Shirai Yuki, Sasaki Narie, Kishi Yoshiro, Izumi Akiko, Itoh Kie, Sameshima Masazumi, Kobayashi Tetsuyuki, Murakami-Murofushi Kimiko
Department of Biology, Ochanomizu University, Bunkyo-ku, Tokyo 112-8610, Japan.
Cell Motil Cytoskeleton. 2006 Feb;63(2):77-87. doi: 10.1002/cm.20110.
Under various environmental stresses, the true slime mold Physarum polycephalum converts into dormant forms, such as microcysts, sclerotia, and spores, which can survive in adverse environments for a considerable period of time. In drought-induced sclerotia, actin is threonine phosphorylated, which blocks its ability to polymerize into filaments. It is known that fragmin and actin-fragmin kinase (AFK) mediate this phosphorylation event. In this work, we demonstrate that high levels of actin threonine phosphorylation are also found in other dormant cells, including microcysts and spores. As the threonine phosphorylation of actin in microcysts and sclerotia were induced by drought stress but not by other stresses, we suggest that drought stress is essential for actin phosphorylation in both cell types. Although characteristic filamentous actin structures (dot- or rod-like structures) were observed in microcysts, sclerotia, and spores, actin phosphorylation was not required for the formation of these structures. Prior to the formation of both microcysts and sclerotia, AFK mRNA expression was activated transiently, whereas fragmin mRNA levels decreased. Our results suggest that drought stress and AFK might be involved in the threonine phosphorylation of actin.
在各种环境胁迫下,真黏菌多头绒泡菌会转变为休眠形式,如微囊肿、菌核和孢子,这些休眠形式能够在不利环境中存活相当长的时间。在干旱诱导形成的菌核中,肌动蛋白会发生苏氨酸磷酸化,这会阻碍其聚合成丝的能力。已知凝溶蛋白和肌动蛋白 - 凝溶蛋白激酶(AFK)介导了这一磷酸化事件。在这项研究中,我们证明在包括微囊肿和孢子在内的其他休眠细胞中也发现了高水平的肌动蛋白苏氨酸磷酸化。由于微囊肿和菌核中肌动蛋白的苏氨酸磷酸化是由干旱胁迫诱导的,而非其他胁迫,我们认为干旱胁迫对于这两种细胞类型中肌动蛋白的磷酸化至关重要。尽管在微囊肿、菌核和孢子中观察到了典型的丝状肌动蛋白结构(点状或棒状结构),但这些结构的形成并不需要肌动蛋白磷酸化。在微囊肿和菌核形成之前,AFK mRNA表达会短暂激活,而凝溶蛋白mRNA水平则会下降。我们的结果表明,干旱胁迫和AFK可能参与了肌动蛋白的苏氨酸磷酸化过程。