Résumé
Xanthomonas albilineans (Xa) is a systemic, xylem-invading pathogen that causes sugarcane leaf scald. Symptoms vary from a single, white, narrow, sharply defined stripe to complete wilting and necrosis of infected leaves, leading to plant death. Xa produces the toxin albicidin that blocks chloroplast differentiation, resulting in white foliar stripe symptoms. Albicidin is the only previously known pathogenicity factor in Xa, yet albicidin-deficient mutant strains are still able to efficiently colonize sugarcane. The complete genome of Xa strain GPE PC73 from Guadeloupe was recently sequenced and annotated (project by Genoscope and four French teams working on plant pathogenic xanthomonads). The genome size (3.769 Mb) is about 25% smaller than that of other already sequenced xanthomonads. Interestingly, Xa lacks both the xanthan gum gene cluster and a type III secretion system (T3SS) of the Hrp1 and Hrp2 injectisome families. Surprisingly, Xa possesses a T3SS SPI-1 gene cluster that is predicted to interact with animal cells. Four percent of the Xa genome encodes 12 large non-homologous non-ribosomal peptide synthetases (NRPSs) in six regions. Three of these NRPSs, encoded in the same gene cluster, were previously described as involved in albicidin biosynthesis. In attempts to identify additional pathogenicity genes, we used site-directed deletions of candidate genes and also random Tn5 mutagenesis, both followed by inoculation of sugarcane plants with newly introduced mutations. Mutation of quorum sensing genes rpfF and xanB2 did not appear to affect albicidin production nor sugarcane colonization by Xa strain FL07-1 from Florida. However, four independent Tn5 mutations of an OmpA family gene strongly affected both disease symptom development and sugarcane stalk colonization without affecting in vitro albicidin production in Xa strain FL07-1. Other candidate pathogenicity genes are currently being investigated. (Résumé d'auteur)