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Type IV pili (T4P) are one of the most common forms of bacterial and archaeal surface structures, involved in adherence, motility, competence for DNA uptake, and pathogenesis. Pseudomonas aeruginosa has emerged as one of the key model systems for the investigation of T4P structure and function. Although its reputation as a serious nosocomial and opportunistic pathogen is well deserved, its facile growth requirements and the ready availability of molecular tools have allowed for rapid advances in our understanding of how T4P are assembled; their contributions to motility, biofilm formation and virulence; and their complex regulation. This review covers recent findings concerning the three different types of T4P found in P. aeruginosa (type IVa, type IVb, and Tad) and provides details about the modes of translocation mediated by T4aP, the architecture and function of the T4aP assembly system, and the complex regulation of T4aP biogenesis and function.
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Supplemental Figure 1: Factors regulating Pseudomonas aeruginosa twitching motility.
Twitching motility is regulated directly and indirectly by both extrinsic and intrinsic factors, some of which are listed in white boxes. Proteins or conditions related to these factors are listed in blue circles. Dotted lines indicate additional connections between factors: Quorum sensing indirectly affects twitching through effects on Vfr (1, 2); the RhlIR quorum-sensing system and iron levels regulate the expression of RhlAB, enzymes involved in production of the biosurfactant rhamnolipid (4); and the Pil-Chp chemotaxis system has cAMP-dependent and cAMP-independent effects on T4aP function (3). Factors not discussed in the main text include Crc (catabolite repression control), which regulates PilA transcription (5), and Ppk (polyphosphate kinase), which does not affect pilus expression but is required for full twitching motility (6).
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Supplemental Movie 1: Pseudomonas aeruginosa spreads rapidly across a surface by twitching motility. Download movie file (MOV)