Iron response regulator (IrrB) in Magnetospirillum gryphiswaldense MSR-1, is a member of the ferric uptake regulatory (Fur) protein family and plays an important role in maintaining the balance between iron and oxygen metabolism in MSR-1. In this study, we conducted RNA-seq analysis to investigate the expression patterns of differentially expressed genes at various growth stages and under different iron conditions following irrB deletion. The RNA-seq analysis unveiled that IrrB exerts a more pronounced regulatory role under conditions of low iron availability compared to high iron levels. It primarily regulates cellular signal transduction, signal maintenance, and the metabolism of amino acids and inorganic ions for the maintenance of cellular homeostasis, as indicated by COG analysis. The ChIP-seq analysis revealed that IrrB has the ability to selectively bind to the promoter regions of 75 genes under low iron conditions. The integrated analysis of ChIP-seq and RNA-seq, coupled with in vitro validation using EMSA, demonstrated that IrrB exerts direct regulatory control over the genes MGMSRv2₀423, 2151, 2215, and irrC. Additionally, unlike Irr proteins in non-magnetic bacteria, MSR-1 IrrB also plays a role in processes such as amino acid metabolism and electron transport, while simultaneously regulating the expression of magnetosome island (MAI) genes. The results illustrate that within the framework of global OxyR regulation, MSR-1 IrrB works in conjunction with Fur and IrrC to finely regulate the balance between intracellular iron and oxygen. This process forms an integral component of a comprehensive regulatory network in MSR-1. This study exhibits the IrrB-OxyR-Fur regulatory network in MSR-1, which coregulates iron-oxygen homeostasis with magnetosome biosynthesis and metabolism, providing key insights for developing magnetosome-based biomedical nanomaterials.
Wang et al. (Mon,) studied this question.