A gain‐of‐function mutation in Msl10 triggers cell death and wound‐induced hyperaccumulation of jasmonic acid in Arabidopsis

Abstract

Jasmonates (JAs) are rapidly induced after wounding and act as key regulators for wound induced signaling pathway. However, what perceives the wound signal and how that triggers JA biosynthesis remains poorly understood. To identify components involved in Arabidopsis wound and JA signaling pathway, we screened for mutants with abnormal expression of a luciferase reporter, which is under the control of a wound-responsive promoter of an ethylene response factor (ERF) transcription factor gene, RAP2.6 (Related to APetala 2.6). The rea1 (RAP2.6 expresser in shoot apex) mutant constitutively expressed the RAP2.6-LUC reporter gene in young leaves. Along with the typical JA phenotypes including shorter petioles, loss of apical dominance, accumulation of anthocyanin pigments and constitutive expression of JA response gene, rea1 plants also displayed cell death and accumulated high levels of JA in response to wounding. The phenotype of rea1 mutant is caused by a gain-of-function mutation in the C-terminus of a mechanosensitive ion channel MscS-like 10 (MSL10). MSL10 is localized in the plasma membrane and is expressed predominantly in root tip, shoot apex and vascular tissues. These results suggest that MSL10 is involved in the wound-triggered early signal transduction pathway and possibly in regulating the positive feedback synthesis of JA.

Plant mechanosensitive ion channels: an ocean of possibilities

“…However, overexpression of MSL10 results in dwarfing, ROS accumulation, and ectopic lesions, and all of these effects are negatively regulated by phosphorylation of the N-terminus [43]. Dwarfing and ectopic lesions are also observed in response to a single EMS-induced point mutation in the C-terminus of MSL10 [44], suggesting that these overexpression phenotypes reflect some aspect of the normal gene function. In addition, a recent study implicated MSL4 in pathogen-triggered immunity [45], and MSL6 phosphorylation was observed in response to oligogalacturonide treatment [46].…”

Nonpolar residues in the presumptive pore‐lining helix of mechanosensitive channel MSL10 influence channel behavior and establish a nonconducting function

“…MSL10 is required for the predominant MS ion channel activity in root cells (Haswell et al., ), but to date no other loss‐of‐function phenotype has been established. Fortunately, gain‐of‐function phenotypes have been revealing; overexpression of MSL10 leads to cell death, as does a single ethyl methanesulfonate‐induced point mutation in the MSL10 C terminus, S640L ( rea1 ) (Veley et al., ; Zou et al., ). Overexpression of the soluble N terminus of MSL10 is sufficient to induce cell death in tobacco epidermal cells (Veley et al., ).…”

The Tension-sensitive Ion Transport Activity of MSL8 is Critical for its Function in Pollen Hydration and Germination

“…It remains formally possible, though unlikely, that the Ile711Ser or Phe720Leu mutations affect both the characteristics of the channel and the function of other domains important for signaling independent of ion transport. Lesions in both the soluble N-terminus (Veley et al, 2014) and the soluble C-terminus (Zou et al, 2015) affect the cell death signaling function of MSL10, but lesions to the predicted pore-lining domain have not yet been tested. Future work will be required to understand how MSL8 functions alongside established ion channels and the tightly regulated ion fluxes that are essential for pollen germination and tube growth (Michard et al, 2009).…”