A translational regulator that binds mRNA to regulate translation initiation and/or mRNA stability. Usually binds in the 5'-UTR at or near the Shine-Dalgarno sequence preventing ribosome-binding, thus repressing translation. Binds mRNA; 77% of enriched bound RNA is for flagellin A (flaA) while another 13% encodes other flagellar or motility-related genes. Binds mRNA in 5'-UTR or intergenic regions, binds consensus 5'-AAGGA-3' in the loop of a predicted stem-loop structure. Binds at least 2 sites in the 5'-UTR of flaA mRNA and represses its translation; mutation of the binding sites abolishes binding and leads to increased amounts of FlaA protein. Translation repression is antagonized by FliW, probably by its direct binding to CsrA, which allows translation of FlaA and probably other flagellar proteins (PubMed:27229370). Influences the localization of flaA transcripts to poles of short, probably elongating, cells. Homodimer; the beta-strands of each monomer intercalate to form a hydrophobic core while the alpha-helices form wings that extend away from the core (By similarity). Binds to FliW (PubMed:27229370). Constitutively expressed (at protein level). No visible growth phenotype, increased expression of the flagellin A (flaA) the major flagellar filament component. Flagella appear normal, the average swimming distance decreases about 20%. Expression of other flagellar genes is not visibly affected unless flaA is also mutated, when an increase in their expression is then seen. mRNA for flaA remain localized to the cell pole. A double csrA-fliW deletion expresses the same amount of flagellin A as the csrA deletion, has 2 wild-type length flagella, a wild-type swimming distance and restored cell pole localization of flaA mRNA. Belongs to the CsrA/RsmA family.