Bacteria develop a variety of adaptations at transcriptomic, metabolomic and proteomic levels in order to survive potentially damaging environmental perturbations. Present study is exploring the fluctuations in proteome of E. coli P4 to knob Cd+2-induced cytotoxicity. An attempt was also made to integrate all these approaches to gain comprehensive insight of Cd+2 stress response in E. coli P4. This study is exposing the altered behavior of various proteins and their underlying metabolic pathways which have previously not been reported with reference to Cd+2 stress such as sulfoquinovose biosynthesis and degradation pathway. Some of the responses studied on all integrated levels followed same dynamics and strategies to conserve energy by down regulating carbohydrate metabolism (depicted by the repression of succinyl-CoA ligase) and growth stasis (down regulation of ftsZ). Moreover, proteomic analysis clearly revealed the affection of Cd+2 stress on various proteins expression including Rrf, MdaB, DapA, GpmA,Cdd, FabI, DsbA, ZnuA and YihW found modulating key cellular metabolic pathways enabling E. coli P4 to withstand Cd+2-induced toxic effects. Furthermore, over-expression of Mn-SOD provided evidence that Cd+2exposure induces superoxide free radicals mediated oxidative stress rather than hydrogen peroxide (H2O2). EnvZ/OmpR -a two component cell envelope regulatory system was observed operating to homeostat the cell's internal environment. Cd+2 bioremediation potential of E. coli P4 and its kinetic and thermodynamic basis were studied by applying different isotherm models which nominated E. coli P4 a good bioresource for green chemistry to eradicate environmental Cd+2.
Keywords: 2-D gel electrophoresis; Cadmium stress; E. coli P4; Proteome analysis.
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