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Full-Text Articles in Genetics and Genomics
Functional Dissection Of The Glucose Signaling Pathways That Regulate The Yeast Glucose Transporter Gene (Hxt) Repressor Rgt1, David J. Jouandot Ii, Adhiraj Roy, Jeong-Ho Kim
Functional Dissection Of The Glucose Signaling Pathways That Regulate The Yeast Glucose Transporter Gene (Hxt) Repressor Rgt1, David J. Jouandot Ii, Adhiraj Roy, Jeong-Ho Kim
Faculty Publications
The yeast Rgt1 repressor is a bifunctional protein that acts as a transcriptional repressor and activator. Under glucose-limited conditions, Rgt1 induces transcriptional repression by forming a repressive complex with its corepressors Mth1 and Std1. Here, we show that Rgt1 is converted from a transcriptional repressor into an activator under high glucose conditions and this occurs through two independent but consecutive events mediated by two glucose signaling pathways: (1) disruption of the repressive complex by the Rgt2/Snf3 pathway; (2) phosphorylation of Rgt1 by the cAMP-dependent protein kinase (cAMP-PKA) pathway. Rgt1 is phosphorylated by PKA at four serine residues within its amino-terminal …
The Nuclear Pore Complex Mediates Binding Of The Mig1 Repressor To Target Promoters, Nayan J. Sarma, Thomas D. Buford, Terry Haley, Kellie Barbara-Haley, George M. Santangelo, Kristine A. Willis
The Nuclear Pore Complex Mediates Binding Of The Mig1 Repressor To Target Promoters, Nayan J. Sarma, Thomas D. Buford, Terry Haley, Kellie Barbara-Haley, George M. Santangelo, Kristine A. Willis
Faculty Publications
All eukaryotic cells alter their transcriptional program in response to the sugar glucose. In Saccharomyces cerevisiae, the best-studied downstream effector of this response is the glucose-regulated repressor Mig1. We show here that nuclear pore complexes also contribute to glucose-regulated gene expression. NPCs participate in glucose-responsive repression by physically interacting with Mig1 and mediating its function independently of nucleocytoplasmic transport. Surprisingly, despite its abundant presence in the nucleus of glucose-grown nup120Δ or nup133Δ cells, Mig1 has lost its ability to interact with target promoters. The glucose repression defect in the absence of these nuclear pore components therefore appears …