Nakano Shunji, Zheng Guolu, Nakano Michiko M, Zuber Peter
Department of Biochemistry and Molecular Biology, OGI School of Science & Engineering, Oregon Health & Science University, Beaverton, Oregon 97006-8921, USA.
J Bacteriol. 2002 Jul;184(13):3664-70. doi: 10.1128/JB.184.13.3664-3670.2002.
ATP-dependent proteases degrade denatured or misfolded proteins and are recruited for the controlled removal of proteins that block activation of regulatory pathways. Among the ATP-dependent proteases, those of the Clp family are particularly important for the growth and development of Bacillus subtilis. Proteolytic subunit ClpP, together with regulatory ATPase subunit ClpC or ClpX, is required for the normal response to stress, for development of genetic competence, and for sporulation. The spx (formally yjbD) gene was previously identified as a site of mutations that suppress defects in competence conferred by clpP and clpX. The level of Spx in wild-type cells grown in competence medium is low, and that in clpP mutants is high. This suggests that the Spx protein is a substrate for ClpP-containing proteases and that accumulation of Spx might be partly responsible for the observed pleiotropic phenotype resulting from the clpP mutation. In this study we examined, both in vivo and in vitro, which ClpP protease is responsible for degradation of Spx. Western blot analysis showed that Spx accumulated in clpX mutant to the same level as that observed in the clpP mutant. In contrast, a very low concentration of Spx was detected in a clpC mutant. An in vitro proteolysis experiment using purified proteins demonstrated that Spx was degraded by ClpCP but only in the presence of one of the ClpC adapter proteins, MecA or YpbH. However, ClpXP, either in the presence or in the absence of MecA and YpbH, was unable to degrade Spx. Transcription of spx, as measured by expression of spx-lacZ, was slightly increased by the clpX mutation. To exclude a possible effect of clpX and clpP on spx transcription, the spx gene was placed under the control of the IPTG (isopropyl-beta-D-thiogalactopyranoside)-inducible Pspac promoter. In this strain, Spx accumulated when ClpX or ClpP was absent, suggesting that ClpX and ClpP are required for degradation of Spx. Taken together, these results suggest that Spx is degraded by both ClpCP and ClpXP. The putative proteolysis by ClpXP might require another adapter protein. Spx probably is degraded by ClpCP under as yet unidentified conditions. This study suggests that the level of Spx is tightly controlled by two different ClpP proteases.
ATP 依赖性蛋白酶可降解变性或错误折叠的蛋白质,并被招募用于可控地清除那些阻碍调节途径激活的蛋白质。在 ATP 依赖性蛋白酶中,Clp 家族的蛋白酶对于枯草芽孢杆菌的生长和发育尤为重要。蛋白水解亚基 ClpP 与调节性 ATP 酶亚基 ClpC 或 ClpX 一起,是正常应激反应、遗传感受态发育和芽孢形成所必需的。spx(原称 yjbD)基因先前被鉴定为抑制 clpP 和 clpX 所导致的感受态缺陷的突变位点。在感受态培养基中生长的野生型细胞中,Spx 的水平较低,而在 clpP 突变体中则较高。这表明 Spx 蛋白是含 ClpP 蛋白酶的底物,并且 Spx 的积累可能部分导致了由 clpP 突变所观察到的多效性表型。在本研究中,我们在体内和体外都研究了哪种 ClpP 蛋白酶负责 Spx 的降解。蛋白质印迹分析表明,Spx 在 clpX 突变体中的积累水平与在 clpP 突变体中观察到的水平相同。相比之下,在 clpC 突变体中检测到的 Spx 浓度非常低。使用纯化蛋白进行的体外蛋白水解实验表明,Spx 仅在存在一种 ClpC 衔接蛋白 MecA 或 YpbH 的情况下被 ClpCP 降解。然而,无论是否存在 MecA 和 YpbH,ClpXP 都无法降解 Spx。通过 spx - lacZ 的表达来衡量,spx 的转录因 clpX 突变而略有增加。为了排除 clpX 和 clpP 对 spx 转录的可能影响,将 spx 基因置于 IPTG(异丙基 -β -D -硫代半乳糖苷)诱导型 Pspac 启动子的控制之下。在该菌株中,当不存在 ClpX 或 ClpP 时,Spx 会积累,这表明 ClpX 和 ClpP 是 Spx 降解所必需的。综上所述,这些结果表明 Spx 可被 ClpCP 和 ClpXP 降解。推测的 ClpXP 蛋白水解作用可能需要另一种衔接蛋白。Spx 可能在尚未明确的条件下被 ClpCP 降解。这项研究表明,Spx 的水平受到两种不同的 ClpP 蛋白酶的严格控制。