Finally a role for AMI1 in Arabidopsis
So proud and happy that our latest work on AMI1 has finally found a home in the Journal of Experimental Botany, and that we have been able to associate AMI1 with a precise role in controlling the tradeoff between growth and plant stress responses in Arabidopsis. A huge shout-out to the teams of Henrik Aronsson and Robert Björk from the University of Gothenburg for their help and patience. The article reports that the accumulation of the auxin precursor indole-3-acetamide in ami1 mutants triggers abscisic acid biosynthesis through a regulatory loop that results in the induction of NCED3 and, thereby, links auxin homeostasis with plant stress responses.
The evolutionary success of plants relies to a large extent on their extraordinary ability to adapt to changes in their environment. These adaptations require that plants balance their growth with their stress responses. Plant hormones are crucial mediators orchestrating the underlying adaptive processes. However, whether and how the growth-related hormone auxin and the stress-related hormones jasmonic acid (JA), salicylic acid, and abscisic acid (ABA) are coordinated remains largely elusive. Here, we analyze the physiological role of AMIDASE 1 (AMI1) in plant growth and its possible connection to plant adaptations to abiotic stresses. AMI1 contributes to cellular auxin homeostasis by catalyzing the conversion of indole-acetamide into the major plant auxin indole-3-acetic acid. Functional impairment of AMI1 increases the plants’ stress status rendering mutant plants more susceptible to abiotic stresses. Transcriptomic analysis of ami1 mutants disclosed the reprogramming of a considerable number of stress-related genes, including JA and ABA biosynthesis genes. The ami1 mutants exhibit only moderately repressed growth, but an enhanced ABA accumulation, which suggests a role for AMI1 in the crosstalk between auxin and ABA. Altogether, our results suggest that AMI1 is involved in coordinating the trade-off between plant growth and stress responses, balancing auxin with ABA homeostasis.