Abstract
Monilinia fructicola is a devastating pathogen on stone fruits, causing blossom blight and fruit rot. Little is known about pathogenic mechanisms in M. fructicola and related Monilinia species. In this study, five endopolygalacturonase (endo-PG) genes were cloned and functionally characterized in M. fructicola. Quantitative reverse-transcriptase PCR (qRT-PCR) revealed that the five MfPG genes are differentially expressed during pathogenesis and in culture under various pH regimes and carbon and nitrogen sources. MfPG1 encodes the major endo-PG and is expressed to significantly higher levels compared to the other four MfPGs in culture and in planta. MfPG1 function during pathogenesis was evaluated by examining the disease phenotypes and gene expression patterns in M. fructicola MfPG1-overexpressing strains and in strains carrying the ÎČ-glucuronidase (GUS) reporter gene fused with MfPG1 (MfPG1-GUS). The MFPG1-GUS reporter was expressed in situ in conidia and hyphae following inoculation of flower petals, and qRT-PCR analysis confirmed MfPG1 expression during pathogenesis. MfPG1-overexpressing strains produced smaller lesions and higher levels of reactive oxygen species (ROS) on the petals of peach and rose flowers than the wild-type strain, suggesting that MfPG1 affecting fungal virulence might be in part resulted from the increase of ROS in the PrunusâM. fructicola interactions.
Highlights
Brown rot blossom blight and fruit rot caused by the fungal pathogen Monilinia fructicola
Only SSPG1d is highly expressed during infection [7]. These findings point to the complex role of fungal endo-PGs during pathogenesis and suggest that the expression of these cell wall-degrading enzymes (CWDEs) must be tightly coordinated for optimal colonization of the host by the pathogen
To provide a better understanding of M. fructicola pathogenicity, we focused on genes that are involved in plant cell wall degradation and investigated their function on brown rot disease development
Summary
Brown rot blossom blight and fruit rot caused by the fungal pathogen Monilinia fructicola Biochemical analyses suggest that cell wall-degrading enzymes (CWDEs) produced by the pathogen play a critical role during M. fructicola pathogenesis [1]. Inactivation of the BcPG1 gene in B. cinerea resulted in a strain that causes significantly smaller lesions on tomato leaves relative to the wild-type, supporting a virulence function of this endo-PG in gray mold disease [5]. Only SSPG1d is highly expressed during infection [7] These findings point to the complex role of fungal endo-PGs during pathogenesis and suggest that the expression of these CWDEs must be tightly coordinated for optimal colonization of the host by the pathogen. To provide a better understanding of M. fructicola pathogenicity, we focused on genes that are involved in plant cell wall degradation and investigated their function on brown rot disease development. The results indicate that overexpression of MfPG1 increases reactive oxygen species (ROS) accumulation and reduces lesion development in M. fructicola host interactions
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
