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Bapaume, L.

Publications and source records attributed to Bapaume, L..

2 recordsLinked to original sources

VAPYRIN attenuates defence by repressing PR gene induction and localized lignin accumulation during arbuscular mycorrhizal symbiosis of Petunia hybrids

O_LIThe intimate association of host and fungus in arbuscular mycorrhizal (AM) symbiosis can potentially trigger induction of host defence mechanisms against the fungus, implying that successful symbiosis requires suppression of defence. C_LIO_LIWe addressed this phenomenon by using AM-defective vapyrin (vpy) mutants in Petunia hybrida, including a new allele (vpy-3) with a transposon insertion close to the ATG start codon. We explore whether abortion of fungal infection in vpy mutants is associated with the induction of defence markers such as cell wall alterations, accumulation of reactive oxygen species (ROS), defence hormones, and induction of pathogenesis-related (PR) genes. C_LIO_LIWe show that vpy mutants exhibit a strong resistance against intracellular colonization, which is associated with the generation of thick cell wall appositions (papillae) with lignin impregnation at fungal entry sites, while no accumulation of defence hormones, ROS, or callose was observed. Systematic analysis of PR gene expression revealed that several PR genes are induced in mycorrhizal roots of the wild type, and even more in vpy plants. Some PR genes are induced exclusively in vpy mutants. C_LIO_LITaken together, these results suggest that VPY is involved in avoiding or suppressing the induction of a cellular defence syndrome that involves localized lignin deposition and PR gene induction. C_LI

plant biology↗

A bacterial GW-effector targets Arabidopsis AGO1 to promote pathogenicity and induces Effector-triggered immunity by disrupting AGO1 homeostasis

Pseudomonas syringae type III effectors were previously shown to suppress the Arabidopsis microRNA (miRNA) pathway through unknown mechanisms. Here, we first show that the HopT1-1 effector promotes bacterial growth by suppressing the Arabidopsis Argonaute 1 (AGO1)-dependent miRNA pathway. We further demonstrate that HopT1-1 interacts with Arabidopsis AGO1 through conserved glycine/tryptophan (GW) motifs, and in turn suppresses miRNA function. This process is not associated with a general decrease in miRNA accumulation. Instead, HopT1-1 reduces the level of AGO1-associated miRNAs in a GW-dependent manner. Therefore, HopT1-1 alters AGO1-miRISC activity, rather than miRNA biogenesis or stability. In addition, we show that the AGO1-binding platform of HopT1-1 is essential to suppress the production of reactive oxygen species (ROS) and of callose deposits during Pattern-triggered immunity (PTI). These data imply that the RNA silencing suppression activity of HopT1-1 is intimately coupled with its virulence function. Overall, these findings provide sound evidence that a bacterial effector has evolved to directly target a plant AGO protein to suppress PTI and cause disease.

plant biology↗