Department of Pathogen Biology, School of Medicine, Nantong University, Nantong, China.
FEMS Yeast Res. 2013 Feb;13(1):85-96. doi: 10.1111/1567-1364.12012. Epub 2012 Nov 19.
In Saccharomyces cerevisiae cells, both of the two PP2C protein phosphatases ScPtc2p and ScPtc3p and the PP4 protein phosphatase ScPph3 are responsible for ScRad53p dephosphorylation after the DNA methylation agent methylmethane sulfonate (MMS)-induced DNA damage. In this study, we show that CaPtc2p is not required for the CaRad53p dephosphorylation during the recovery from DNA damage, as is CaPph3p in Candida albicans. However, deletion of CaPPH3 has an additive effect on the sensitivity of C. albicans cells lacking CaPTC2 to MMS and the DNA synthesis inhibitor hydroxyurea (HU). In addition, deletion of CaPPH3 promotes in vitro filamentation of C. albicans cells. Furthermore, mutation of CaPTC2 is epistatic to that of CaPPH3 in the sensitivity of C. albicans cells to rapamycin. Therefore, CaPtc2p and CaPph3p might play a role in the target of rapamycin (TOR) signaling in C. albicans cells.
在酿酒酵母细胞中，两种 PP2C 蛋白磷酸酶 ScPtc2p 和 ScPtc3p 以及 PP4 蛋白磷酸酶 ScPph3 都负责在甲基甲烷磺酸（MMS）诱导的 DNA 损伤后使 ScRad53p 去磷酸化。在这项研究中，我们表明，CaPtc2p 并不像 Candida albicans 中的 CaPph3p 那样，在 DNA 损伤恢复过程中不需要 CaRad53p 去磷酸化。然而，CaPPH3 的缺失对缺乏 CaPTC2 的 C. albicans 细胞对 MMS 和 DNA 合成抑制剂羟基脲（HU）的敏感性有附加效应。此外，CaPPH3 的缺失促进了 C. albicans 细胞体外的丝状生长。此外，CaPTC2 的突变在 C. albicans 细胞对雷帕霉素的敏感性方面与 CaPPH3 的突变呈上位性。因此，CaPtc2p 和 CaPph3p 可能在 C. albicans 细胞中的雷帕霉素（TOR）信号通路中发挥作用。
