Sebbagh M, Renvoizé C, Hamelin J, Riché N, Bertoglio J, Bréard J
INSERM U461, Faculté de Pharmacie, 92296 Châtenay-Malabry, France.
Nat Cell Biol. 2001 Apr;3(4):346-52. doi: 10.1038/35070019.
Increased phosphorylation of myosin light chain (MLC) is necessary for the dynamic membrane blebbing that is observed at the onset of apoptosis. Here we identify ROCK I, an effector of the small GTPase Rho, as a new substrate for caspases. ROCK I is cleaved by caspase-3 at a conserved DETD1113/G sequence and its carboxy-terminal inhibitory domain is removed, resulting in deregulated and constitutive kinase activity. ROCK proteins are known to regulate MLC-phosphorylation, and apoptotic cells exhibit a gradual increase in levels of phosphorylated MLC concomitant with ROCK I cleavage. This phosphorylation, as well as membrane blebbing, is abrogated by inhibition of caspases or ROCK proteins, but both processes are independent of Rho activity. We also show that expression of active truncated ROCK I induces cell blebbing. Thus, activation of ROCK I by caspase-3 seems to be responsible for bleb formation in apoptotic cells.
在凋亡开始时观察到的动态细胞膜起泡现象中,肌球蛋白轻链(MLC)磷酸化增加是必要的。在此,我们确定小GTP酶Rho的效应器ROCK I是一种新的半胱天冬酶底物。ROCK I在保守的DETD1113/G序列处被半胱天冬酶-3切割,其羧基末端抑制结构域被去除,导致激酶活性失控和组成性激活。已知ROCK蛋白可调节MLC磷酸化,凋亡细胞中磷酸化MLC水平会随着ROCK I的切割而逐渐升高。这种磷酸化以及细胞膜起泡现象可通过抑制半胱天冬酶或ROCK蛋白而消除,但这两个过程均独立于Rho活性。我们还表明,活性截短型ROCK I的表达会诱导细胞起泡。因此,半胱天冬酶-3对ROCK I的激活似乎是凋亡细胞中气泡形成的原因。