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J. Biol. Chem., Vol. 279, Issue 21, 22010-22019, May 21, 2004

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Expression of the HXT1 Low Affinity Glucose Transporter Requires the Coordinated Activities of the HOG and Glucose Signalling Pathways^*

Lidia Tomás-Cobos¶, Laura Casadomé||**, Glòria Mas||**, Pascual Sanz, and Francesc Posas||

From the Instituto de Biomedicina de Valencia, Jaime Roig 11, 46010 Valencia and the ^||Cell Signaling Unit, Departament de Ciencies Experimentals i de la Salut, Universitat Pompeu Fabra, 08003 Barcelona, Spain

Expression of the HXT1 gene, which encodes a low affinity glucose transporter in Saccharomyces cerevisiae, is regulated positively in response to glucose by the general glucose induction pathway, involving the Snf3/Rgt2 membrane glucose sensors, the SCF-Grr1 ubiquitination complex and the Rgt1 transcription factor. In this study we show that, in addition to the glucose signaling pathway, regulation of HXT1 expression also requires the HOG pathway. Deletion of components in the glucose signaling pathway or in the HOG pathway results in impaired HXT1 expression. Genetic analyses showed that, whereas the glucose signaling pathway regulates HXT1 through modulation of the Rgt1 transcription factor, the HOG pathway modulates HXT1 through regulation of the Sko1-Tup1-Ssn6 complex. Coordinated regulation of the two signaling pathways is required for expression of HXT1 by glucose and in response to osmostress.

Received for publication, January 20, 2004

^* This work was supported in part by the Spanish Ministry of Science and Technology (MCyT) (Grant BMC2002-00208 to P. S.) and by the Ministry of Science and Technology (Grants PM99-0028 and BMC2003-00321), Distinció de la Generalitat de Catalunya per a la Promoció dela Recerca Universitaria. Joves Investigadors DURSI (Generalitat de Catalunya), and the EMBO YIP program (to F. P.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Both authors contributed equally to this work.

^¶ Supported by a fellowship from the MCyT (Spain).

^** Recipients of a Formación Personal Universitario pre-doctoral fellowship from the Ministry of Education and Culture (Spain).

To whom correspondence should be addressed. Tel.: 34-96-339-1760; Fax: 34-96-369-0800; E-mail: sanz{at}ibv.csic.es.

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