Abstract

Xanthomonas axonopodis pv. glycines (Xag) causes bacterial pustule disease on soybean. This bacterium is present worldwide around hot and humid growing regions such as Southeast Asia. To understand if the gene coding for hemin transport protein (hem) is involved in virulence of the pathogen in soybean, we generated a hem mutant in Xag by overlapping PCR mutagenesis. Disruption of hem significantly reduced the population size and the disease incidence when sprayed on soybean but not when injected directly to soybean. The hem mutant caused the hypersensitive response induction on tobacco as an Xag wildtype. Interestingly, the hem expression was also reduced when the Xag wildtype grow in planta. The hemin transporter protein involved in the production of extracellular polysaccharide, biofilm formation, motility and attachment but not for extracellular enzymes. This confirmed that epiphytic fitness of Xag strongly required hem functions. These results suggest that hem gene is essential for virulence of Xag on soybean during the infection process.

Key words: Bacterial pustule disease, virulence factors, iron uptake system, hem gene, epiphytic fitness.