Figure 6.

Role of Fur in the transcriptional, translational and post-translational regulation of sodA and sodB. (A) Repression of sodA by Fur is depicted in addition to the role of Fur in iron homeostasis. Iron is known to bind to the active site of MnSODs that leads to inactivation of the enzyme [106,124]. Increased expression of MnSOD was detected only when excess Mn2+ was added to the media in order to out compete the Fe2+. Deletion of fur under iron replete conditions results in increase transcription of sodA, but incorportation of Fe2+ into the active site of SodA resulting in SodA-Fe and an inactive enzyme. Addition of excess Mn2+ to the culture media can out compete Fe2+ for the active site of SodA resulting in SodA-Mn and an active enzyme. (B) Indirect regulation of SodB by Fur in S. Typhimurium. The small RNAs rfrA and rfrB of S. Typhimurium are likely to function as their homolog ryhB in E. coli in regards to SodB regulation [88]. Our data confirms the Hfq-dependent function of reduced FeSOD activity in Δfur. Previous work confirmed the role of Hfq and Fur in SodB expression [39]. Deletion of fur results in increased transcription of the sRNAs (rfrA and rfrB) that can pair with mRNA of sodB in an Hfq-dependent fashion and result in the degradation of sodB mRNA. However, a combined deletion of hfq in Δfur results in loss of rfrAB-mediated degradation of sodB, and results in the synthesis of SodB protein that gets activated to FeSOD in the presence of Fe2+.

Troxell et al. BMC Microbiology 2011 11:236   doi:10.1186/1471-2180-11-236
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