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The  Bradyrhizobium japonicum  transcriptional regulator Irr (iron response regulator) is a key regulator of the iron homeostasis, which is degraded in response to heme binding via a mechanism that involves oxidative modification of the protein. Here, we show that heme-bound Irr activates O 2  to form highly reactive oxygen species (ROS) with the “active site conversion” from heme iron to non-heme iron to degrade itself. In the presence of heme and reductant, the ROS scavenging experiments show that Irr generates H 2 O 2  from O 2  as found for other hemoproteins, but H 2 O 2  is less effective in oxidizing the peptide, and further activation of H 2 O 2  is suggested. Interestingly, we find a time-dependent decrease of the intensity of the Soret band and appearance of the characteristic EPR signal at g = 4.3 during the oxidation, showing the heme degradation and the successive formation of a non-heme iron site. Together with the mutational studies, we here propose a novel “two-step self-oxidative modification” mechanism, during which O 2  is activated to form H 2 O 2  at the heme regulatory motif (HRM) site and the generated H 2 O 2  is further converted into more reactive species such as ·OH at the non-heme iron site in the His-cluster region formed by the active site conversion.

Protein oxidation mediated by heme-induced active site conversion specific for heme-regulated transcription factor, iron response regulator