How Certain Gens in the Stewart’s Wilt Causal Pathogen Pantoea stewartii Affect the Pathogen Spread and Biofilm Formation

Abstract

Stewart’s wilt caused by the bacterial pathogen, Pantoea stewartii (Ps), is posing a potential threat to the corn industry in the US. The disease symptom development of infected corn plants depends largely on the pathogen’s spread in the host plants. This study uses a wild-type Ps strain and its two mutants (Δwceo and Δrtx2, either of which presumably has an impaired production of exopolysaccharide) to investigate how the wceo and rtx2 genes may affect the pathogen’s spread and biofilm formation in sweet corn. Our results have indicated that Ps spread from the inoculation site in a sweet corn occurred differently among its three genotypes with the wild-type Ps occurring fastest and Δrtx2 mutant slowest. The wild-type Ps were found to become systemic in symptomatic corn leaves and be present both inside and outside of the leaf’s vascular bundles while the Δwceo and Δrtx2 Ps were more restricted in their spread and localized within the leaf’s vascular bundles. The three Ps genotypes also showed significant differences in quantity in host plants. In terms of biofilm formation, the wild-type Ps cells often occurred in largest clusters, which were mostly embedded in biofilm. Δwceo mutant cells aggregated into much smaller clusters of various sizes. As a conclusion, we believe that the rtx2 and wceo genes may facilitate the pathogen’s spread and biofilm production in sweet corn plants. This information is essential to understand Ps-host plant interactions, contributing to the analysis of the Stewart’s wilt susceptibility mechanism of corns and other host species.