Proteins P24 and P41 Function in the Regulation of Terminal-Organelle Development and Gliding Motility in Mycoplasma pneumoniae

摘要: Mycoplasma pneumoniae is a major cause of bronchitis and atypical pneumonia in humans. This cell wall-less bacterium has complex terminal organelle that functions cytadherence gliding motility. The mechanism unknown but coordinated with terminal-organelle development during division. Disruption M. open reading frame MPN311 results loss protein P41 downstream gene product P24. localizes to the base required anchor body, division, insertion mutants also fail properly regulate nascent spatially or activity temporally. We measured velocity frequency used fluorescent fusions time-lapse imaging assess roles P24 individually function. was necessary for normal proper spatial positioning new organelles, while formation at wild-type rates. However, essential function, absence P41, exhibited dynamic localization pattern. Finally, P28 requires stability, analysis P28− mutant established phenotype not function P28.