Xanthomonas oryzae pv. Oryzae Avirulence Genes Contribute Differently and Specifically to Pathogen Aggressiveness

Abstract

Genomic copies of three Xanthomonas oryzae pv. oryzae avirulence (avr) genes, avrXa7, avrXal0, and avrxa5, and four homologous genes, aB3.5, aB3.6, aB4.3, and aB4.5, were mutagenized individually or in combination to study the roles of avr genes in one component of pathogen fitness, i.e., aggressiveness or the amount of disease X. oryzae pv. oryzae causes in susceptible rice lines. These X. oryzae pv. oryzae genes are members of the highly related Xanthomonas avrBs3 gene family. Compared to the wild-type strain, X. oryzae pv. oryzae strains with mutations in avrXa7, avrxa5, and the four homologous genes caused shorter lesions on rice line IR24, which contains no resistance genes relevant to the wild-type strain. The contribution of each gene to lesion length varied, with avrXa7 contributing the most and avrXal0 showing no measurable effect on aggressiveness. The functional, plasmidborne copies of avrXa7, aB4.5, and avrxa5 restored aggressiveness only to strains with mutations in avrXa7, aB4.5, and avrxa5, respectively. Mutations in avrXa7 were not complemented by plasmids carrying any other avr gene family members. These data indicate that some, but not all, avr family members contribute to pathogen aggressiveness and that the contributions are quantitatively different. Furthermore, despite their sequence similarity, the aggressiveness functions of these gene family members are not interchangeable. The results suggest that selection and pyramiding resistance genes can be guided by the degree of fitness penalty that is empirically determined in avr gene mutations.

Identification of amino acids of the beet necrotic yellow vein virus p25 protein required for induction of the resistance response in leaves of Beta vulgaris plants

“…The copy number of the 34 aa repeat unit of the AvrBs3 protein determines the specificity of recognition by the Bs3 resistance gene (Herbers et al, 1992), whereas in p25 protein it is determined by single amino acid changes ( Table 2) that influence known properties of p25 (Klein et al, 2007). Some members of the AvrBs3 family are involved in disease symptom formation (Swarup et al, 1992;Yang et al, 1996;Bai et al, 2000), and in those cases, the protein displays a virulence phenotype in one host, but not in other hosts. In contrast, p25 is responsible for the induction of rhizomania disease and clearly functions at the cultivar-specific level.…”

Genome Sequence of Xanthomonas oryzae pv. oryzae Suggests Contribution of Large Numbers of Effector Genes and Insertion Sequences to Its Race Diversity

“…To our knowledge, there are no reports of natural mechanisms of how new avr genes or race differentiation are generated. Mutational analyses of avrBs3/ pth genes revealed that the order and type of repeats in the central domain were important for race-specificity or pathogen fitness 3,38,39 . In general, repetitive regions of DNA are known to be active sites for homologous recombination 28 .…”

Genetic Structure and Population Dynamics of Xanthomonas axonopodis pv. manihotis in Colombia from 1995 to 1999

“…The RFLP-EcoRI analysis performed in this study may not detect changes in the copies of the avr genes that are causing a variation in the virulence patterns of the strains. Changes in the avr structure that cause a variation in the virulence pattern of the strain can be due to single mutations at the 3Ј terminus of the avrXa7 alleles (4,26). One strategy could be to sequence the copies of the plasmid-borne avr gene copies in the new pathotypes.…”