Abstract

Nitric oxide (NO) and lipoxygenase (LOX)-derived oxylipins play important roles in stomatal closure in plants, and LOX-NO crosstalk has been indicated in mesophyll cells. However, whether the crosstalk also exists in guard cells is not clear and the detailed mechanisms remain unknown. Here, we report that exogenous sodium nitroprusside (SNP, a NO donor)-induced stomatal closure was clearly impaired in the AtLOX2 null mutant lox2-1 compared with wild-type (WT) Arabidopsis thaliana (L.) Heynh. Patch clamp analysis showed that the SNP-suppressed activity of inward-rectifying potassium channels in lox2-1 guard cell protoplasts was reduced. Moreover, SNP promoted an increase in cytosolic Ca2+ concentration in guard cells of lox2-1 mutants was inhibited compared with the WT. These results suggest that AtLOX2 plays an important role in NO-induced stomatal closure by affecting the cytosolic Ca2+ concentration increase and the activity of inward-rectifying potassium channels in guard cells. Furthermore, lox2-1 mutants showed a higher rate of leaf water loss and a relatively wider stomatal aperture than the WT under normal growth conditions. These data imply that AtLOX2 might modulate stomatal movement by increasing oxylipin generation in A. thaliana.

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