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Polyadenylation is recognized as part of a surveillance machinery for eliminating defective RNA molecules in eukaryotes and prokaryotes. Escherichia coli strains, deficient in poly(A)polymerase I (PAP I), expressed less flagellin compared to wild-type strains. Because flagellin synthesis is a late step in the flagellar biosynthesis pathway, we assessed the role of PAP I in this cascade and in flagella function. Transcription of flhDC, fliA, and fliC was decreased in the PAP I mutant. These results provide evidence that polyadenylation positively controls the expression of genes belonging to the flagellar biosynthesis pathway and that this effect is mediated through the FlhDC master regulator. However, the downshift in flagella gene expression in the mutant strain did not provoke any noticeable defects in the synthesis of flagella, in biofilm formation and in swimming speed although there was a reduction in motility on soft agar. Our data support an alternative hypothesis that the reduced motility of the mutant resulted from an alteration of the cell membrane composition caused in part by the higher level of GlmS (Glucosamine-6P synthase) which accumulates in the mutant. In agreement with this hypothesis the mutant is more sensitive to hydrophobic agents and antibiotics and in particular to vancomycin. We propose that PAP I participates in the ability of the bacteria to adapt to and survive detrimental conditions by constantly monitoring and adjusting to its environment.