Li Wenzhou, Zhang Siwei, Numata Osamu, Nozawa Yoshinori, Wang Shulin
State Key Laboratory of Genetic Engineering, Institute of Genetics, Fudan University School of Life Sciences, Shanghai 200433, PR China.
Cell Biochem Funct. 2009 Aug;27(6):364-9. doi: 10.1002/cbf.1583.
TpMRK was identified as a stress-responsive mitogen activated protein kinase (MAPK)-related kinase and has been shown to play a critical role in the stress signalling in Tetrahymena cells. Here, we found that the mRNA expression of TpMRK was correlated with cell division of Tetrahymena with decreased expression occurring in cells prior to entering synchronous cell division induced by heat treatment. Notably, cell division was delayed with a lower division index of 40% after exposure to hydrogen peroxide while 85% of cells underwent cell division synchronously at 75 min after heat treatment without the oxidative exposure. Furthermore, inactivation of TpMRK signalling by p38 MAPK inhibitor SB203580 or MEK inhibitor PD 98059 partially derepressed cell division induced by hydrogen peroxide. Our data suggest that oxidative stimuli might cause aberration of synchronous cell division of Tetrahymena through activating the TpMRK cascade.
TpMRK被鉴定为一种应激反应性丝裂原活化蛋白激酶（MAPK）相关激酶，并且已证明其在四膜虫细胞的应激信号传导中起关键作用。在此，我们发现TpMRK的mRNA表达与四膜虫的细胞分裂相关，在热诱导的同步细胞分裂之前，细胞中TpMRK的表达降低。值得注意的是，暴露于过氧化氢后，细胞分裂延迟，分裂指数较低，为40%，而在未进行氧化暴露的情况下，85%的细胞在热处理后75分钟时同步进行细胞分裂。此外，p38 MAPK抑制剂SB203580或MEK抑制剂PD 98059使TpMRK信号失活，部分解除了过氧化氢诱导的细胞分裂抑制。我们的数据表明，氧化刺激可能通过激活TpMRK级联反应导致四膜虫同步细胞分裂异常。
