Stern B, Nurse P
Cell Cycle Laboratory, Imperial Cancer Research Fund, London, UK.
EMBO J. 1997 Feb 3;16(3):534-44. doi: 10.1093/emboj/16.3.534.
Yeast pheromones block cell cycle progression in G1 in order to prepare mating partners for conjugation. We have investigated the mechanism underlying pheromone-induced G1 arrest in the fission yeast Schizosaccharomyces pombe. We find that the G1-specific transcription factor p65cdc10-p72res1/sct1 which controls the expression of S-phase genes is fully activated in pheromone, unlike the analogous control in budding yeast. In contrast, the G1 function of p34cdc2 acting after activation of the G1-specific transcription is blocked. Pheromone inhibits the p34cdc2 kinase associated with both the G1-specific B-type cyclin p45cig2 and the B-type cyclin p56cdc13 and overexpression of p45cig2 or p47cdc13delta90 overcomes the pheromone-induced G1 arrest. G1 arrest is compromised in enlarged cells. We suggest that onset of S-phase is controlled by pheromone inhibiting the B-cyclin-associated kinase in G1, and that increasing cell size contributes to the mechanism for pheromone adaptation. Thus, pheromone in fission and budding yeast acts similarly in inhibiting the G1 cyclin-dependent kinase (CDK), but differs in its effects on the G1/S transcriptional control, suggesting that inhibition of CDKs may be a more general mechanism for the control of G1 progression compared with G1/S transcriptional control.
酵母信息素可阻断G1期的细胞周期进程，以便让交配伴侣为接合做好准备。我们研究了裂殖酵母粟酒裂殖酵母中信息素诱导G1期停滞的潜在机制。我们发现，控制S期基因表达的G1期特异性转录因子p65cdc10 - p72res1/sct1在信息素作用下被完全激活，这与芽殖酵母中的类似调控不同。相比之下，在G1期特异性转录激活后发挥作用的p34cdc2的G1期功能被阻断。信息素抑制与G1期特异性B型细胞周期蛋白p45cig2和B型细胞周期蛋白p56cdc13相关的p34cdc2激酶，p45cig2或p47cdc13delta90的过表达可克服信息素诱导的G1期停滞。在体积增大的细胞中，G1期停滞受到损害。我们认为，S期的起始由信息素抑制G1期的B型细胞周期蛋白相关激酶来控制，细胞体积增大有助于信息素适应机制的形成。因此，裂殖酵母和芽殖酵母中的信息素在抑制G1期细胞周期蛋白依赖性激酶（CDK）方面作用相似，但在对G1/S转录调控的影响上有所不同，这表明与G1/S转录调控相比，抑制CDK可能是控制G1期进程的更普遍机制。
