Department of Botany, University of Texas, 78713, Austin, TX, USA.
Planta. 1991 Dec;186(1):17-26. doi: 10.1007/BF00201493.
Ultrastructural changes in the cortical cytoskeleton during wound-induced cytoplasmic contraction were examined in the coenocytic green alga Ernodesmis verticillata. Both calmodulin (CaM) and actin were localized in intact and contracting cells by immunogold labeling. Within 5 min after wounding, compact microfilament (MF) bundles were observed which increase in diameter as cytoplasmic contraction proceeds. Calmodulin labeling is associated with amorphous material studding the MF bundles, whereas actin labeling occurs along the individual MFs. No MF bundles were ever observed during contraction that were not also labeled with anti-CaM antibodies. In cells treated with the CaM antagonist W-7 (N-[6-aminohexyl]-5-chloro-1-naphtha-lenesulfonamide), MF bundles do not form, and the formation of loosely arranged MFs (similar to nascent bundles in untreated cells) is greatly retarded. We propose that CaM binds indirectly to actin by activating an actin-binding regulatory protein which functions in early stages of the transduction sequence leading to functional MF bundles. Additionally, ultrastructural evidence is presented for a plasma-membrane skeleton or undercoating in this alga.
在创伤诱导的细胞质收缩过程中,皮层细胞骨架的超微结构变化在多核绿藻 Ernodesmis verticillata 中进行了研究。用免疫金标记法定位了完整细胞和收缩细胞中的钙调蛋白(CaM)和肌动蛋白。在创伤后 5 分钟内,观察到了直径增大的致密微丝(MF)束,随着细胞质的收缩而增加。CaM 标记与 MF 束上的无定形物质有关,而肌动蛋白标记则发生在单个肌动蛋白上。在收缩过程中从未观察到没有用抗 CaM 抗体标记的 MF 束。在用 CaM 拮抗剂 W-7(N-[6-氨基己基]-5-氯-1-萘磺酰胺)处理的细胞中,MF 束不会形成,并且松散排列的 MF(类似于未处理细胞中的新生束)的形成大大延迟。我们提出,CaM 通过激活在导致功能性 MF 束的转导序列的早期阶段起作用的肌动蛋白结合调节蛋白间接与肌动蛋白结合。此外,还提出了该藻类中存在质膜骨架或底层的超微结构证据。