Sun Qi, Bi Lifu, Su XiuLan, Tsurugi Kunio, Mitsui Kazuhiro
Department of Biochemistry 2nd, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, 1110 Shimokato, Chuou, Yamanashi 409-3898, Japan.
FEBS Lett. 2007 Aug 21;581(21):3991-5. doi: 10.1016/j.febslet.2007.07.030. Epub 2007 Jul 25.
We investigated the participation of HDACs in VPA induced apoptosis in Saccharomyces cerevisiae. VPA (20 mM) induced apoptosis in several HDAC mutants, including PRD3 and HDA1-disrupted cells and SIR2 over expressing cells, as well as in wild-type cells but not SIR2-disrupted cells. Intracellular reactive oxygen species and neutral lipid content increased markedly in all kinds of HDAC mutant cells tested except for SIR2-disrupted cells. Thus, these results suggest that 20 mM VPA induces neutral lipid accumulation and apoptosis-like features in S. cerevisiae, and that VPA-induced apoptosis was evaded by deletion of SIR2.
我们研究了组蛋白去乙酰化酶（HDACs）在丙戊酸（VPA）诱导的酿酒酵母细胞凋亡中的作用。VPA（20 mM）可诱导包括PRD3和HDA1基因敲除细胞、SIR2过表达细胞以及野生型细胞在内的多种HDAC突变体细胞发生凋亡，但SIR2基因敲除细胞除外。除SIR2基因敲除细胞外，在所有测试的HDAC突变体细胞中，细胞内活性氧和中性脂质含量均显著增加。因此，这些结果表明，20 mM VPA可诱导酿酒酵母细胞中性脂质积累和凋亡样特征，且SIR2基因缺失可避免VPA诱导的细胞凋亡。
