A motile pseudorevertant of ΔrodZ isolated possessed
a near rod-shaped cell morphology, indicating that RodZ is not absolutely required for the elongation of the lateral cell wall and the synthesis of functional flagella. Most membrane proteins of bacteria are involved in the complex metabolic and signal transduction network (Sargent, 2007), and consequently, elucidation of their functions and the detailed molecular mechanisms is awaited. Recently, we performed a genome-wide screening for genes that resulted in a reduced biofilm phenotype when disrupted and identified yfgA, a predicted Escherichia coli gene for a membrane protein, as one such gene. Mutants of yfgA were nonmotile and showed phenotypes characteristic of membrane deficiency (Niba et al., 2007). Flagella of E. coli are synthesized under the tight regulation
of coordinated transcription of over 50 genes categorized into three classes (Chilcott & Hughes, 2000). The Epacadostat mouse class one genes flhD and flhC form the master operon, which is the sole determinant of the fate of flagella biogenesis and motility. FlhD and FlhC proteins form a heterotetrameric complex that binds and regulates promoters of class two genes necessary for hook and basal body formation as well as the flagella-specific sigma factor, Dabrafenib fliA, which in turn is required for the expression of class three genes such as fliC that encodes flagellin. Motility and flagellar assembly are dependent on environmental factors represented by stresses that are sensed
by flhDC. In E. coli, several global regulators such as H-NS (Bertin et al., 1994), OmpR (Shin & Park, 1995), CRP-cAMP (Soutourina et al., 1999), LrhA (Lehnen et al., 2002) and RcsAB (Francez-Charlot et al., 2003) are directly involved in the complex genetic regulatory hierarchy that assures ordered assembly of flagellar components. In rod-shaped cells, a connection between flagellar biosynthesis and cell morphogenesis has been reported. Without flhD, the cell morphology switched from rods to spheres (Prüss & Matsumura, 1996). Furthermore, microarray analysis of the flhD/flhC-regulated promoters identified mreBCD genes that are responsible for rod-shape determination (Prüss et al., 2001). Cell shape is mainly maintained by peptidoglycans Farnesyltransferase that form a protective layer to ensure that cells are not lysed by high internal osmotic pressure (review by den Blaauwen et al., 2008; Vollmer & Bertsche, 2008). Reports have shown that elongation and septation of the peptidoglycan layer are the basis for cell division and growth. MreB, MreC, MreD and RodA as well as the penicillin-binding protein PBP2 are essential for peptidoglycan elongation. A defect in any of these proteins causes cells to become spherical. A number of proteins, including PBP3, are involved in septation, and their loss leads to a filamentous cell morphology. More recently, yfgA has been shown to participate in rod-shape determination and hence it was named rodZ (Shiomi et al.
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