Pathogen-induced methylglyoxal negatively regulates rice bacterial blight resistance by inhibiting OsCDR1 protease activity

Xanthomonas oryzae pv.oryzae(Xoo)causes bacterial blight(BB),a globally devastating disease of rice(Oryza sativa)that is responsible for significant crop loss.Sugars and sugar metabolites are important for pathogen infection,providing energy and regulating events associated with defense responses;howev-er,the mechanisms by which they regulate such events in BB are unclear.As an inevitable sugar metabolite,methylglyoxal(MG)is involved in plant growth and responses to various abiotic stresses,but the underlying mechanisms remain enigmatic.Whether and how MG functions in plant biotic stress responses is almost completely unknown.Here,we report that the Xoo strain PXO99 induces OsWRKY62.1 to repress transcrip-tion of OsGLY Il genes by directly binding to their promoters,resulting in overaccumulation of MG.MG negatively regulates rice resistance against Pxo99:osglyll2 mutants with higher MG levels are more sus-ceptible to the pathogen,whereas OsGLYIl2-overexpressing plants with lower MG content show greater resistance than the wild type.Overexpression of OsGLYll2 to prevent excessive MG accumulation confers broad-spectrum resistance against the biotrophic bacterial pathogens Xoo and Xanthomonas oryzae pv.oryzicola and the necrotrophic fungal pathogen Rhizoctonia solani,which causes rice sheath blight.Further evidence shows that MG reduces rice resistance against PXO99 through CONSTITUTIVE DISEASE RESISTANCE 1(OsCDR1).MGmodifies the Arg97 residue of OsCDR1to inhibit its aspartic protease activ-ity,which is essential for OsCDR1-enhanced immunity.Taken together,these findings illustrate how Xoo promotes infection by hijacking a sugar metabolite in the host plant.

Hydrogen peroxide sulfenylates and inhibits the photorespiratory enzyme PGLP1 to modulate plant thermotolerance

Climate change is resulting in more frequent and rapidly changing temperatures at both extremes that severely affect the growth and production of plants,particularly crops.Oxidative stress caused by high temperatures is one of the most damaging factors for plants.However,the role of hydrogen peroxide(H_(2)O_(2))in modulating plant thermotolerance is largely unknown,and the regulation of photorespiration essential for C3 species remains to be fully clarified.Here,we report that heat stress promotes H2O2 accumulation in chloroplasts and that H2O2 stimulates sulfenylation of the chloroplast-localized photorespiratory enzyme 2-phosphoglycolate phosphatase 1(PGLP1)at cysteine 86,inhibiting its activity and promoting the accumulation of the toxic metabolite 2-phosphoglycolate.We also demonstrate that PGLP1 has a positive function in plant thermotolerance,as PGLP1 antisense lines have greater heat sensitivity and PGLP1-overexpressing plants have higher heat-stress tolerance than the wild type.Together,our results demonstrate that heat-induced H2O2 in chloroplasts sulfenylates and inhibits PGLP1 to modulate plant thermotolerance.Furthermore,targeting CATALASE2 to chloroplasts can largely prevent the heatinduced overaccumulation of H2O2 and the sulfenylation of PGLP1,thus conferring thermotolerance without a plant growth penalty.These findings reveal that heat-induced H2O2 in chloroplasts is important for heat-caused plant damage.

Coordination of plant growth and abiotic stress responses by tryptophan synthase β subunit 1 through modulation of tryptophan and ABA homeostasis in Arabidopsis

To adapt to changing environments, plants have evolved elaborate regulatory mechanisms balancing their growth with stress responses. It is currently unclear whether and how the tryptophan (Trp), the growth-related hormone auxin, and the stress hormone abscisic acid (ABA) are coordinated in this trade-off. Here, we show that tryptophan synthase β subunit 1 (TSB1) is involved in the coordination of Trp and ABA, thereby affecting plant growth and abiotic stress responses. Plants experiencing high salinity or drought display reduced TSB1 expression, resulting in decreased Trp and auxin accumulation and thus reduced growth. In comparison with the wild type, amiR-TSB1 lines and TSB1 mutants exhibited repressed growth under non-stress conditions but had enhanced ABA accumulation and stress tolerance when subjected to salt or drought stress. Furthermore, we found that TSB1 interacts with and inhibits β-glucosidase 1 (BG1), which hydrolyses glucose-conjugated ABA into active ABA. Mutation of BG1 in the amiR-TSB1 lines compromised their increased ABA accumulation and enhanced stress tolerance. Moreover, stress-induced H2O2 disrupted the interaction between TSB1 and BG1 by sulfenylating cysteine-308 of TSB1, relieving the TSB1-mediated inhibition of BG1 activity. Taken together, we revealed that TSB1 serves as a key coordinator of plant growth and stress responses by balancing Trp and ABA homeostasis.