ABLs and TMKs are co-receptors for extracellular auxin

Abstract

Extracellular perception of auxin, an essential phytohormone in plants, has been debated for decades. Auxin binding protein 1 (ABP1) physically interacts with quintessential transmembrane kinases (TMKs) and was proposed to act as an extracellular auxin receptor, but its role was disputed because abp1 knockout mutants lack obvious morphological phenotypes. Here we identified two new auxin-binding proteins, ABL1 and ABL2, that are localized to the apoplast and directly interact with the extracellular domain of TMKs in an auxin-dependent manner. Furthermore, functionally redundant ABL1 and ABL2 genetically interact with TMKs and exhibit functions that are overlapping with those of ABP1 as well as independent of ABP1. Importantly, the extracellular domain of TMK1 itself binds auxin and synergizes with either ABP1 or ABL1 in auxin binding. Thus, our findings discovered new auxin receptors ABL1 and ABL2 having functions overlapping with but distinct from ABP1 and acting together with TMKs as co-receptors for extracellular auxin.

Bioengineering secreted proteases converts divergent Rcr3 orthologs and paralogs into extracellular immune co-receptors

“…Decoy bioengineering may provide an alternative route for the generation of synthetic resistance genes targeting important plant pathogens in the future. Finally, it is important to note that Cf-2 is not the only cell-surface receptor that has been shown to require additional apoplastic factors for ligand recognition, as the apoplastic protein auxin-binding protein 1 (ABP1) and ABP1-LIKE 1 and 2 (ABL1/2) physically interacts with the LRR-RLK transmembrane kinase (TMK) family receptor-like kinases to form an auxin-sensing complex in the apoplast (Yu et al, 2023).…”

Cell surface auxin signalling directly targets PIN-mediated auxin fluxes for adaptive plant development

“…Consistent with these notions, auxin canalization and canalization-mediated vascular tissue regeneration are severely defective in abp1 and tmk mutants 15 . Despite these strong, specific defects, overall growth and development is not strongly affected following single-gene lesions within the ABP1-TMK pathway, which can be explained by the genetic redundancy between TMKs 46 and between ABP1 and its homologues 55 . Thus, ABP1-TMK cell surface signalling is a likely input component of the positive feedback central to the auxin canalization mechanism.…”

PIN2-mediated self-organizing transient auxin flow contributes to auxin maxima at the tip of Arabidopsis cotyledons

“…The PC interdigitation event occurs with specific auxin signaling coordination throughout the cotyledon 2 . The small molecule phytohormone auxin acts as both a local and global signal to coordinate the PC interdigitation 3–6 . Local auxin activates cell surface signaling cascades that are independent of auxin-induced gene transcription and directly leads to PC interdigitation by regulating ROP GTPase-dependent cytoskeletal reorganization 1,3,4,6,7 .…”

“…The small molecule phytohormone auxin acts as both a local and global signal to coordinate the PC interdigitation 3–6 . Local auxin activates cell surface signaling cascades that are independent of auxin-induced gene transcription and directly leads to PC interdigitation by regulating ROP GTPase-dependent cytoskeletal reorganization 1,3,4,6,7 . Auxin maxima and gradients peaking in a specific region of developing organs are a common feature in plants 8,9 .It serves as guidance for proper patterning, growth regulation, cell type differentiation and organogenesis 10 .…”