Abstract
A plant's capability to cope with environmental challenges largely relies on signal transmission through mitogen-activated protein kinase (MAPK) cascades. In Arabidopsis thaliana, MPK3 is particularly strongly associated with numerous abiotic and biotic stress responses. Identification of MPK3 substrates is a milestone towards improving stress resistance in plants. Here, we characterize AZI1, a lipid transfer protein (LTP)-related hybrid proline-rich protein (HyPRP), as a novel target of MPK3. AZI1 is phosphorylated by MPK3 in vitro. As documented by co-immunoprecipitation and bimolecular fluorescence complementation experiments, AZI1 interacts with MPK3 to form protein complexes in planta. Furthermore, null mutants of azi1 are hypersensitive to salt stress, while AZI1-overexpressing lines are markedly more tolerant. AZI1 overexpression in the mpk3 genetic background partially alleviates the salt-hypersensitive phenotype of this mutant, but functional MPK3 appears to be required for the full extent of AZI1-conferred robustness. Notably, this robustness does not come at the expense of normal development. Immunoblot and RT-PCR data point to a role of MPK3 as positive regulator of AZI1 abundance.
Highlights
IntroductionPlants face a multitude of biotic and abiotic stresses. In order to survive, they need to react appropriately to modest or severe, transient or permanent, single or co-occurring stresses
During their lifespan, plants face a multitude of biotic and abiotic stresses
The sequence alignment (Figure 1) shows the four members of the EARLI hybrid proline-rich protein (HyPRP) family as well as the distantly related DIR1, a well-characterized lipid transfer protein (LTP) involved in the pathogen response (Maldonado et al, 2002)
Summary
Plants face a multitude of biotic and abiotic stresses. In order to survive, they need to react appropriately to modest or severe, transient or permanent, single or co-occurring stresses. To maintain cellular integrity under stress, plants have developed various adaptation strategies, including the synthesis of osmo-protectants, ‘hardening’ of the cell boundary by callose apposition, or by modifying plasma membrane composition and/or fluidity. These adaptation responses are preceded by rapidly stress-induced lipid and kinase signaling pathways (Munnik and Vermeer, 2010; Testerink and Munnik, 2011; Arisz et al, 2013)
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