Tanabe Kaori, Tanaka Katsunori, Matsuda Hideyuki, Kawamukai Makoto
Department of Life Science and Biotechnology, Faculty of Life and Environmental Science, Shimane University, Shimane, Japan.
Biosci Biotechnol Biochem. 2004 Jan;68(1):266-70. doi: 10.1271/bbb.68.266.
We previously reported that expression of Sla1DeltaC, a truncated form of Sla1, induces ectopic meiosis in heterothallic fission yeast and this was possibly due to the inhibition of Pat1 kinase by Sla1DeltaC. Here we found mei2 mRNA and the Mei2 protein accumulated and stability of the Mei2 protein increased when Sla1DeltaC was expressed. The former two results are considered to be the consequence of de-repression of Ste11, which is the transcription factor of mei2 and negatively regulated by Pat1 kinase. The latter result reflects the consequence of deregulation of Mei2 by Pat1 kinase. In addition, Ste11 accumulated in the nucleus when Sla1DeltaC was expressed. All these data consistently support the idea that the action of Sla1DeltaC is to inactivate Pat1 kinase.
我们之前报道过,截短形式的Sla1即Sla1DeltaC的表达会在异宗配合的裂殖酵母中诱导异位减数分裂,这可能是由于Sla1DeltaC对Pat1激酶的抑制作用。在此我们发现,当表达Sla1DeltaC时,mei2 mRNA和Mei2蛋白会积累,并且Mei2蛋白的稳定性增加。前两个结果被认为是Ste11去抑制的结果,Ste11是mei2的转录因子且受到Pat1激酶的负调控。后一个结果反映了Pat1激酶对Mei2调控失调的结果。此外,当表达Sla1DeltaC时,Ste11会在细胞核中积累。所有这些数据一致支持这样的观点,即Sla1DeltaC的作用是使Pat1激酶失活。