Zoospores of the filamentous actinomycete Actinoplanes missouriensis swim vigorously using flagella and stop swimming to initiate germination in response to nutrient exposure. However, the molecular mechanisms underlying swimming cessation remain unknown. A protein (FtgA) of unknown function encoded by a chemotaxis gene cluster (che cluster-1) was found to be required for flagellar rotation arrest; the zoospores of ftgA-knockout mutants kept swimming awkwardly after germination. An ftgA-overexpressing strain exhibited a non-flagellated phenotype. Isolation of a suppressor strain from this strain and further in vivo experiments revealed that the extended N-terminal region of FliN, a component of the C-ring of the flagellar basal body, was involved in the function of FtgA; FliN-P101S canceled the flagellar rotation arrest by FtgA, as well as the negative effect of ftgA-overexpression on flagellation. Furthermore, bacterial two-hybrid assays suggested that FtgA interacted not only with the C-terminal core region of FliN but also with chemotaxis regulatory proteins CheA1 and CheW1-2, which are encoded by che cluster-1. We propose the following working model of motility regulation in A. missouriensis zoospores: the chemotaxis sensory complex initially captures FtgA to allow zoospores to swim and then releases FtgA to stop flagellar rotation (i.e., swimming) in response to external nutrient signals.
© 2024. The Author(s).