Baroni M D, Martegani E, Monti P, Alberghina L
Dipartimento di Fisiologia e Biochimica Generali, Università degli Studi di Milano, Italy.
Mol Cell Biol. 1989 Jun;9(6):2715-23. doi: 10.1128/mcb.9.6.2715-2723.1989.
A detailed kinetic analysis of the cell cycle of cdc25-1, RAS2Val-19, or cdc25-1/RAS2Val-19 mutants during exponential growth is presented. At the permissive temperature (24 degrees C), cdc25-1 cells show a longer G1/unbudded phase of the cell cycle and have a smaller critical cell size required for budding without changing the growth rate in comparison to an isogenic wild type. The RAS2Val-19 mutation efficiently suppresses the ts growth defect of the cdc25-1 mutant at 36 degrees C and the increase of G1 phase at 24 degrees C. Moreover, it causes a marked increase of the critical cell mass required to enter into a new cell division cycle compared with that of the wild type. Since the critical cell mass is physiologically modulated by nutritional conditions, we have also studied the behavior of these mutants in different media. The increase in cell size caused by the RAS2Val-19 mutation is evident in all tested growth conditions, while the effect of cdc25-1 is apparently more pronounced in rich culture media. CDC25 and RAS2 gene products have been showed to control cell growth by regulating the cyclic AMP metabolic pathway. Experimental evidence reported herein suggests that the modulation of the critical cell size by CDC25 and RAS2 may involve adenylate cyclase.
本文对指数生长期间cdc25-1、RAS2Val-19或cdc25-1/RAS2Val-19突变体的细胞周期进行了详细的动力学分析。在允许温度(24摄氏度)下,与同基因野生型相比,cdc25-1细胞的细胞周期G1/未出芽期更长,出芽所需的临界细胞大小更小,但生长速率不变。RAS2Val-19突变有效抑制了cdc25-1突变体在36摄氏度时的温度敏感生长缺陷以及在24摄氏度时G1期的增加。此外,与野生型相比,它导致进入新细胞分裂周期所需的临界细胞质量显著增加。由于临界细胞质量受营养条件的生理调节,我们还研究了这些突变体在不同培养基中的行为。RAS2Val-19突变引起的细胞大小增加在所有测试的生长条件下都很明显,而cdc25-1的影响在丰富培养基中显然更明显。已表明CDC25和RAS2基因产物通过调节环磷酸腺苷代谢途径来控制细胞生长。本文报道的实验证据表明,CDC25和RAS2对临界细胞大小的调节可能涉及腺苷酸环化酶。