2). With 10% SDS, the effect of the mutations on survival varied. Some mutants (yadC, ybdA, yfbQ, ykfM, yrbB, ybcM, and emrK) were less susceptible to killing than wild-type E. coli, while ycdO, yibA, and rfbC mutants were more readily killed (Fig. 2). In summary, 14 mutant genes were associated with hyperlethality to https://www.selleckchem.com/products/4egi-1.html nalidixic acid and were more readily killed by mitomycin C and peroxide; 9 were more readily killed by UV irradiation. Only 3 of the mutants were more readily

killed by SDS, none by high temperature. Below we consider what has been reported previously about the diverse set of genes identified by our screening procedure. None of that information leads to an expectation of hyperlethality to nalidixic acid. Putative function of genes exhibiting hyperlethality to nalidixic acid Eight of the mutant genes (yadC, rfbX, rfbC, ycdO, PI3K Inhibitor Library yrbB, ybdA, emrK, and emrY) were annotated in Genbank as outer membrane proteins or proteins whose function is related to the outer membrane. The MIC99s of these mutants for nalidixic acid

were in the same range as that of the wild-type strain; consequently, hyperlethality caused by these mutations was unlikely to be due to increased accumulation of drug. Since the genes were involved in protecting from the effects of nalidixic acid, mitomycin C, and hydrogen peroxide, it is likely that protection from UV irradiation also occurred at the level of downstream effects of irradiation rather than through screening cells from UV light. The yadC mutant, which was among the more sensitive to DNA Daporinad manufacturer damaging agents, was considerably less sensitive than the wild-type strain to SDS. YadC is a fimbrial-like protein whose amino acid sequence suggests that it may contain β-barrel structure(s) [19]. In E. coli, pili are adherence factors that could, in principle, protect some cells in a population from antimicrobial treatment. However, we detected no difference with respect to cellular aggregation when the yadC mutant

and the wild-type strain, growing exponentially, were examined by light microscopy (not shown). Thus, the hyperlethal phenotype of the mutant was not likely to be due to lack of cellular self-association. yadC is induced immediately after Flucloronide exposure to the biocide polyhexamethylene biguanide [20], which is consistent with its involvement in a cellular response to stress. The two rfb mutants were strikingly different in their response to UV: the rfbX mutant showed little effect, while the rfbC mutant was one of the most susceptible (Fig. 2). RfbX, also known as WzxB, is a member of the polysaccharide transporter (PST) family [21], and hydropathy analysis suggests that RfbX has 12 transmembrane segments [22]. rfbC encodes dTDP-4-dehydrorhamnose 3,5-epimerase [23]. Although the rfb genes are thought to be involved in O-antigen biosynthesis in enteric bacteria, such as Salmonella, Shigella, Klebsiella, and some serovars of E.