PLEIOTROPIC EFFECTS OF A YERSINIA-PESTIS FUR MUTATION

A Yersinia pestis fur mutation was constructed by insertionally disrup ting the fur open reading frame. Analysis of a Fur-regulated beta-gala ctosidase reporter gene revealed a loss of iron regulation as a result of the fur mutation. trans complementation with the cloned Y. pestis fur gene restored iron regulation. The expression of most iron-regulat ed proteins was also deregulated by this mutation; however, a number o f iron-repressible and two iron-inducible polypeptides retained normal regulation. Mutations in fur or hmsH, a gene encoding an 86-kDa surfa ce protein required for hemin storage, increased the sensitivity of Y. pestis cells to the bacteriocin pesticin. Interestingly, the Y. pesti s fur mutant lost temperature control of hemin storage; however, expre ssion of the HmsH polypeptide was not deregulated. When growth with ex cess iron, a Y. pestis fur mutant possessing the 102-kb pigmentation l ocus exhibited severe growth inhibition and a dramatic increase in the number of spontaneous nonpigmented chromosomal deletion mutants prese nt at late log phase. These results suggest that the Fur protein of Y. pestis is an important global regulator and that a separate Fur-indep endent iron regulatory system may exist.