Cannon J F, Tatchell K
Department of Biology, University of Pennsylvania, Philadelphia 19104.
Mol Cell Biol. 1987 Aug;7(8):2653-63. doi: 10.1128/mcb.7.8.2653-2663.1987.
Mutations in the SRA1 or SRA3 gene eliminate the requirement for either RAS gene (RAS1 or RAS2) in Saccharomyces cerevisiae. We cloned SRA1 and SRA3 and determined their DNA sequences. SRA1 encodes the regulatory subunit of the cyclic AMP (cAMP)-dependent protein kinase and therefore is identical to REG1 and BCY1. This gene is not essential, but its deletion confers many traits: reduction of glycogen accumulation, temperature sensitivity, reduced growth rate on maltose and sucrose, inability to grow on galactose and nonfermentable carbon sources, and nitrogen starvation intolerance. SRA3 is homologous to protein kinases that phosphorylate serine and threonine and likely encodes the catalytic subunit of the cAMP-dependent protein kinase. The wild-type SRA3 gene either triplicated in the chromosome or on episomal, low-copy plasmids behaves like spontaneous dominant SRA3 mutations by suppressing ras2-530 (RAS2::LEU2 disruption), cdc25, and cdc35 mutations. These findings indicate that the yeast RAS genes are dispensable if there is constitutive cAMP-dependent protein kinase activity.
SRA1或SRA3基因的突变消除了酿酒酵母中任一RAS基因（RAS1或RAS2）的需求。我们克隆了SRA1和SRA3并确定了它们的DNA序列。SRA1编码环磷酸腺苷（cAMP）依赖性蛋白激酶的调节亚基，因此与REG1和BCY1相同。该基因并非必需，但缺失它会赋予许多性状：糖原积累减少、温度敏感性、在麦芽糖和蔗糖上生长速率降低、无法在半乳糖和不可发酵碳源上生长以及对氮饥饿不耐受。SRA3与磷酸化丝氨酸和苏氨酸的蛋白激酶同源，可能编码cAMP依赖性蛋白激酶的催化亚基。野生型SRA3基因在染色体上三倍体化或存在于附加型低拷贝质粒上时，通过抑制ras2 - 530（RAS2::LEU2破坏）、cdc25和cdc35突变，表现得如同自发显性SRA3突变。这些发现表明，如果存在组成型cAMP依赖性蛋白激酶活性，酵母RAS基因是可有可无的。
