Matsuura A, Treinin M, Mitsuzawa H, Kassir Y, Uno I, Simchen G
Institute of Applied Microbiology, University of Tokyo, Japan.
EMBO J. 1990 Oct;9(10):3225-32. doi: 10.1002/j.1460-2075.1990.tb07521.x.
Entry into meiosis in Saccharomyces cerevisiae cells is regulated by starvation through the adenylate cyclase/cAMP-dependent protein kinase (AC/PK) pathway. The gene IME1 is also involved in starvation control of meiosis. Multicopy IME1 plasmids overcome the meiotic deficiency of bcy1 and of RASval19 diploids. Double mutants ime1 cdc25 and ime1 ras2 are sporulation deficient. These results suggest that IME1 comes after the AC/PK cascade. Furthermore, the level of IME1 transcripts is affected by mutations in the AC/PK genes CDC25, CYR1 and BCY1. Moreover, the addition of cAMP to a cyr1-2 diploid suppresses IME1 transcription. The presence in a bcy1 diploid of IME1 multicopy plasmids does not cure the failure of bcy1 cells to arrest as unbudded cells following starvation and to enter the G0 state (thermotolerance, synthesis of unique G0 proteins). This indicates that the pathway downstream of the AC/PK cascade branches to control meiosis through IME1, and to control entry into G0 and cell cycle initiation, independently of IME1.
酿酒酵母细胞进入减数分裂受饥饿通过腺苷酸环化酶/依赖于cAMP的蛋白激酶（AC/PK）途径调控。IME1基因也参与减数分裂的饥饿控制。多拷贝IME1质粒可克服bcy1和RASval19二倍体的减数分裂缺陷。双突变体ime1 cdc25和ime1 ras2存在孢子形成缺陷。这些结果表明IME1位于AC/PK级联反应之后。此外，IME1转录本水平受AC/PK基因CDC25、CYR1和BCY1突变的影响。而且，向cyr1 - 2二倍体中添加cAMP可抑制IME1转录。在bcy1二倍体中存在IME1多拷贝质粒并不能解决bcy1细胞在饥饿后无法停滞为未出芽细胞并进入G0期（耐热性、独特G0蛋白的合成）的问题。这表明AC/PK级联反应下游的途径分支，通过IME1控制减数分裂，并独立于IME1控制进入G0期和细胞周期起始。
