Plants, being sessile, have developed complex signaling and response mechanisms to cope with biotic and abiotic stressors. Recent investigations have revealed the significant contribution of phytohormones in enabling plants to endure unfavorable conditions. Among these phytohormones, jasmonic acid (JA) and its derivatives, collectively referred to as jasmonates (JAs), are of particular importance and are involved in diverse signal transduction pathways to regulate various physiological and molecular processes in plants, thus protecting plants from the lethal impacts of abiotic and biotic stressors. Jasmonic acid has emerged as a central player in plant defense against biotic stress and in alleviating multiple abiotic stressors in plants, such as drought, salinity, vernalization, and heavy metal exposure. Furthermore, as a growth regulator, JA operates in conjunction with other phytohormones through a complex signaling cascade to balance plant growth and development against stresses. Although studies have reported the intricate nature of JA as a biomolecular entity for the mitigation of abiotic stressors, their underlying mechanism and biosynthetic pathways remain poorly understood. Therefore, this review offers an overview of recent progress made in understanding the biosynthesis of JA, elucidates the complexities of its signal transduction pathways, and emphasizes its pivotal role in mitigating abiotic and biotic stressors. Moreover, we also discuss current issues and future research directions for JAs in plant stress responses.

Gray leaf spot (GLS), caused by the fungal pathogens Cercospora zeae-maydis and Cercospora zeina, is a major foliar disease of maize worldwide (Zea mays L.). Here we demonstrate that ZmWAKL encoding cell-wall-associated receptor kinase-like protein is the causative gene at the major quantitative disease resistance locus against GLS. The ZmWAKL^Y protein, encoded by the resistance allele, can self-associate and interact with a leucine-rich repeat immune-related kinase ZmWIK on the plasma membrane. The ZmWAKL^Y/ZmWIK receptor complex interacts with and phosphorylates the receptor-like cytoplasmic kinase (RLCK) ZmBLK1, which in turn phosphorylates its downstream NADPH oxidase ZmRBOH4. Upon pathogen infection, ZmWAKL^Y phosphorylation activity is transiently increased, initiating immune signaling from ZmWAKL^Y, ZmWIK, ZmBLK1 to ZmRBOH4, ultimately triggering a reactive oxygen species burst. Our study thus uncovers the role of the maize ZmWAKL–ZmWIK–ZmBLK1–ZmRBOH4 receptor/signaling/executor module in perceiving the pathogen invasion, transducing immune signals, activating defense responses and conferring increased resistance to GLS.

Questions such as the following often arise: “Should reciprocal crosses be included in a diallel?” and “Would their inclusion in a diallel impact grain yield (GY), estimates of general (GCA) and specific combining ability (SCA) effects, and heterotic group classification in maize (Zea mays L.)?” We evaluated a 12‐parent maize diallel cross (Griffing's Method 3 and Method 4) in three environments to determine (i) if reciprocal crosses impact GY of crosses and GCA and SCA effects, (ii) if reciprocal crosses influence the GCA and SCA and residual variance estimates in a diallel analysis, and (iii) if reciprocal crosses impact maize heterotic group classification. The results showed that inclusion of reciprocal crosses in a diallel greatly impacted GY and estimates of GCA and SCA effects. Under the assumption of a random‐effects model, the inclusion of reciprocal crosses caused the residual and GCA variances to decrease and the SCA variances to increase as the number of parental lines increased in a diallel cross. Because inclusion of reciprocal crosses impacted GY and SCA estimates, reciprocal crosses would have great impact on maize heterotic group classification. The maize heterotic groups might be classified differently with and without the inclusion of reciprocal crosses. Based on our dataset from southwest China, three heterotic groups seemed to be an ideal number for improving maize‐breeding efficiency.

Quality protein maize (QPM; Zea mays L.) has effectively enhanced levels of the amino acids, lysine, and tryptophan, over normal maize and provided balanced dietary protein for the health and development of monogastric animals and humans. However, as in normal maize, QPM varieties are low in provitamin A (ProVA), a precursor of vitamin A, which can lead to vitamin A deficiency in humans when maize is a significant part of their diet. In this study, maize inbred Hp321-1 carrying the favorable alleles crtRB1-5′TE-2 and crtRB1-3′TE-1 that can enhance levels of ProVA, was used as donor for improving ProVA in QPM inbred lines CML161 and CML171. Functional markers for identifying the favorable alleles crtRB1-5′TE-2 and crtRB1-3′TE-1 were used in foreground selection, and simple sequence repeat markers were used in background selection for the BC₁F₁, BC₂F₁, and BC₂F₂ generations. The background recovery rates were 77.4 and 84.5 % for CML161 and CML171 populations, respectively, in the BC₁F₁ generation, and 89.9 and 92.1 % in the BC₂F₂ generation. With foreground and background selection, the mean ProVA concentration has been improved from 1.60 µg g⁻¹ in the parent of CML161 to 5.25 µg g⁻¹ in its BC₂F₃ offspring, from 1.80 µg g⁻¹ in the parent of CML171 to 8.14 µg g⁻¹ in its BC₂F₃ offspring while maintaining similar QPM characteristics of the recurrent parents. The success from this study offers maize breeders a procedure for increasing ProVA in QPM lines, which will greatly mitigate vitamin A deficiency and protein-energy malnutrition in developing countries.

Gray leaf spot, northern leaf blight and southern leaf blight are three of the most destructive foliar diseases affecting maize (Zea mays L.). Here we identified a gene, ZmCPK39, that encodes a calcium-dependent protein kinase and negatively regulates quantitative resistance to these three diseases. The ZmCPK39 allele in the resistant line displayed significantly lower pathogen-induced gene expression than that in the susceptible line. A marked decrease in ZmCPK39 abundance mitigated the phosphorylation and degradation of the transcription factor ZmDi19. This led to elevated expression of ZmPR10, a gene known to encode an antimicrobial protein, thereby enhancing maize resistance to foliar diseases. Moreover, the F₁ hybrid with reduced ZmCPK39 expression favored disease resistance, thereby increasing yield. Hence, the discovery of the ZmCPK39–ZmDi19–ZmPR10 immune module provides insight into the mechanisms underlying broad-spectrum quantitative disease resistance and also offers a new avenue for the genetic control of maize foliar diseases.