In ， the ferric uptake regulator (Fur) protein controls both metabolism and virulence in response to iron availability. Differently from other bacteria， attempts to obtain deletion mutants of failed， leading to the assumption that Fur is an essential protein in this bacterium. By investigating a conditional mutant， we demonstrate that Fur is not essential for growth in liquid media， biofilm formation， and pathogenicity in an insect model of infection. Conversely， Fur is essential for growth on solid media since Fur-depleted cells are severely impaired in colony formation. Transposon-mediated random mutagenesis experiments identified pyochelin siderophore biosynthesis as a major cause of the colony growth defect of the conditional mutant， and deletion mutagenesis confirmed this evidence. Impaired colony growth of pyochelin-proficient Fur-depleted cells does not depend on oxidative stress， since Fur-depleted cells do not accumulate higher levels of reactive oxygen species (ROS) and are not rescued by antioxidant agents or overexpression of ROS-detoxifying enzymes. Ectopic expression of genes revealed that pyochelin production has no inhibitory effects on a deletion mutant of pv. ， suggesting that the toxicity of the locus in Fur-depleted cells involves a -specific pathway(s). Members of the ferric uptake regulator (Fur) protein family are bacterial transcriptional repressors that control iron uptake and storage in response to iron availability， thereby playing a crucial role in the maintenance of iron homeostasis. While null mutants of many bacteria have been obtained， Fur appears to be essential in for still unknown reasons. We obtained Fur-depleted cells by conditional mutagenesis and showed that Fur is dispensable for planktonic growth， while it is required for colony formation. This is because Fur protects colonies from toxicity exerted by the pyochelin siderophore. This work provides a functional basis to the essentiality of Fur in and highlights unique properties of the Fur regulon in this species.