation was originally attributed to mechanistic Tor protein kinase complex 1 (mTorC1)-mediated control of Gln3. However, we recently showed that two regulatory systems act cumulatively to maintain cytoplasmic Gln3 sequestration, only one of which is mTorC1. Present experiments demonstrate that the other previously elusive component is uncharged transfer RNA-activated, Gcn2 protein kinase-mediated general amino acid control (GAAC). Gcn2 and Gcn4 are required for NCR-sensitive nuclear Gln3-Myc 13 localization, and from epistasis experiments Gcn2 appears to function upstream of Ure2. Bmh1/2 are also required for nuclear Gln3-Myc 13 localization and appear to function downstream of Ure2. Overall, Gln3 phosphorylation levels decrease upon loss of Gcn2, Gcn4, or Bmh1/2. Our results add a new dimension to nitrogenresponsive GATA-factor regulation and demonstrate the cumulative participation of the mTorC1 and GAAC pathways, which respond oppositely to nitrogen availability, in the nitrogen-responsive control of catabolic gene expression in yeast.

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“…Therefore, it is not too surprising that control of pathways generating and using nitrogenous precursors might share similarities on the one hand and exhibit distinct differences on the other. An analogous situation occurs with general amino acid control by the GCN proteins ( Riego et al 2002 ; Sosa et al 2003 ; Hernandez et al 2011 ). It is well known that the regulation of protein synthesis by the GCN proteins is mechanistically distinct from the NCR-sensitive regulation of Gln3 and its control of nitrogen catabolism even though Gln3 provides the nitrogen for that protein biosynthesis.…”

Section: Discussionmentioning

confidence: 95%

GATA Factor Regulation in Excess Nitrogen Occurs Independently of Gtr-Ego Complex-Dependent TorC1 Activation

Tate

Georis

Rajendra

et al. 2015

G3 Genes|Genomes|Genetics

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The TorC1 protein kinase complex is a central component in a eukaryotic cell’s response to varying nitrogen availability, with kinase activity being stimulated in nitrogen excess by increased intracellular leucine. This leucine-dependent TorC1 activation requires functional Gtr1/2 and Ego1/3 complexes. Rapamycin inhibition of TorC1 elicits nuclear localization of Gln3, a GATA-family transcription activator responsible for the expression of genes encoding proteins required to transport and degrade poor nitrogen sources, e.g., proline. In nitrogen-replete conditions, Gln3 is cytoplasmic and Gln3-mediated transcription minimal, whereas in nitrogen limiting or starvation conditions, or after rapamycin treatment, Gln3 is nuclear and transcription greatly increased. Increasing evidence supports the idea that TorC1 activation may not be as central to nitrogen-responsive intracellular Gln3 localization as envisioned previously. To test this idea directly, we determined whether Gtr1/2- and Ego1/3-dependent TorC1 activation also was required for cytoplasmic Gln3 sequestration and repressed GATA factor-mediated transcription by abolishing the Gtr-Ego complex proteins. We show that Gln3 is sequestered in the cytoplasm of gtr1Δ, gtr2Δ, ego1Δ, and ego3Δ strains either long term in logarithmically glutamine-grown cells or short term after refeeding glutamine to nitrogen-limited or -starved cells; GATA factor−dependent transcription also was minimal. However, in all but a gtr1Δ, nuclear Gln3 localization in response to nitrogen limitation or starvation was adversely affected. Our data demonstrate: (i) Gtr-Ego-dependent TorC1 activation is not required for cytoplasmic Gln3 sequestration in nitrogen-rich conditions; (ii) a novel Gtr-Ego-TorC1 activation-independent mechanism sequesters Gln3 in the cytoplasm; (iii) Gtr and Ego complex proteins participate in nuclear Gln3-Myc13 localization, heretofore unrecognized functions for these proteins; and (iv) the importance of searching for new mechanisms associated with TorC1 activation and/or the regulation of Gln3 localization/function in response to changes in the cells’ nitrogen environment.

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Gln3–Gcn4 hybrid transcriptional activator determines catabolic and biosynthetic gene expression in the yeast Saccharomyces cerevisiae

Cited by 12 publications

References 32 publications

Five Conditions Commonly Used to Down-regulate Tor Complex 1 Generate Different Physiological Situations Exhibiting Distinct Requirements and Outcomes

Five Conditions Commonly Used to Down-regulate Tor Complex 1 Generate Different Physiological Situations Exhibiting Distinct Requirements and Outcomes

General Amino Acid Control and 14-3-3 Proteins Bmh1/2 Are Required for Nitrogen Catabolite Repression-Sensitive Regulation of Gln3 and Gat1 Localization

GATA Factor Regulation in Excess Nitrogen Occurs Independently of Gtr-Ego Complex-Dependent TorC1 Activation

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