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Originally published as Genetics Published Articles Ahead of Print on June 18, 2006.
Genetics, Vol. 174, 617-626, October 2006, Copyright © 2006
doi:10.1534/genetics.106.059766
Connection Between the Rag4 Glucose Sensor and the KlRgt1 Repressor in Kluyveromyces lactis
Stéphane Rolland1, Martina Hnatova, Marc Lemaire, Juana Leal-Sanchez2 and Micheline Wésolowski-Louvel3
Génétique des Levures, UMR 5122 Microbiologie et Génétique, Université Claude Bernard Lyon 1, 69622 Villeurbanne, France
3 Corresponding author: Unité Microbiologie et Génétique UMR 5122 CNRS/UCBL/INSA, Université Claude Bernard Lyon 1, 43, Boulevard du 11 Novembre 1918, 69622 Villeurbanne Cédex, France.
E-mail: louvel{at}univ-lyon1.fr
The RAG4 gene encodes for the sole transmembrane glucose sensor of Kluyveromyces lactis. A rag4 mutation leads to a fermentation-deficient phenotype (Rag– phenotype) and to a severe defect in the expression of the major glucose transporter gene RAG1. A recessive extragenic suppressor of the rag4 mutation has been identified. It encodes a protein (KlRgt1) 31% identical to the Saccharomyces cerevisiae Rgt1 regulator of the HXT genes (ScRgt1). The Klrgt1 null mutant displays abnormally high levels of RAG1 expression in the absence of glucose but still presents an induction of RAG1 expression in the presence of glucose. KlRgt1 is therefore only a repressor of RAG1. As described for ScRgt1, the KlRgt1 repressor function is controlled by phosphorylation in response to high glucose concentration and this phosphorylation is dependent on the sensor Rag4 and the casein kinase Rag8. However, contrary to that observed with ScRgt1, KlRgt1 is always bound to the RAG1 promoter. This article reveals that the key components of the glucose-signaling pathway are conserved between S. cerevisiae and K. lactis, but points out major differences in Rgt1 regulation and function that might reflect different carbon metabolism of these yeasts.
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