ABSTRACTIron is an essential element for growth and survival of pathogenic bacteria. However, how these bacteria sense and respond to iron starvation or excess is still not fully understood. Here, we show that xfeA (a homolog of fepA) in Xanthomonas oryzae, can sense the extra-cytoplasmic iron concentration and change the 3D structure of ligand channel domain by A-to-I RNA editing. The percentage of A-to-I RNA editing was increased to 76.87% under iron-starvation, facilitating iron to pass through the XfeA channel without any interference to the strongest Iron(III)–siderophore [Fe-(Ent)]3−. However, under high iron concentration, the percentage of A-to-I editing to xfeA was reduced, thereby restricting the Fe-Ent to pass iron through the channel of XfeA. The variations in concentration of Fe-Ent was sensed by methyl-accepting chemotaxis proteins (MCPs) at cytoplasmic membrane, which influences the expression of a number of chemotaxis related genes. This regulation drives the bacteria to move further towards the iron-rich direction. Overall, our results revealed a new signaling mechanism that bacterial iron sense and homeostasis are modulated through A-to-I RNA editing.IMPORTANCEA-to-I RNA editing, which is catalyzed by the adenosine deaminase, acts on RNA family of enzymes, is one of the most prevalent type of post-transcriptional modification in metazoans. However, the research of A-to-I editing in bacteria is limited and the importance of this editing is still underestimated. In this study, we found that bacteria may use A-to-I editing (xfeA, a homolog of fepA) as an alternative strategy in iron metabolic uptake, as the editing event level can precisely regulate the RNA and the protein sequence within relatively short physiological time scales comparing with the traditional switch “on” and “off” regulation. To best of our knowledge, it is a new identified inching-switch-like mechanism by which pathogens may absorb iron better in order to compete with the hosts.