Poster
Jana Hucklenbroich
Max Planck Institute for Plant Breeding Research
Cologne, Nordrhein-Westfalen, Germany
Zoe Prockl
Faculty of Science, Hokkaido University
Cologne, Nordrhein-Westfalen, Germany
Fiqih Ramadhan
Faculty of Science, Hokkaido University
Sapporo, Hokkaido, Japan
Silvina Perin
Max Planck Institute for Plant Breeding Research
Cologne, Nordrhein-Westfalen, Germany
Tomohisa Shimasaki
Faculty of Science, Hokkaido University
Sapporo, Hokkaido, Japan
Ryohei Thomas Nakano
Faculty of Science, Hokkaido University
Sapporo, Hokkaido, Japan
The plant growth-defense tradeoff is a well-documented phenomenon in which chronic activation of plant immunity inhibits growth. This tradeoff has significant ecological and agricultural implications, yet its modulation by root-associated commensal bacteria remains largely unexplored. We previously identified bacterial strains capable of mitigating this tradeoff, allowing sustained plant growth even under prolonged immune activation by the microbe-associated molecular pattern (MAMP) flg22 or the damage-associated molecular pattern (DAMP) AtPep1. Here, we investigate the genetic basis underlying this bacterial suppression of pattern-triggered growth inhibition. Using a forward genetic screen based on mTn5-mediated random mutagenesis, we identified six bacterial mutants defective in this suppressive activity, most of which retained their ability to colonize host roots. Among them, one mutant harbored a transposon insertion in AhcY, a gene encoding adenosylhomocysteinase, an enzyme involved in the methionine metabolic cycle. Functional analysis revealed that this metabolic pathway plays a critical role in regulating the bacterial ability to influence the plant growth-defense tradeoff. We hypothesize that disruptions in the methionine cycle alter bacterial DNA methylation patterns, leading to transcriptional changes that suppress the production and/or secretion of the active compound responsible for tradeoff manipulation.