Analyses of molecular mechanisms of regulation of bacterial shape by cytoskeletal protein complex.

本课题的目的是了解细菌细胞形态调控的分子机制。对RODZ突变体的抑制突变体的分析表明，RODZ调节MreB细丝的组装。这一结果发表于2012年。为了分析带正电荷的残基在膜旁结构域中的重要性，我在残基中引入了丙氨酸并删除了该结构域。我发现带正电荷的残基对于RODZ函数是可有可无的，而结构域的长度是关键的。我还分析了组成超分子机械的蛋白质之间的相互作用，伸长体。我发现RODZ与MreB、MreC、PBP2和RodA相互作用，并且存在两个亚复合体，即MreB/MreC和PBP2/RodA复合体。结果表明，RODZ连接了亚复合体。我还应用了体内特定部位的光交联法来检测RODZ与其他蛋白质的相互作用。我可以检测到交联物。

Purpose of this project was to understand molecular mechanism to regulate bacterial cell shape. Analyses of the suppressor mutants of the rodZ mutant suggested that RodZ regulates assembly of MreB filaments. This result was published in 2012. In order to analyze the importance of the positively-charged residues in the juxta-membrane domain, I introduced Alanine into the residues and deleted the domain. I found that the positively-charged residues is dispensable for the RodZ function while the length of the domain is critical. I also analyzes the interaction among proteins constituting supramolecular machinery, elongasome. I found that RodZ interacts with MreB, MreC, PBP2, and RodA and that there are two sub-complexes in the complex, that is, MreB/MreC and PBP2/RodA complexes. The results indicate that RodZ bridges the sub-complexes. I also applied site-specific in vivo photo crosslink assay to detect interaction between RodZ and other proteins. I could detect crosslinked products.