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Burkholderia pseudomallei  is the causative agent of melioidosis. The complete genome sequences of this pathogen have been revealed, which explain some pathogenic mechanisms. In various hostile conditions, for example, during nitrogen and amino acid starvation, bacteria can utilize alternative sigma factors such as RpoS and RpoN to modulate genes expression for their adaptation and survival. In this study, we demonstrate that mutagenesis of  rpoN2 , which lies on chromosome 2 of  B. pseudomallei  and encodes a homologue of the sigma factor RpoN, did not alter nitrogen and amino acid utilization of the bacterium. However, introduction of  B. pseudomallei rpoN2  into  E. coli  strain deficient for  rpoN  restored the ability to utilize amino acids. Moreover, comparative partial proteomic analysis of the  B. pseudomallei  wild type and its  rpoN2  isogenic mutant was performed to elucidate its amino acids utilization property which was comparable to its function found in the complementation assay. By contrast, the  rpoN2  mutant exhibited decreased  katE  expression at the transcriptional and translational levels. Our finding indicates that  B. pseudomallei  RpoN2 is involved in a specific function in the regulation of catalase E expression.

Role ofBurkholderia pseudomalleiSigma N2 in Amino Acids Utilization and in Regulation of Catalase E Expression at the Transcriptional Level