Nitrogen catabolite repression of arginase (CAR1) expression in Saccharomyces cerevisiae is derived from regulated inducer exclusion

Author:

Cooper T G1,Kovari L1,Sumrada R A1,Park H D1,Luche R M1,Kovari I1

Affiliation:

1. Department of Microbiology and Immunology, University of Tennessee, Memphis 38163.

Abstract

Expression of the Saccharomyces cerevisiae arginase (CAR1) gene is regulated by induction and nitrogen catabolite repression (NCR). Arginine was demonstrated to be the native inducer. CAR1 sensitivity to NCR has long been accepted to be accomplished through a negative control mechanism, and cis-acting sites for it have been hypothesized. In search of this negatively acting site, we discovered that CAR1 sensitivity to NCR derives from regulated inducer (arginine) exclusion. The route of catabolic entry of arginine into the cell, the general amino acid permease (GAP1), is sensitive to NCR. However, CAR1 expression in the presence of sufficient intracellular arginine is NCR insensitive.

Publisher

American Society for Microbiology

Subject

Molecular Biology,Microbiology

Reference40 articles.

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3. Saturation mutagenesis of the UASNTR (GATAA) responsible for nitrogen catabolite repression-sensitive transcriptional activation of the allantoin pathway genes in Saccharomyces cerevisiae;Bysani N.;J. Bacteriol.,1991

4. Cooper T. G. 1982. Nitrogen metabolism in Saccharomyces cerevisiae p. 39-99. In J. Strathern E. Jones and J. Broach (ed.) Molecular biology of the yeast Saccharomyces: metabolism and gene expression. Cold Spring Harbor Laboratory Cold Spring Harbor N.Y.

5. Cooper T. G. 1982. Transport in Saccharomyces cerevisiae p. 399-461. In J. Strathern E. Jones and J. Broach (ed.) Molecular biology of the yeast Saccharomyces: metabolism and gene expression. Cold Spring Harbor Laboratory Cold Spring Harbor N.Y.

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