The fungal effector Mlp37347 unlock the gateway to intercellular trafficking
Résumé
Melampsora larici-populina is the most devastating pathogen of poplar trees; it causes poplar leaf rust. Genomic studies revealed that it possesses a repertoire of 1184 small secreted proteins. Some of them are characterized as candidate effectors. How these effectors promote virulence is still a blurred picture. This study was designed to investigate the candidate effector Mlp37347’s role during infection. We developed a stable transgenic Arabidopsis line expressing the effector tagged with the GFP. In confocal microscopy image, we found that the effector accumulated exclusively in plasmodesmata (PD). Transcriptome profiling and gene ontology (GO) analysis of transgenic lines and wild-type (WT) revealed that glucan catabolic process genes are specifically up-regulated in effector expressed lines, suggesting that the deposition of the polysaccharide callose at PD will control the movement of endogenous macromolecules. This effector has previously been shown to interact with glutamate decarboxylase 1 (GAD1) and in silico docking of Mlp37347-GAD1 also showed strong binding affinity. The virulence activities of the effector in WT, and transgenic lines using bacterial and oomycete pathogens disclosed that the effector promotes oomycete (fungus-like) growth but bacterial. Further diffusion assay established that effector makes the dilation of PD and facilitates PD flux level. To conclude, the effector Mlp37347 targets PD in host cells, promote infection by regulating PD flux.