Rice GLUTATHIONE PEROXIDASE1-mediated oxidation of bZIP68 positively regulates ABA-independent osmotic stress signaling.

Osmotic stress caused by drought and high salinity is a significant environmental threat that limits plant growth and agricultural yield. Redox regulation plays an important role in plant stress responses, but the mechanisms by which plants perceive and transduce redox signals are still underexplored. Here, we report a critical function for the thiol peroxidase GPX1 in osmotic stress response in rice, where it serves as a redox sensor and transducer. GPX1 is quickly oxidized upon exposure to osmotic stress and forms an intramolecular disulfide bond, which is required for the activation of bZIP68, a VRE-like basic leucine zipper (bZIP) transcription factor involved in the ABA-independent osmotic stress response pathway. The disulfide exchange between GPX1 and bZIP68 induces homo-tetramerization of bZIP68 and thus positively regulates osmotic stress response by regulating osmotic-responsive gene expression. Furthermore, we discovered that the nuclear translocation of GPX1 is regulated by its acetylation under osmotic stress. Taken together, our findings not only uncover the redox regulation of the GPX1-bZIP68 module during osmotic stress but also highlight the coordination of protein acetylation and redox signaling in plant osmotic stress responses.

Hydrogen sulfide, a signaling molecule in plant stress responses.

Gaseous molecules, such as hydrogen sulfide (H2 S) and nitric oxide (NO), are crucial players in cellular and (patho)physiological processes in biological systems. The biological functions of these gaseous molecules, which were first discovered and identified as gasotransmitters in animals, have received unprecedented attention from plant scientists in recent decades. Researchers have arrived at the consensus that H2 S is synthesized endogenously and serves as a signaling molecule throughout the plant life cycle. However, the mechanisms of H2 S action in redox biology is still largely unexplored. This review highlights what we currently know about the characteristics and biosynthesis of H2 S in plants. Additionally, we summarize the role of H2 S in plant resistance to abiotic stress. Moreover, we propose and discuss possible redox-dependent mechanisms by which H2 S regulates plant physiology.

The coordination of guard-cell autonomous ABA synthesis and DES1 function in situ regulates plant water deficit responses.

INTRODUCTION: Drought stress triggers the synthesis and accumulation of the phytohormone abscisic acid (ABA), which regulates stomatal aperture and hence reducing plant water loss. Hydrogen sulfide (H2S), which is produced by the enzyme L-cysteine desulfhydrase 1 (DES1) that catalyzes the desulfuration of L-cysteine in Arabidopsis, also plays a critical role in the regulation of drought-induced stomatal closure. However, little is known about the regulation of DES1 or the crosstalk between H2S and ABA signaling in response to dehydration. OBJECTIVES: To demonstrate the potential crosstalk between DES1-dependent H2S and ABA signaling in response to dehydration and its regulation mechanism. METHODS: Firstly, by introducing guard cell-specific MYB60 promoter, to produce complementary lines of DES1 or ABA3 into guard cell of des1 or aba3 mutant. And the related genes expression and water loss under ABA, NaHS, or dehydration treatment in these mutant or transgenics lines were determinate. RESULTS: We found that dehydration-induced expression of DES1 is abolished in the abscisic acid deficient 3 (aba3) mutants that are deficient in ABA synthesis. Both the complementation of ABA3 expression in guard cells of the aba3 mutants and ABA treatment rescue the dehydration-induced expression of DES1, as well as the wilting phenotype observed in these mutants. Moreover, the drought-induced expression of ABA synthesis genes was suppressed in des1 mutants. While the addition of ABA or the expression of either ABA3 or DES1 in the guard cells of the aba3/des1 double mutant did not alter the wilting phenotype of these mutants, the wild type phenotype was fully restored by the expression of both ABA3 and DES1, or by the application of NaHS. CONCLUSION: These results demonstrate that the coordinated synthesis of ABA and DES1 expression is required for drought-induced stomatal closure in Arabidopsis.

Abscisic acid-triggered guard cell l-cysteine desulfhydrase function and in situ hydrogen sulfide production contributes to heme oxygenase-modulated stomatal closure.

Recent studies have demonstrated that hydrogen sulfide (H2 S) produced through the activity of l-cysteine desulfhydrase (DES1) is an important gaseous signaling molecule in plants that could participate in abscisic acid (ABA)-induced stomatal closure. However, the coupling of the DES1/H2 S signaling pathways to guard cell movement has not been thoroughly elucidated. The results presented here provide genetic evidence for a physiologically relevant signaling pathway that governs guard cell in situ DES1/H2 S function in stomatal closure. We discovered that ABA-activated DES1 produces H2 S in guard cells. The impaired guard cell ABA phenotype of the des1 mutant can be fully complemented when DES1/H2 S function has been specifically rescued in guard cells and epidermal cells, but not mesophyll cells. This research further characterized DES1/H2 S function in the regulation of LONG HYPOCOTYL1 (HY1, a member of the heme oxygenase family) signaling. ABA-induced DES1 expression and H2 S production are hyper-activated in the hy1 mutant, both of which can be fully abolished by the addition of H2 S scavenger. Impaired guard cell ABA phenotype of des1/hy1 can be restored by H2 S donors. Taken together, this research indicated that guard cell in situ DES1 function is involved in ABA-induced stomatal closure, which also acts as a pivotal hub in regulating HY1 signaling.