Perturbation of Auxin Homeostasis and Signaling by PINOID Overexpression Induces Stress Responses in Arabidopsis

Abstract

Under normal and stress conditions plant growth require a complex interplay between phytohormones and reactive oxygen species (ROS). However, details of the nature of this crosstalk remain elusive. Here, we demonstrate that PINOID (PID), a serine threonine kinase of the AGC kinase family, perturbs auxin homeostasis, which in turn modulates rosette growth and induces stress responses in Arabidopsis plants. Arabidopsis mutants and transgenic plants with altered PID expression were used to study the effect on auxin levels and stress-related responses. In the leaves of plants with ectopic PID expression an accumulation of auxin, oxidative burst and disruption of hormonal balance was apparent. Furthermore, PID overexpression led to the accumulation of antioxidant metabolites, while pid knockout mutants showed only moderate changes in stress-related metabolites. These physiological changes in the plants overexpressing PID modulated their response toward external drought and osmotic stress treatments when compared to the wild type. Based on the morphological, transcriptome, and metabolite results, we propose that perturbations in the auxin hormone levels caused by PID overexpression, along with other hormones and ROS downstream, cause antioxidant accumulation and modify growth and stress responses in Arabidopsis. Our data provide further proof for a strong correlation between auxin and stress biology.

Osmotic stress inhibits leaf growth of Arabidopsis thaliana by enhancing ARF‐mediated auxin responses

“…The T‐DNA insertion lines axr4‐1 ( N8018 ), axr5 ( N16234 ), aux1‐7 ( N9583 ), nit1‐3 ( N3738 ) and tir1‐1 ( N3798 ) were obtained from Nottingham Arabidopsis Stock Centre. The auxin response factor (arf) 7-1 , arf19-1 and pinoid14 mutants were a kind gift from Kris Vissenberg (Saini et al , 2017; Schoenaers et al , 2018).…”

Investigation of a Novel Salt Stress-Responsive Pathway Mediated by Arabidopsis DEAD-Box RNA Helicase Gene AtRH17 Using RNA-Seq Analysis

“…ABR increases the ABR-dependent phosphorylation of PIN2, which activates auxin efflux, alters auxin accumulation, and promotes root growth under salt stress conditions [31,32]. T-DNA insertional mutants of ABR are hypersensitive to salt stress in primary root elongation and do not respond to PA [31,32]. These results suggest that the upregulated LEA4-5, TSPO, and ABR confer salt stress-tolerance in AtRH17 OXs.…”

“…The interaction between TSPO and PIP2;7 triggers the reduction of PIP2;7 channels present in the plasma membrane and reduces the water transport activity [20,21]. ABR is a Ser/Thr kinase and interacts with phospholipase D-derived phosphatidic acid (PA) [31,32]. ABR increases the ABR-dependent phosphorylation of PIN2, which activates auxin efflux, alters auxin accumulation, and promotes root growth under salt stress conditions [31,32].…”

“…ABR is a Ser/Thr kinase and interacts with phospholipase D-derived phosphatidic acid (PA) [31,32]. ABR increases the ABR-dependent phosphorylation of PIN2, which activates auxin efflux, alters auxin accumulation, and promotes root growth under salt stress conditions [31,32]. T-DNA insertional mutants of ABR are hypersensitive to salt stress in primary root elongation and do not respond to PA [31,32].…”

Arabidopsis ERF109 regulates auxin transport-related genes in root development

“…Loss-of-function mutants of the PID display apical organogenesis defects and the decline of auxin transport, which is similar to the pin1 mutant (Benjamins et al , 2001; Bennett et al , 1995). The overexpression of PID causes the reduction of lateral auxin transport due to the preferential stimulation of downward directed PAT to the root apex by PID , which leads to the loss of auxin of root apex and peripheral cells, and subsequently results in the reduction of lateral roots, shortened hypocotyl and root, and the loss of gravitropism and phototropism (Benjamins et al , 2001; Haga and Sakai, 2015; Saini et al , 2017a; Sukumar et al , 2009; Willige and Chory, 2015). Recent studies have revealed that PID is a crucial contributor of the regulation of apical-basal PIN polarity (Friml et al , 2004; Kleine-Vehn et al , 2009; Saini et al , 2017b; Wang et al , 2019; Zourelidou et al , 2014).…”