[ODP22] 5. 病原性-b. 毒素・エフェクター・生理活性物質

[ODP-118/W6-6] 気管支敗血症菌が産生するBcr4によるIII型分泌装置制御機構の解析

後藤 雅貴¹，桑江 朝臣¹，花輪 智子²，阿部 章夫¹ (¹北里大・院・感染制御科学府・分子細菌，²杏林大・医・感染症)

Bordetella bronchiseptica injects virulence proteins called effectors into host cells via a type III secretion system (T3SS) conserved among many Gram-negative bacteria. Small proteins called chaperones are required for stabilizing some T3SS components or localizing them to the T3SS machinery. In a previous study, we identified a chaperone-like protein named Bcr4 that regulates T3SS activity in Bordetella bronchiseptica. Bcr4 does not show strong sequence similarity to well-studied T3SS proteins of other bacteria, and its function remains to be elucidated. Here, we investigated the mechanism by which Bcr4 controls T3SS activity. A pull-down assay revealed that Bcr4 interacts with BscI, based on its homology to other bacterial proteins, to be an inner rod protein of the T3SS machinery. Moreover, the deletion of BscI abolished the secretion of type III secreted proteins from Bordetella bronchiseptica and the translocation of a cytotoxic effector into cultured mammalian cells. Finally, we showed that BscI is unstable in the absence of Bcr4. These results suggest that Bcr4 supports the construction of the T3SS machinery by stabilizing BscI. This is the first demonstration of a chaperone for the T3SS inner rod protein among the virulence bacteria possessing the T3SS.