Exogenous abscisic acid (ABA) and jasmonate (JA) promote metabolic regulation in Jacarandá-Pardo (Machaerium villosum Vog.) seedlings under PEG-induced water deficit

Abstract

Plant hormones are essential in regulating plant responses to water deficit. However, there is little information on their effects on the growth of Cerrado plants under water deficit. This study aimed to investigate how exogenous abscisic acid (ABA) and jasmonic acid (JA), used separately, can minimize the effects of induced water deficit by polyethylene glycol (PEG-6000) in Machaerium villosum seedlings. The experiment had four treatments: 1) control: half-strength Hoagland's nutrient solution; (2) PEG-water deficit: Hoagland's solution supplemented with PEG (−1.0 MPa); (3) PEG-water deficit + 100 μM ABA; and (4) PEG-water deficit + 100 μM JA. Seedlings of M. villosum were collected separately at 0, 3, 7, and 14 days after treatment. At the end of 14 days, the relative water content (RWC) substantially decreased by 29.69% in the PEG treatment, followed by 14.59 and 13.83% in the PEG+ABA and PEG+JA treatments, respectively. The PSII photochemistry quantum yield (Fv/Fm) differed significantly between control and PEG treatments at seven days. Oxidative stress was detected after three days of water deficit. The superoxide anion (O₂⁻) content gradually increased in the PEG and PEG + ABA treatments, while the PEG + JA treatment interacted positively with the suppression of O₂⁻ production. Hydrogen peroxide (H2O2) production increased by 132.2 and 66.2% at seven days and 277.4 and 131.3% at 14 days in the PEG and PEG + ABA treatments, respectively. Metabolic profiling analysis showed that ABA and JA affected common water deficit-induced metabolic pathways. PEG and PEG + ABA treatments accumulated carbohydrates and some amino acids responsible for osmotic adjustment and energy production. Conversely, the PEG + JA treatment accumulated caffeic acid, vanillic acid, and quinic acid related to secondary metabolism, antioxidant compounds, and fatty acids, important membrane repair agents.