Inhibition of NPR1 activity Leads to Shoot Growth Improvement under Low-Calcium Conditions in Arabidopsis.

Under low-Ca conditions, plants accumulate salicylic acid (SA) and induce SA-responsive genes. However, the relationship between SA and low-Ca tolerance remains unclear. Here, we demonstrated that the inhibition or suppression of NPR1 activity, a major regulator of the SA signaling pathway in the defense response, improves shoot growth under low-Ca conditions. Furthermore, mutations in PAD4 or EDS1, which are upstream regulators of NPR1, improved shoot growth under low-Ca conditions, suggesting that the NPR1 suppressed growth under low-Ca conditions. In contrast, the growth of sid2-2, which is an SA-deficient mutant, was sensitive to low-Ca levels, suggesting that SA accumulation by SID2 was not related to growth inhibition under low-Ca conditions. Additionally, npr1-1 showed low-Ca tolerance, and the application of tenoxicam-an inhibitor of the NPR1-mediated activation of gene expression-also improved shoot growth under low-Ca conditions. The low-Ca tolerance of double mutants pad4-1 npr1-1 and eds1-22 npr1-1 were similar to that of the single mutants, suggesting that PAD4 and EDS1 are involved in the same genetic pathway in suppressing growth under low-Ca conditions as NPR1. Cell death and low-Ca tolerance were not correlated among the mutants, suggesting that growth improvement in the mutants was not due to cell death inhibition. In conclusion, we revealed that NPR1 suppresses plant growth under low-Ca conditions, and that the other SA-related genes influence plant growth and cell death.