Tor Pathway Control of the Nitrogen-responsive DAL5 Gene Bifurcates at the Level of Gln3 and Gat1 Regulation in Saccharomyces cerevisiae

Georis, Isabelle; Tate, Jennifer J.; Cooper, Terrance G.; Dubois, Evelyne

doi:10.1074/jbc.m708811200

Cited by 51 publications

(168 citation statements)

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“…In case of S. cerevisiae, the TOR pathway is involved in the intracellular localization of the GATA-type TFs, Gln3 and Gat1, in response to the nitrogen status as mentioned in Introduction (6)(7)(8). Recently, it was revealed that the TOR pathway also plays an important regulatory role in NCR sensitive transcription even after Gln3 is localized to the nucleus (27). Given the conserved structure and functions of TOR kinase among eukaryotes, it would be natural to postulate that the TOR pathway also plays a central role in the regulation of nitrogen assimilation genes through modification of the R2R3-type MYB TFs in plant cells.…”

Section: Discussionmentioning

confidence: 99%

R2R3-type MYB transcription factor, CmMYB1, is a central nitrogen assimilation regulator in Cyanidioschyzon merolae

Imamura

Kanesaki

Ohnuma

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

117

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Plant cells sense environmental nitrogen levels and alter their gene expression accordingly to survive; however, the underlying regulatory mechanisms still remains to be elucidated. Here, we identified and characterized a transcription factor that is responsible for expression of nitrogen assimilation genes in a unicellular red alga Cyanidioschyzon merolae . DNA microarray and Northern blot analyses revealed that transcript of the gene encoding CmMYB1, an R2R3-type MYB transcription factor, increased 1 h after nitrogen depletion. The CmMYB1 protein started to accumulate after 2 h and reached a peak after 4 h after nitrogen depletion, correlating with the expression of key nitrogen assimilation genes, such as CmNRT , CmNAR , CmNIR , CmAMT , and CmGS . Although the transcripts of these nitrogen assimilation genes were detected in nitrate-grown cells, they disappeared upon the addition of preferred nitrogen source such as ammonium or glutamine, suggesting the presence of a nitrogen catabolite repression (NCR) mechanism. The nitrogen depletion-induced gene expression disappeared in a CmMYB1 -null mutant, and the mutant showed decreased cell viability after exposure to the nitrogen-depleted conditions compared with the parental strain. Chromatin immunoprecipitation analysis demonstrated that CmMYB1 specifically occupied these nitrogen-responsive promoter regions only under nitrogen-depleted conditions, and electrophoretic mobility shift assays using crude cell extract revealed specific binding of CmMYB1, or a complex containing CmMYB1, to these promoters. Thus, the presented results indicated that CmMYB1 is a central nitrogen regulator in C. merolae .

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Section: Discussionmentioning

confidence: 99%

R2R3-type MYB transcription factor, CmMYB1, is a central nitrogen assimilation regulator in Cyanidioschyzon merolae

Imamura

Kanesaki

Ohnuma

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

117

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“…6, A and B, ure2⌬ Gln, of Ref. 48), whereas Gat1-Myc 13 similarly relocates in less than 1 ⁄ 3 of them and remains exclusively cytoplasmic in almost half of them (Fig. 6, C and D, ure2⌬ Gln, of Ref.…”

Section: Discussionmentioning

confidence: 99%

“…Work to this point has provided a detailed view of conditions and phosphatase requirements affecting the intracellular localization of Gln3-Myc 13 . Unfortunately, similar information for Gat1 was lacking except for the observations that rapamycin treatment did not demonstrably affect the electrophoretic mobility of Gat1-Myc 13 (44), and rapamycin-induced nuclear Gat1-Myc 13 localization occurred similarly in wild type and sit4⌬ cells (48).…”

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confidence: 99%

“…(v) In the absence of Pph21/22-Tpd3-Cdc55/ Rts1 activity, Gln3-Myc 13 , which is dephosphorylated to the same level as in glutamine-grown, rapamycin-treated wild type cells, remains localized to the cytoplasm (47). (vi) nuclear targeting of Gln3-Myc 13 alone is insufficient for its recruitment to the DAL5 promoter (48). (vii) Gln3-Myc 13 is not uniformly distributed in the cytoplasm of cells grown under repressive conditions but is associated with a cytoplasmic membrane system (49,50).…”

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confidence: 99%

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Distinct Phosphatase Requirements and GATA Factor Responses to Nitrogen Catabolite Repression and Rapamycin Treatment in Saccharomyces cerevisiae

Tate

Georis

Dubois

et al. 2010

Journal of Biological Chemistry

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In yeast, rapamycin (Rap)-inhibited TorC1, and the phosphatases it regulates (Sit4 and PP2A) are components of a conserved pathway regulating the response of eukaryotic cells to nutrient availability. TorC1 and intracellular nitrogen levels regulate the localization of Gln3 and Gat1, the activators of nitrogen catabolite repression (NCR)-sensitive genes whose products are required to utilize poor nitrogen sources. In nitrogen excess, Gln3 and Gat1 are cytoplasmic, and NCR-sensitive transcription is repressed. During nitrogen limitation or Rap treatment, Gln3 and Gat1 are nuclear, and transcription is derepressed. We previously demonstrated that the Sit4 and Pph21/22-Tpd3-Cdc55/Rts1 requirements for nuclear Gln3 localization differ. We now show that Sit4 and Pph21/22-Tpd3-Cdc55/Rts1 requirements for NCR-sensitive and Rap-induced nuclear Gat1 localization markedly differ from those of Gln3. Our data suggest that Gln3 and Gat1 localizations are controlled by two different regulatory pathways. Gln3 localization predominantly responds to intracellular nitrogen levels, as reflected by its stronger NCR-sensitivity, weaker response to Rap treatment, and strong response to methionine sulfoximine (Msx, a glutamine synthetase inhibitor). In contrast, Gat1 localization predominantly responds to TorC1 regulation as reflected by its weaker NCR sensitivity, stronger response to Rap, and immunity to the effects of Msx. Nuclear Gln3 localization in prolinegrown (nitrogen limited) cells exhibits no requirement for Pph21/22-Tpd3/Cdc55, whereas nuclear Gat1 localization under these conditions is absolutely dependent on Pph21/22-Tpd3/Cdc55. Furthermore, the extent to which Pph21/22-Tpd3-Cdc55 is required for the TorC1 pathway (Rap) to induce nuclear Gat1 localization is regulated in parallel with Pph21/22-Tpd3-Cdc55-dependent Gln3 dephosphorylation and NCRsensitive transcription, being highest in limiting nitrogen and lowest when nitrogen is in excess.One consequence of motif, gene, or genome duplication is the subsequent existence of multiple proteins with the same or overlapping functions. In some cases the duplicated genes evolve, acquiring easily distinguishable new functions or regulatory profiles (1-4). In others, the differences are more subtle, and a more careful study is required before they become apparent. This is the case with the Saccharomyces cerevisiae GATA family transcription factors, Gln3 and Gat1/Nil1. Both Gln3 and Gat1 are responsible for nitrogen catabolite repression (NCR) 2 -sensitive expression of genes encoding the transport and enzyme proteins needed to scavenge poor nitrogen sources (e.g. proline) when more readily usable ones are limiting or unavailable (5-8). Gln3 and Gat1 binding sites in NCR-sensitive promoters contain the core sequence GATAA that binds the well characterized zinc finger motif that defines this family of proteins (9 -11).The most apparent differences in the regulation of the GATA factors occur at the level of transcription. GAT1 expression is NCR-sensitive, Gln3-dependent, Gat1-auto-a...

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“…Rapamycin treatment also triggers nuclear import of Gat1 (Beck et al 1999). How TORC1 regulates this process is unclear, yet it appears to be different from TORC1-dependent Gln3 control and does not involve Ure2 or Sit4 (Kuruvilla et al 2001;Crespo et al 2002;Georis et al 2008).…”

Section: Rapamycin-sensitive Signalling Via Torc1mentioning

confidence: 98%

Life in the midst of scarcity: adaptations to nutrient availability in Saccharomyces cerevisiae

et al. 2010

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Cells of all living organisms contain complex signal transduction networks to ensure that a wide range of physiological properties are properly adapted to the environmental conditions. The fundamental concepts and individual building blocks of these signalling networks are generally well-conserved from yeast to man; yet, the central role that growth factors and hormones play in the regulation of signalling cascades in higher eukaryotes is executed by nutrients in yeast. Several nutrient-controlled pathways, which regulate cell growth and proliferation, metabolism and stress resistance, have been defined in yeast. These pathways are integrated into a signalling network, which ensures that yeast cells enter a quiescent, resting phase (G 0 ) to survive periods of nutrient scarceness and that they rapidly resume growth and cell proliferation when nutrient conditions become favourable again. A series of well-conserved nutrient-sensory protein kinases perform key roles in this signalling network: i.e. Snf1, PKA, Tor1 and Tor2, Sch9 and Pho85-Pho80. In this review, we provide a comprehensive overview on the current understanding of the signalling processes mediated via these kinases with a particular focus on how these individual pathways converge to signalling networks that ultimately ensure the dynamic translation of extracellular nutrient signals into appropriate physiological responses.

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Tor Pathway Control of the Nitrogen-responsive DAL5 Gene Bifurcates at the Level of Gln3 and Gat1 Regulation in Saccharomyces cerevisiae

Cited by 51 publications

References 49 publications

R2R3-type MYB transcription factor, CmMYB1, is a central nitrogen assimilation regulator in Cyanidioschyzon merolae

R2R3-type MYB transcription factor, CmMYB1, is a central nitrogen assimilation regulator in Cyanidioschyzon merolae

Distinct Phosphatase Requirements and GATA Factor Responses to Nitrogen Catabolite Repression and Rapamycin Treatment in Saccharomyces cerevisiae

Life in the midst of scarcity: adaptations to nutrient availability in Saccharomyces cerevisiae

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