Experimental study reveals that AtPLC1 deficiency exacerbates salt-alkali damage in Arabidopsis thaliana, indicating its vital role in stomatal control and stress resistance.
Soil salinization poses a major environmental threat to global agriculture, affecting approximately 20% of cultivated land and 50% of irrigated land worldwide. Developing salt–alkali tolerant plant varieties represents a sustainable strategy for utilizing these marginal lands. Phosphatidylinositol-specific phospholipase C (PI-PLC) is a key enzyme in the phosphoinositide signaling system and has been implicated in plant stress responses; however, its function under salt–alkali stress remains poorly understood. In this study, the function of AtPLC1 in salt–alkali tolerance was investigated, and only the atplc1 mutant exhibited a pronounced stress-sensitive phenotype, with AtPLC1 being predominantly expressed in roots and leaves, with peak expression at 6 h of treatment. Compared with wild-type, atplc1 mutants displayed significantly reduced seedling survival, retarded root growth, decreased biomass, water content, chlorophyll, and soluble sugar contents, yet accumulated higher levels of Na+, malondialdehyde, H2O2, and superoxide anions under salt–alkali stress. Notably, atplc1 mutants showed increased stomatal conductance and decreased leaf surface temperature, as detected by thermal imaging, indicating impaired water regulation. Collectively, our findings demonstrate that AtPLC1 positively regulates salt–alkali tolerance and provides a candidate gene for molecular breeding of stress-resistant crops.
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