SnRK1α1 Antagonizes Cell Death Induced by Transient Overexpression of Arabidopsis thaliana ABI5 Binding Protein 2 (AFP2)

Abstract

Plants are continuously exposed to environmental stressors. They have thus evolved complex signaling pathways to govern responses to a variety of stimuli. The hormone abscisic acid (ABA) has been implicated in modulating both abiotic and biotic stress responses in plants. ABI5 Binding Proteins (AFPs) are a family of negative regulators of bZIP transcription factors of the AREB/ABF family, which promote ABA responses. AFP2 interacts with Snf1-Related protein Kinase 1 (SnRK1), which belongs to a highly conserved heterotrimeric kinase complex that is activated to re-establish energy homeostasis following stress. However, the role of this interaction is currently unknown. Here, we show that transient overexpression of Arabidopsis thaliana AFP2 in Nicotiana benthamiana leaves induces cell death (CD). Using truncated AFP2 constructs, we demonstrate that CD induction by AFP2 is dependent on the EAR domain. Co-expression of the catalytic subunit SnRK1α1, but not SnRK1α2, rescues AFP2-induced CD. Overexpression of SnRK1α1 has little effect on AFP2 protein level and does not affect AFP2 subcellular localization. Our results show that a high level of AFP2 is detrimental for cell function and that SnRK1α1 antagonizes AFP2-induced CD most likely through a mechanism that does not involve AFP2 protein degradation or a change in subcellular localization.

AFP2 inhibits ABA responses during germination without ABI5 degradation but DWAs reduce desiccation tolerance

“…Consistent with these expression patterns, genetic analyses have shown that AFP1 and AFP2 act redundantly to reduce ABA sensitivity at germination (Garcia et al, 2008) and AFP2 breaks high temperature-induced secondary dormancy via effects on GA and ABA metabolism by suppressing ABI5- and DELLA-mediated SOMNUS (SOM) expression (Chang et al, 2018). In addition, AFP2 attenuation of responses to salt and osmotic stress may be mediated via interactions with SnRK1 kinases (Carianopol et al, 2020), and AFP2 can promote cell death when transiently overexpressed (Carianopol and Gazzarrini, 2020). Later in development AFP2 and AFP3 act redundantly to inhibit flowering under long day conditions by reducing expression of CO and its downstream targets FT and SOC1 (Chang et al, 2019).…”