Edskes H K, Hanover J A, Wickner R B
Laboratory of Biochemistry and Genetics, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892-0830, USA.
Genetics. 1999 Oct;153(2):585-94. doi: 10.1093/genetics/153.2.585.
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: NH(3) dash, vertical Mks1p dash, vertical Ure2p dash, vertical Gln3p --> DAL5. Either overproduction of Mks1p or deletion of MKS1 interferes with pseudohyphal growth.
氮的供应调节影响酵母氮分解代谢、假菌丝生长和减数分裂孢子形成的基因。酿酒酵母的Ure2p是氮分解代谢的负调节因子,它抑制Gln3p(DAL5的正调节因子)以及其他氮同化基因。当细胞在如脯氨酸这样的贫氮源上生长时,尿囊酸通透酶Dal5p允许尿苷琥珀酸摄取(Usa(+))。我们发现过量表达Mks1p可使细胞在氨上摄取尿苷琥珀酸,而缺失Mks1p则会阻止细胞在脯氨酸上摄取尿苷琥珀酸或表达Dal5p。过量表达Mks1p不影响细胞中Ure2p的水平。mks1 ure2双突变体在氨或脯氨酸上都能摄取尿苷琥珀酸。此外,过量表达Ure2p会抑制过量表达Mks1p使细胞在氨上摄取尿苷琥珀酸的能力。这些结果表明Mks1p在Ure2p上游参与氮调控,具体如下:NH(3) ︱ Mks1p ︱ Ure2p ︱ Gln3p --> DAL5。过量表达Mks1p或缺失MKS1都会干扰假菌丝生长。