ALBERT

Description: 〈p〉Publication date: 13 August 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Cell Reports, Volume 28, Issue 7〈/p〉 〈p〉Author(s): Jakob Neuser, Caroline C. Metzen, Bernd H. Dreyer, Claudio Feulner, Joost T. van Dongen, Romy R. Schmidt, Jos H.M. Schippers〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Plants continuously need to adapt to their environment and prioritize either growth or defense responses to secure survival and reproduction. Trade-offs between growth and defense are often attributed to the allocation of energy for growth to adaptation responses. Still, the exact mechanisms underlying growth and defense trade-offs are poorly understood. Here, we demonstrate that the growth-related transcription factor HOMOLOG OF BEE2 INTERACTING WITH IBH 1 (HBI1) regulates apoplastic reactive oxygen species (ROS) homeostasis by differentially controlling the expression of NADPH oxidases (NOXs) and peroxidases (POXs). The HBI1 target genes 〈em〉RESPIRATORY BURST OXIDASE HOMOLOG A〈/em〉 (〈em〉RbohA〈/em〉) and 〈em〉RbohC〈/em〉 have contrasting effects on the regulation of cell size. In addition, the HBI1-controlled 〈em〉NOX〈/em〉s and 〈em〉POX〈/em〉s oppositely regulate susceptibility toward 〈em〉Pseudomonas syringae〈/em〉. Our findings reveal that the incompatibility between growth and defense programs can be attributed to the way apoplastic ROS homeostasis is modulated during both processes.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S221112471930926X-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉