Plant hormone receptors: new perceptions

Abstract

Plant growth and development require the integration of a variety of environmental and endogenous signals that, together with the intrinsic genetic program, determine plant form. Central to this process are several growth regulators known as plant hormones or phytohormones. Despite decades of study, only recently have receptors for several of these hormones been identified, revealing novel mechanisms for perceiving chemical signals and providing plant biologists with a much clearer picture of hormonal control of growth and development.

Figure 1.

Ubiquitin-ligase based receptors. (A) Under subthreshold auxin concentrations, auxin-responsive genes are repressed by Aux/IAA proteins heterodimerizing with ARF transcription factors. Upon an auxin stimulus, the TIR1 F-box protein subunit of the SCF^TIR1 ubiquitin-ligase binds auxin, enabling the recruitment of Aux/IAA proteins to the SCF complex for ubiquitination. Subsequent Aux/IAA degradation by the 26S proteasome derepresses the ARF transcription factors. (B) JAZ proteins negatively regulate jasmonate response by repressing MYC2 transcriptional activity. Upon binding jasmonate, the SCF^COI1 ubiquitin-ligase targets JAZ proteins for ubiquitin-mediated proteolysis, derepressing MYC2. (C) DELLA proteins repress GA response by negatively regulating PIF3, PIF4, and presumably other transcription factors that control the expression of GA-inducible genes. DELLA proteins also promote the expression of several GA-repressible genes, several of which encode GA biosynthetic enzymes and components of the response pathway including the GID1 receptors. Upon binding GA, the GID1 receptor interacts with DELLA. The GID1-GA-DELLA complex is then recognized by the SCF^GID2 ubiquitin-ligase, which targets DELLA for ubiquitin-mediated degradation. The red arrows in A–C indicate the effects of the respective hormone on the Aux/IAA, JAZ, and DELLA repressors.

Figure 2.

ABA receptors act at different cellular locations. The RNA-binding protein FCA acts in the nucleus together with the mRNA 3′-end processing factor FY to control the abundance of FLC, an inhibitor of flowering. Upon binding ABA, FCA and FY dissociate, leading to the accumulation of FLC and inhibition of flowering. In the chloroplast, the Mg-chelatase H subunit (CHLH) binds to ABA and acts as a positive regulator of ABA signaling by an unknown mechanism. This function appears to be separable from CHLH's role in plastid-to-nucleus signaling and chlorophyll synthesis. GPCRs have been proposed to function as ABA receptors on the plasma membrane. Genetic studies have implicated GCR1 and RGS1 as potential ABA receptors, but ABA binding activity has not been demonstrated. The GPCR-related protein GCR2 does bind ABA. However, it is currently unclear whether or not GCR2 is a canonical serpentine GPCR or a peripheral membrane protein. Genetic studies have implicated G-proteins and several potential downstream effectors and secondary messengers in ABA response. (PLD) Phospholipase D; (PP2C) protein phosphatase 2C; (MAPK) mitogen-activated kinase; (SnRK) SNF1-related kinase; (PA) phosphatidic acid; (ROS) reactive oxygen species; (NO) nitric oxide.