These observations suggest that the sE-dependent increase in fdhD expression is not specific to Crp4-induced damage but rather signifies a generalized stress response to cytoplasmic membrane damage .
Crp4 induce expression of rpoE Complementation of P2 susceptibility of rpoE mutant S. Typhimurium by fdhD overexpression suggested a possible regulatory link between fdhD .
Crp4 induce expression of rpoE Complementation of P2 susceptibility of rpoE mutant S. Typhimurium by fdhD overexpression suggested a possible regulatory link between sE .
Crp4 induce expression of fdhD Complementation of P2 susceptibility of rpoE mutant S. Typhimurium by fdhD overexpression suggested a possible regulatory link between fdhD .
Crp4 induce expression of fdhD Complementation of P2 susceptibility of rpoE mutant S. Typhimurium by fdhD overexpression suggested a possible regulatory link between fdhD .
Crp4 induce expression of fdhD Complementation of P2 susceptibility of rpoE mutant S. Typhimurium by fdhD overexpression suggested a possible regulatory link between sE .
Crp4 induce expression of fdhD Complementation of P2 susceptibility of rpoE mutant S. Typhimurium by fdhD overexpression suggested a possible regulatory link between sE .
While it is clear that Crp4 kill Salmonella by distinct actions , the targeting of the cytoplasmic membrane in both cases may be responsible for the common ability of these peptides to activate the E s-dependent induction of fdhD expression .