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The plant hormone jasmonate (JA) plays crucial roles in regulating plant responses to herbivorous insects and microbial pathogens and is an important regulator of plant growth and development1–7. Key mediators of JA signaling include MYC transcription factors, which are repressed by JAZ transcriptional repressors at the resting state. In the presence of active JA, JAZ proteins function as JA co-receptors by forming a hormone-dependent complex with COI1, the F-box subunit of an SCF-type ubiquitin E3 ligase8–11. The hormone-dependent formation of the COI1–JAZ co-receptor complex leads to ubiquitination and proteasome-dependent degradation of JAZ repressors and release of MYC proteins from transcriptional repression3,10,12. The mechanism by which JAZ proteins repress MYC transcription factors and how JAZ proteins switch between the repressor function in the absence of hormone and the co-receptor function in the presence of hormone remain enigmatic. Here we show that Arabidopsis MYC3 undergoes pronounced conformational changes when bound to the conserved Jas motif of the JAZ9 repressor. The Jas motif, previously shown to bind to hormone as a partially unwound helix, forms a complete α-helix that displaces the N-terminal helix of MYC3 and becomes an integral part of the MYC N-terminal fold. In this position, the Jas helix competitively inhibits MYC3 interaction with the MED25 subunit of the transcriptional Mediator complex. Our study elucidates a novel molecular switch mechanism that governs the repression and activation of a major plant hormone pathway.

Hydrogen sulfide (H 2 S) is a gaseous signaling molecule that regulates diverse cellular signaling pathways through persulfidation, which involves the post-translational modification of specific cysteine residues to form persulfides.However, the mechanisms that underlie this important redox-based modification remain poorly understood in higher plants. We have, therefore, analyzed how protein persulfidation acts as a specific and reversible signaling mechanism during the abscisic acid (ABA) response in Arabidopsis thaliana.Here we show that ABA stimulates the persulfidation of L-CYSTEINE DESULFHYDRASE 1 (DES1), an important endogenous H 2 S enzyme, at Cys44 and Cys205 in a redox-dependent manner. Moreover, sustainable H 2 S accumulation drives persulfidation of the NADPH oxidase RESPIRATORY BURST OXIDASE HOMOLOG PROTEIN D (RBOHD) at Cys825 and Cys890, enhancing its ability to produce reactive oxygen species. Physiologically, S-persulfidation-induced RBOHD activity is relevant to ABA-induced stomatal closure. Together, these processes form a negative feedback loop that fine-tunes guard cell redox homeostasis and ABA signaling. These findings not only expand our current knowledge of H 2 S function in the context of guard cell ABA signaling, but also demonstrate the presence of a rapid signal integration mechanism involving specific and reversible redox-based post-translational modifications that occur in response to changing environmental conditions.

Gaseous molecules, such as hydrogen sulfide (H2S) 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 H2S is synthesized endogenously and serves as a signaling molecule throughout the plant life cycle. However, the mechanisms of H2S action in redox biology is still largely unexplored. This review highlights what we currently know about the characteristics and biosynthesis of H2S in plants. Additionally, we summarize the role of H2S in plant resistance to abiotic stress. Moreover, we propose and discuss possible redox‐dependent mechanisms by which H2S regulates plant physiology.

Fusarium graminearum (teleomorph, Gibberella zeae) causes head blight of cereals and contaminates grains with trichothecene mycotoxins that are harmful to humans and domesticated animals. Control of Fusarium head blight relies on carbendazim (MBC) in China, but resistance to MBC in F. graminearum is now widespread. Sixty-seven strains were evaluated for trichothecene production in shake culture or in the field. The strains included 60 wild-type strains (30 MBC-resistant and 30 MBC-sensitive), three MBC-resistant site-directed mutants at codon 167 in beta(2)-tubulin, three MBC-sensitive site-directed mutants at codon 240 in beta(2)-tubulin, and their MBC-sensitive wild-type progenitor strain ZF21. The incidence of infected spikelets and the amount of F. graminearum DNA in field grain (AFgDNA) also were evaluated for all strains. MBC resistance increased trichothecene production in shake culture or in the field. Although MBC resistance did not change the incidence of infected spikelets, it did increase AFgDNA. Tri5 gene expression increased in MBC-resistant strains grown in shake culture. We found a significant exponential relationship between trichothecene production and Tri5 gene expression in shake culture and a linear relationship between the incidence of infected spikelets or AFgDNA and trichothecene production in field grain.

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Fusarium head blight (FHB) of wheat and other cereals, caused mainly by Fusarium graminearum, is one of the most economically important diseases worldwide, especially in the United States and China. The benzimidazole fungicides, particularly carbendazim (MBC), have been consistently used during the period of wheat heading and flowering in areas with warm and moist weather to control FHB in China for over 30 years. The effectiveness of MBC, however, has been threatened by the emergence of resistant pathogen populations in the field. JS399-19 (experimental number; a.i. 2-cyano-3-amino-3-phenylancryic acetate) is a novel cyanoacrylate fungicide discovered and patented by the Jiangsu Branch of National Pesticide Research & Development South Center of China. To evaluate the potential risk of resistance development in MBC-resistant F. graminearum isolates to this new fungicide JS399-19, five isolates each of MBC-resistant or -sensitive, which were classified into three different sensitivity phenotypes, such as sensitive (S), moderately resistant (MR), and highly resistant (HR) to MBC, were selected to induce JS399-19-resistant mutants by selecting resistance on potato sucrose agar (PSA) plates amended with JS399-19 at 10 microg/ml. In this way, a total of 24 JS399-19-resistant mutants were obtained from all tested MBC-resistant or -sensitive isolates. All 50 single-spore progenies of each of the resistant mutants could grow normally on PSA plates amended with JS399-19 at 10 microg/ml, indicating stability of resistance to this fungicide. Also, all of the resistant mutants maintained their resistance to JS399-19 and/or MBC through eight transfers on PSA plates for 40 days and when stored on PSA slants at 4 degrees C for 60 days. The mycelial growth and conidial production capacity were decreased in 52.4% of the resistant mutants, indicating that a fitness cost was associated with JS399-19-resistant phenotypes of F. graminearum isolates. However, most of the mutants resistant to both MBC and JS399-19 exhibited high sexual reproduction capacity and pathogenicity as their parental isolates. Nevertheless, the majority of these mutants possessed fitness levels comparable to their parents. The results on the efficacy of the two fungicides for controlling FHB incited by the fungicide-resistant mutants were generally consistent with those of the in vitro sensitivity tests. JS399-19 was effective in controlling FHB caused by MBC-resistant isolates under field conditions, while it was not effective in controlling FHB caused by isolates resistant to JS399-19 or those that were resistant to both MBC and JS399-19. Moreover, the efficacy of the mixture of MBC and JS399-19 was also significantly lower in controlling FHB caused by the isolates resistant to both MBC and JS399-19 than the efficacy against the disease caused by the sensitive isolates, the MBC-resistant isolates, or the JS399-19-resistant isolates. The results suggest that JS399-19 possessed a high risk in development of resistance in MBC-resistant and -sensitive F. gramin...