Graphical Abstract Highlights d Arabidopsis HBI1 is a transcriptional regulator of ROS homeostasis d HBI1 promotes leaf cell expansion through RbohC d RbohA negatively regulates growth but promotes disease resistance d The growth defense trade-off results from incompatible ROS requirements SUMMARYPlants continuously need to adapt to their environment and prioritize either growth or defense responses to secure survival and reproduction. Tradeoffs 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 RESPIRATORY BURST OXIDASE HOMOLOG A (RbohA) and RbohC have contrasting effects on the regulation of cell size. In addition, the HBI1-controlled NOXs and POXs oppositely regulate susceptibility toward Pseudomonas syringae. 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.

Superoxide dismutase (SOD) is a primary antioxidant enzyme that can be found in organisms from all kingdoms of life. Its date of origin indicates a pivotal role in the evolution of life on our planet. The SOD family is subdivided into different classes based upon the metal‐cofactor these enzymes use. In this article, we specifically emphasise the role and appearance of the youngest enzyme, copper‐zinc SOD (CuZnSOD). We discuss the evolution of CuZnSODs and the emergence of COPPER CHAPERONE FOR SUPEROXIDE DISMUTASE (CCS) proteins. SODs were initially appreciated for their antioxidant properties and potential to improve plant stress tolerance. However, recent findings indicate a role for SODs in maintaining reactive oxygen species (ROS) gradients to guide plant developmental processes. Moreover, after nearly 50 years of research on SODs, these enzymes still hold many surprises as evidenced by the recent finding that SOD in yeast acts as a transcriptional regulator. In this article, we aim at giving an overview of the current knowledge on SODs in plants and highlight avenues for future research endeavours, as there is still so much to learn.

In animals, endocytosis of a seven-transmembrane GPCR is mediated by arrestins to propagate or arrest cytoplasmic G protein–mediated signaling, depending on the bias of the receptor or ligand, which determines how much one transduction pathway is used compared to another. In Arabidopsis thaliana, GPCRs are not required for G protein–coupled signaling because the heterotrimeric G protein complex spontaneously exchanges nucleotide. Instead, the seven-transmembrane protein AtRGS1 modulates G protein signaling through ligand-dependent endocytosis, which initiates derepression of signaling without the involvement of canonical arrestins. Here, we found that endocytosis of AtRGS1 initiated from two separate pools of plasma membrane: sterol-dependent domains and a clathrin-accessible neighborhood, each with a select set of discriminators, activators, and candidate arrestin-like adaptors. Ligand identity (either the pathogen-associated molecular pattern flg22 or the sugar glucose) determined the origin of AtRGS1 endocytosis. Different trafficking origins and trajectories led to different cellular outcomes. Thus, in this system, compartmentation with its associated signalosome architecture drives biased signaling.

Abbreviations: Arabidopsis thaliana Regulator of G Signaling (AtRGS1), Clathrin-Mediated 43 Endocytosis (CME), Sterol-Dependent Endocytosis (SDE), Total Internal Reflection 44 Fluorescence Microscopy (TIRF), Clathrin Light Chain (CLC), Flotilin 1 (FLOT1), 45 Vacuolar Protein Sorting 26 (VPS26) 46 SUMMARY 47 Biased signaling occurs when different ligands that are directed at the same receptor launch 48 different cellular outcomes. Because of their pharmacological importance, we know the most 49 about biased ligands and little is known about other mechanisms to achieve signaling bias. 50 In the canonical animal G protein system, endocytosis of a 7-transmembrane GPCR 51 desensitizes a cell from its extracellular signal. β-arrestins facilitate GPCR endocytosis but 52 also propagate cytoplasmic signaling depending on the bias. In Arabidopsis, GPCRs are not 53 required for G protein coupled signaling because the heterotrimeric G protein complex 54 spontaneously exchanges nucleotide. Instead, the prototype 7-transmembrane Regulator of 55 G Signaling 1 protein AtRGS1 modulates G signaling and through ligand-dependent 56 endocytosis, de-repression of signaling is initiated but canonical arrestins are not involved. 57 Endocytosis initiates from two separate pools of plasma membrane: microdomains and a 58 clathrin-accessible neighborhood, each with a select set of discriminators, activators, and 59 newly-discovered arrestin-like adaptors. Different trafficking origins and trajectories lead 60 to different cellular outcomes. Thus, compartmentation with its attendant signalosome 61