Senda T, Horiguchi Y, Umemoto M, Sugimoto N, Matsuda M
Department of Anatomy, Osaka University Medical School, Suita, Japan.
Exp Cell Res. 1997 Jan 10;230(1):163-8. doi: 10.1006/excr.1996.3414.
We recently demonstrated that Bordetella bronchiseptica dermonecrotizing toxin (DNT) modifies a small GTP-binding protein rho and causes assembly of actin stress fibers and focal adhesions in MC3T3-E1 cells, indicating that DNT activates the function of rho protein (Horiguchi et al., 1995, J. Cell Sci. 108, 3243-3251). In this study, we examined by electron microscopy ultrastructural changes in DNT-treated MC3T3-E1 cells under conditions in which DNT elicited the above morphological changes. We found that DNT induced proliferation of cytoplasmic membrane organelles, such as Golgi apparatus, smooth and rough endoplasmic reticulum, and mitochondria, and formation of plasmalemmal caveolae. Therefore we examined also the effect of Clostridium botulinum C3 exoenzyme (C3), which has been known to ADP-ribosylate and inactivate rho protein, and found that C3 exoenzyme inhibited the development of membrane organelles in the MC3T3-E1 cells. These findings show that proliferation of membrane organelles and caveolae formation are controlled by the function of rho, which is the target of DNT action.
我们最近证明,支气管败血波氏杆菌皮肤坏死毒素(DNT)可修饰一种小GTP结合蛋白rho,并导致MC3T3-E1细胞中肌动蛋白应激纤维和粘着斑的组装,这表明DNT激活了rho蛋白的功能(堀口等人,1995年,《细胞科学杂志》108卷,3243 - 3251页)。在本研究中,我们通过电子显微镜检查了在DNT引发上述形态变化的条件下,经DNT处理的MC3T3-E1细胞的超微结构变化。我们发现DNT诱导了细胞质膜细胞器的增殖,如高尔基体、光滑和粗糙内质网以及线粒体,并形成了质膜小窝。因此,我们还研究了已知可使rho蛋白ADP核糖基化并使其失活的肉毒梭菌C3外毒素(C3)的作用,发现C3外毒素抑制了MC3T3-E1细胞中膜细胞器的发育。这些发现表明,膜细胞器的增殖和小窝形成受rho功能的控制,而rho是DNT作用的靶点。