Alleviation by abscisic acid of Al toxicity in rice bean is not associated with citrate efflux but depends on ABI5-mediated signal transduction pathways

Under conditions of aluminum(Al) toxicity,which severely inhibits root growth in acidic soils, plants rapidly alter their gene expression to optimize physiological fitness for survival. Abscisic acid(ABA) has been suggested as a mediator between Al stress and gene expression, but the underlying mechanisms remain largely unknown. Here,we investigated ABA-mediated Al-stress responses, using integrated physiological and molecular biology approaches.We demonstrate that Al stress caused ABA accumulation in the root apex of rice bean(Vigna umbellata [Thunb.] Ohwi &Ohashi), which positively regulated Al tolerance. However,this was not associated with known Al-tolerance mechanisms. Transcriptomic analysis revealed that nearly one-third of the responsive genes were shared between the Al-stress and ABA treatments. We further identified a transcription factor, ABI5, as being positively involved in Al tolerance. Arabidopsis abi5 mutants displayed increased sensitivity to Al, which was not related to the regulation of AtALMT1 and AtMATE expression. Functional categorization of ABI5-mediated genes revealed the importance of cell wall modification and osmoregulation in Al tolerance, a finding supported by osmotic stress treatment on Al tolerance. Our results suggest that ABA signal transduction pathways provide an additional layer of regulatory control over Al tolerance in plants.

Abscisic acid-dependent PMT1 expression regulates salt tolerance by alleviating abscisic acid-mediated reactive oxygen species production in Arabidopsis

Phosphocholine(PCho)is an intermediate metabolite of nonplastid plant membranes that is essential for salt tolerance.However,how PCho metabolism modulates response to salt stress remains unknown.Here,we characterize the role of phosphoethanolamine N-methyltransferase 1(PMT1)in salt stress tolerance in Arabidopsis thaliana using a T-DNA insertional mutant,geneediting alleles,and complemented lines.The pmt1 mutants showed a severe inhibition of root elongation when exposed to salt stress,but exogenous ChoCl or lecithin rescued this defect.pmt1 also displayed altered glycerolipid metabolism under salt stress,suggesting that glycerolipids contribute to salt tolerance.Moreover,pmt1 mutants exhibited altered reactive oxygen species(ROS)accumulation and distribution,reduced cell division activity,and disturbed auxin distribution in the primary root compared with wild-type seedlings.We show that PMT1 expression is induced by salt stress and relies on the abscisic acid(ABA)signaling pathway,as this induction was abolished in the aba2-1 and pyl112458 mutants.However,ABA aggravated the salt sensitivity of the pmt1 mutants by perturbing ROS distribution in the root tip.Taken together,we propose that PMT1 is an important phosphoethanolamine N-methyltransferase participating in root development of primary root elongation under salt stress conditions by balancing ROS production and distribution through ABA signaling.