Heterotrimeric G Protein Signaling in Abiotic Stress

Abstract

As sessile organisms, plants exhibit extraordinary plasticity and have evolved sophisticated mechanisms to adapt and mitigate the adverse effects of environmental fluctuations. Heterotrimeric G proteins (G proteins), composed of α, β, and γ subunits, are universal signaling molecules mediating the response to a myriad of internal and external signals. Numerous studies have identified G proteins as essential components of the organismal response to stress, leading to adaptation and ultimately survival in plants and animal systems. In plants, G proteins control multiple signaling pathways regulating the response to drought, salt, cold, and heat stresses. G proteins signal through two functional modules, the Gα subunit and the Gβγ dimer, each of which can start either independent or interdependent signaling pathways. Improving the understanding of the role of G proteins in stress reactions can lead to the development of more resilient crops through traditional breeding or biotechnological methods, ensuring global food security. In this review, we summarize and discuss the current knowledge on the roles of the different G protein subunits in response to abiotic stress and suggest future directions for research.

Keywords: abiotic stress tolerance; heterotrimeric GTP-binding protein; hormonal signaling; signal transduction.

Figure 1

Heterotrimeric G protein signaling in plant drought and salinity stress (Created with BioRender.com on 17/03/2022). Gα deficiency inhibits Ca2⁺ channel activation and ROS production due to disruption of ABA signaling. Gα acts downstream of S1P to regulate stomatal closure by modulating inward K⁺ channels and slow anion channels. PA and PLDα1 interact with Gα to mediate ABA inhibition of stomatal opening. Binding of PA to Rboh at the N-terminal cytoplasmic region results in the production of ROS. Stomatal regulation by the RALF-FER pathway is associated with Gβ. Gα participates in ExtCaM-induced stomatal closure of guard cells by regulating NO synthesis, and NO synthesis is dependent on H₂O₂ produced by NADPH oxidases through the action of the nitrate reductase Nia1. BR induces the expression of ACS5 and ACS9 to initiate ethylene synthesis, which signals through Gα to synthesize H₂O₂ and before the nitric synthase NOA1 induces the production of NO. Several groups have proven the involvement of Gα in salt stress although the results are contradictory with positive as well as negative roles being proposed for this subunit. Gβ regulates the combination of osmotic and ionic stresses during salt stress by increasing levels of proteins involved in ROS detoxification and osmoprotectant compounds. SphK: sphingosine kinase; RALF1: rapid alkalinization factor 1; FER: receptor-like kinase FERONIA; S1P: sphingosine-1-phosphate; PLDα1: phospholipase D α1; PA: phosphatidic acid; RbohD/F: NADP oxidases RbohD and RbohF; ROS: reactive oxygen species; ExtCaM: extracellular calmodulin; AtNOA1: nitric oxide; Nia1: nitrate reductase.