Genetics, Vol. 153, 585-594, October 1999, Copyright © 1999

Mks1p Is a Regulator of Nitrogen Catabolism Upstream of Ure2p in Saccharomyces cerevisiae

Herman K. Edskesa, John A. Hanoverb, and Reed B. Wicknera
a Laboratory of Biochemistry and Genetics, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892-0830
b Laboratory of Cell Biochemistry and Biology, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892-0830

Corresponding author: Reed B. Wickner, Bldg. 8, Rm. 225, National Institutes of Health, 8 Center Dr., MSC 0830, Bethesda, MD 20892-0830., wickner{at}helix.nih.gov (E-mail)

Communicating editor: A. P. MITCHELL

The supply of nitrogen regulates yeast genes affecting nitrogen catabolism, pseudohyphal growth, and meiotic sporulation. Ure2p of Saccharomyces cerevisiae is a negative regulator of nitrogen catabolism that inhibits Gln3p, a positive regulator of DAL5, and other genes of nitrogen assimilation. Dal5p, the allantoate permease, allows ureidosuccinate uptake (Usa+) when cells grow on a poor nitrogen source such as proline. We find that overproduction of Mks1p allows uptake of ureidosuccinate on ammonia and lack of Mks1p prevents uptake of ureidosuccinate or Dal5p expression on proline. Overexpression of Mks1p does not affect cellular levels of Ure2p. An mks1 ure2 double mutant can take up ureidosuccinate on either ammonia or proline. Moreover, overexpression of Ure2p suppresses the ability of Mks1p overexpression to allow ureidosuccinate uptake on ammonia. These results suggest that Mks1p is involved in nitrogen control upstream of Ure2p as follows: NH3{dashv} Mks1p{dashv} Ure2p{dashv} Gln3p -> DAL5. Either overproduction of Mks1p or deletion of MKS1 interferes with pseudohyphal growth.




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