Turner J E, Minkoff C G, Martin K H, Misra R, Swenson K I
Department of Molecular Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710.
J Cell Biol. 1995 Mar;128(6):1145-62. doi: 10.1083/jcb.128.6.1145.
Cell cycle progression for postembryonic cells requires the activity of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-R), the enzyme which catalyzes the production of the isoprenoid precursor, mevalonate. In this study, we examine the requirements of HMG-R activity for cell cycle progression during the meiotic and early mitotic divisions using oocytes and dividing embryos from the surf clam, Spisula solidissima. Using two different inhibitors of HMG-R, we find that the activity of this enzyme appears to be required at three distinct points of the cell cycle during meiosis. Depending on the stage at which these inhibitors are added to synchronous clam cultures, a reversible cell cycle block is triggered at the time of activation or at metaphase of either meiosis I or II, whereas there is not block to the mitotic cell cycle. Inhibition of HMG-R activity in activated oocytes does not affect the transient activation of p42MAPK but results in a block at metaphase of meiosis I that is accompanied by the stabilization of cyclins A and B and p34cdc2 kinase activity. Our results suggest that metabolites from the mevalonate biosynthetic pathway can act to influence the process of activation, as well as the events later in the cell cycle that lead to cyclin proteolysis and the exit from M phase during clam meiosis.
胚胎后细胞的细胞周期进程需要3-羟基-3-甲基戊二酰辅酶A还原酶(HMG-R)的活性,该酶催化类异戊二烯前体甲羟戊酸的产生。在本研究中,我们使用 surf 蛤(Spisula solidissima)的卵母细胞和分裂胚胎,研究减数分裂和早期有丝分裂过程中细胞周期进程对HMG-R活性的需求。使用两种不同的HMG-R抑制剂,我们发现该酶的活性在减数分裂期间细胞周期的三个不同点似乎是必需的。根据将这些抑制剂添加到同步蛤培养物中的阶段,在激活时或减数分裂I或II的中期会触发可逆的细胞周期阻滞,而有丝分裂细胞周期则没有阻滞。抑制激活的卵母细胞中的HMG-R活性不会影响p42MAPK的瞬时激活,但会导致减数分裂I中期的阻滞,同时伴有细胞周期蛋白A和B的稳定以及p34cdc2激酶活性。我们的结果表明,甲羟戊酸生物合成途径的代谢产物可以影响激活过程,以及细胞周期后期导致细胞周期蛋白降解和蛤减数分裂期间退出M期的事件。