Published online Aug 26, 2015. doi: 10.4331/wjbc.v6.i3.249
Peer-review started: February 4, 2015
First decision: April 10, 2015
Revised: May 21, 2015
Accepted: June 9, 2015
Article in press: June 11, 2015
Published online: August 26, 2015
Processing time: 204 Days and 23.2 Hours
AIM: To identify alkyl hydroperoxide reductase subunit C (AhpC) homologs in Bacillus subtilis (B. subtilis) and to characterize their structural and biochemical properties. AhpC is responsible for the detoxification of reactive oxygen species in bacteria.
METHODS: Two AhpC homologs (AhpC_H1 and AhpC_H2) were identified by searching the B. subtilis database; these were then cloned and expressed in Escherichia coli. AhpC mutants carrying substitutions of catalytically important Cys residues (C37S, C47S, C166S, C37/47S, C37/166S, C47/166S, and C37/47/166S for AhpC_H1; C52S, C169S, and C52/169S for AhpC_H2) were obtained by site-directed mutagenesis and purified, and their structure-function relationship was analyzed. The B. subtilis ahpC genes were disrupted by the short flanking homology method, and the phenotypes of the resulting AhpC-deficient bacteria were examined.
RESULTS: Comparative characterization of AhpC homologs indicates that AhpC_H1 contains an extra C37, which forms a disulfide bond with the peroxidatic C47, and behaves like an atypical 2-Cys AhpC, while AhpC_H2 functions like a typical 2-Cys AhpC. Tryptic digestion analysis demonstrated the presence of intramolecular Cys37-Cys47 linkage, which could be reduced by thioredoxin, resulting in the association of the dimer into higher-molecular-mass complexes. Peroxidase activity analysis of Cys→Ser mutants indicated that three Cys residues were involved in the catalysis. AhpC_H1 was resistant to inactivation by peroxide substrates, but had lower activity at physiological H2O2 concentrations compared to AhpC_H2, suggesting that in B. subtilis, the enzymes may be physiologically functional at different substrate concentrations. The exposure to organic peroxides induced AhpC_H1 expression, while AhpC_H1-deficient mutants exhibited growth retardation in the stationary phase, suggesting the role of AhpC_H1 as an antioxidant scavenger of lipid hydroperoxides and a stress-response factor in B. subtilis.
CONCLUSION: AhpC_H1, a novel atypical 2-Cys AhpC, is functionally distinct from AhpC_H2, a typical 2-Cys AhpC.
Core tip: Two alkyl hydroperoxide reductase subunit C (AhpC) homologs (AhpC_H1 and AhpC_H2) were identified by searching the Bacillus subtilis database. Sequence homology and phylogenetic analyses revealed that AhpC_H1 is an ortholog of Escherichia coli (E. coli) AhpC, a representative of bacterial AhpC. AhpC_H1 forms dimers consisting of atypical 2-Cys subunits, while AhpC_H2 behaves like a typical 2-Cys AhpC. These AhpC homologs may perform their respective physiological functions at different peroxide levels. Structural and catalytic differences between the enzymes indicate that AhpC_H1 is not an ortholog of E. coli AhpC, but a novel type of atypical 2-Cys AhpC.