The Ca /calmodulin2-binding transcription factor TGA3 elevates LCD expression and H S production to bolster Cr tolerance in Arabidopsis.

Heavy metal (HM) contamination on agricultural land not only reduces crop yield but also causes human health concerns. As a plant gasotransmitter, hydrogen sulfide (H S) can trigger various defense responses and help reduce accumulation of HMs in plants; however, little is known about the regulatory mechanisms of H S signaling. Here, we provide evidence to answer the long-standing question about how H S production is elevated in the defense of plants against HM stress. During the response of Arabidopsis to chromium (Cr ) stress, the transcription of L-cysteine desulfhydrase (LCD), the key enzyme for H S production, was enhanced through a calcium (Ca )/calmodulin2 (CaM2)-mediated pathway. Biochemistry and molecular biology studies demonstrated that Ca /CaM2 physically interacts with the bZIP transcription factor TGA3, a member of the 'TGACG'-binding factor family, to enhance binding of TGA3 to the LCD promoter and increase LCD transcription, which then promotes the generation of H S. Consistent with the roles of TGA3 and CaM2 in activating LCD expression, both cam2 and tga3 loss-of-function mutants have reduced LCD abundance and exhibit increased sensitivity to Cr stress. Accordingly, this study proposes a regulatory pathway for endogenous H S generation, indicating that plants respond to Cr stress by adjusting the binding affinity of TGA3 to the LCD promoter, which increases LCD expression and promotes H S production. This suggests that manipulation of the endogenous H S level through genetic engineering could improve the tolerance of grains to HM stress and increase agricultural production on soil contaminated with HMs.