Gibberella stalk rot (GSR) by Fusarium graminearum causes significant losses of maize production worldwide. Jasmonates (JAs) have been broadly known in regulating defense against pathogens through the homeostasis of active JAs and COI-JAZ-MYC function module. However, the functions of different molecular species of JAs and COI-JAZ-MYC module in maize interactions with Fusarium graminearum and regulation of diverse metabolites remain unknown. In this study, we found that exogenous application of MeJA strongly enhanced resistance to GSR. RNA-seq analysis showed that MeJA activated multiple genes in JA pathways, which prompted us to perform a genome-wide screening of key JA signaling components in maize. Yeast Two-Hybrid, Split-Luciferase, and Pull-down assays revealed that the JA functional and structural mimic coronatine (COR) functions as an essential ligand to trigger the interaction between ZmCOIa and ZmJAZ15. By deploying CRISPR-cas9 knockout and Mutator insertional mutants, we demonstrated that coi1a mutant is more resistant, whereas jaz15 mutant is more susceptible to GSR. Moreover, JA-deficient opr7-5opr8-2 mutant displayed enhanced resistance to GSR compared to wild type. Together, these results provide strong evidence that ZmJAZ15 plays a pivotal role, whereas ZmCOIa and endogenous JA itself might function as susceptibility factors, in maize immunity to GSR.

Gibberella ear rot (GER), a prevalent disease caused by Fusarium graminearum (F. graminearum), can result in significant yield loss and carcinogenic mycotoxin contamination in maize worldwide., However, only a few quantitative trait loci (QTLs) for GER resistance have been reported. In this study, we evaluated a Chinese recombinant inbred line (RIL) population comprising of 204 lines, developed from a cross between a resistant parent DH4866 and a susceptible line T877, in three field trial environments under artificial inoculation with F. graminearum. The RIL population and their parents were genotyped with an Affymetrix microarray CGMB56K SNP Array. Based on the genetic linkage map constructed using 1,868 bins as markers, eleven QTLs, including five stable QTLs, were identified by individual environment analysis. Joint multiple environments analysis and epistatic interaction analysis revealed six additive and six epistatic (additive × additive) QTLs, respectively. None of the QTLs could explain more than 10% of phenotypic variation, suggesting that multiple minor-effect QTLs contributed to the genetic component of resistance to GER, and both additive and epistatic effects contributed to the genetic architecture of resistance to GER. A novel QTL, qGER4.09, with largest effect, identified and validated using 588 F2 individuals, was colocalized with genomic regions for FER and Aspergillus ear rot, indicating that this genetic locus likely confers resistance to multiple pathogens, and can be potentially utilized in breeding maize varieties, aimed at improving the resistance not only to GER, but also other ear rot diseases.

Background: Gibberella ear rot (GER), a prevalent disease caused by Fusarium graminearum, can result in yield loss and mycotoxin contamination in maize. Despite that several QTLs related to GER resistance have been reported previously, few of them was identified in Chinese maize inbred lines. In this study, we employed a Chinese recombination inbred line (RIL) population comprising of 204 lines, developed from a cross involving a resistant parent DH4866 and a susceptible line T877. The population was phenotypically evaluated at three field trial locations under artificial inoculation with F. graminearum and genotyped with an Affymetrix microarray CGMB56K SNP Array to detect the quantitative trait loci (QTLs) for resistance to GER. Results: Based on the genetic linkage map constructed using 1,868 bins as markers, a total of 15 QTLs were identified, and both DH4866 and T877 alleles at these QTLs contributed toward resistance. Of these QTLs, five were stably expressed across multiple locations, including three co-localized with previously reported genomic regions. The largest-effect QTL located on chromosome 4, qGER4.2, which accounted for 5.66~17.10% of the phenotypic variation, was detected at all locations. Based on the phenotypic values of the alleles corresponding to the five stable QTLs, a significant correlation (r2 = 0.45) between resistance to GER and the number of resistant alleles was observed. Conclusions: QTL mapping was successfully employed to identify genetic loci conferring resistance to GER by a high-density genetic map constructed from two Chinese maize germplasms. The five stable QTLs identified, especially the large-effect QTL, qGER4.2, will be useful in maize breeding programs aimed at improving GER resistance.