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Systemic resistance (SR) occurs when systemic signals derived from sites of previous pathogen attacks result in increased resistance levels to subsequent pathogenesis at distal sites. Although much research on this phenomenon has been conducted in dicotyledonous species, little is known about SR in monocotyledonous models. In this study, we investigate SR in maize caused by foliar infection with Cochliobolus heterostrophus—the causal agent of southern leaf blight (SLB) disease—and by leaf damage. In juvenile maize, we observed that both prior infection with C. heterostrophus and cutting of the third and fourth leaves led to enhanced resistance to SLB in the fifth leaf. Levels of SR induction were variable between genotypes and between growth conditions. C. heterostrophus infection induced local and systemic expression of the defense-associated transcript ZmPR1. We discuss the implications of these findings that provide insights into the systemic disease resistance response in maize. [Formula: see text] The author(s) have dedicated the work to the public domain under the Creative Commons CC0 “No Rights Reserved” license by waiving all of his or her rights to the work worldwide under copyright law, including all related and neighboring rights, to the extent allowed by law, 2026. 

Heterosis is the increased performance of hybrids relative to their parental genotypes. Heterosis for growth may be mediated by underlying traits, including traits affecting host–microbe interactions. A trade-off between growth and defense is often observed in plant disease studies, such that a stronger defense response is often associated with slower growth and lower yield. We investigated the production of reactive oxygen species (ROS) following treatment with microbial elicitors, an early component of the pattern-triggered immunity (PTI) response, in maize hybrids and their inbred parents. ROS production was often reduced in hybrids compared with inbred parents, and this effect was dependent on genotype, elicitor used, and time of day. These results identify PTI as a response displaying heterosis whose regulation might contribute to heterosis in other traits, such as growth and yield. [Formula: see text] Copyright © 2026 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license . 

How host genotype shapes pathogen tissue tropism remains poorly understood. Vascular and nonvascular tissues represent distinct habitats within a plant for bacteria to colonize. Host plants often utilize different mechanisms to defend themselves against vascular and nonvascular pathogens, and mechanisms of resistance employed by the host can vary by organ. Xanthomonas vasicola pv. vasculorum ( Xvv) is an emerging bacterial maize pathogen, and this pathosystem offers an opportunity to study how host resistance differs in response to the vascular and nonvascular lifestyles exhibited by a single bacterial phytopathogen. We used different inoculation techniques to induce vascular and nonvascular disease and evaluated maize populations using both techniques to map resistance to vascular and nonvascular disease caused by Xvv. Xvv can colonize both vascular and nonvascular tissues, depending on the genotype. Different inoculation techniques can be used to induce vascular or nonvascular colonization. Independent loci control variation in resistance to Xvv during vascular and nonvascular pathogenesis. We confirmed the role of those regions in resistance to vascular and nonvascular infection. This study offers insights into how host resistance shapes how bacterial pathogens adapt to both vascular and nonvascular lifestyles. We show that host genotype can dictate which tissues a pathogen can infect. This system can serve as a model to understand tissue-specific host resistance to plant pathogens and tissue specificity in pathogens. 

Heterosis, or hybrid vigor, refers to the phenotypic superiority of hybrids relative to their parental inbred lines. Recent work showed that manipulation of the soil microbial community consistently altered heterosis, but the direction of the effect was dependent on microbiome composition, environment, or both. Abiotic factors such as temperature, water availability, and soil nutrients are known modifiers of heterosis expression; however, whether interactions between the soil microbial community and abiotic properties affect heterosis is largely unknown. To further understand how microbes influence heterosis, we characterized variation in maize heterosis when grown in soil inocula derived from historical maize farms or prairies. Although we did not observe consistent differences in heterosis among plants grown in these inocula, our observations affirm that microbial effects on heterosis are likely specific to the local microbial community. The introduction of a nutrient amendment resulted in greater heterosis in the presence of an agricultural soil inoculum than in the presence of a prairie soil inoculum. In addition, the interaction between soil inoculum and nutrient treatment structured bacterial and fungal community composition in the root endosphere. Root bacterial diversity was also significantly higher under nutrient-limited conditions. These results suggest that the contributions of genotype-by-environment interactions to heterosis are dependent on microbial context. They also provide direct evidence for the interactive effect of the soil microbial community and abiotic environment on heterosis and suggest that consideration of the soil microbial community may be helpful for breeding hybrid maize varieties for high performance in diverse environmental contexts. [Formula: see text] Copyright © 2026 The Author(s). This is an open access article distributed under the CC BY 4.0 International license . 

ABSTRACT It is more than 40 years since the era of transgenic plants began and more than 30 years after the cloning of the first plant disease resistance genes. Despite extensive progress in our mechanistic understanding and despite considerable sustained efforts in the commercial, nonprofit, academic and governmental sectors, the prospect of commercially viable plant varieties carrying disease resistance traits endowed by biotechnological approaches remains elusive. The cost of complying with the regulations governing the release of transgenic plants is often cited as the main reason for this lack of success. While this is undeniably a substantial hurdle, other transgenic traitshavebeen successfully commercialised. We argue that a significant portion of the challenges of producing crop varieties engineered for disease resistance is intrinsic to the trait itself. In this review, we briefly discuss the main approaches used to engineer plant disease resistance. We further discuss possible reasons why they have not been successful in a commercial context and, finally, we try to derive some lessons to apply to future efforts. 

Abstract Disease resistance in plants can be conferred by single genes of large effect or by multiple genes each conferring incomplete resistance. The latter case, termed quantitative resistance, may be difficult for pathogens to overcome through evolution due to the low selection pressures exerted by the actions of any single gene and, for some diseases, is the only identified source of genetic resistance. We evaluated quantitative resistance to 2 diseases of maize in a biparental mapping population as well as backcrosses to both parents. Quantitative trait locus analysis shows that the genetic architecture of resistance to these diseases is characterized by several modes of gene action including additivity as well as dominance, overdominance, and epistasis. Heterosis or hybrid vigor, the improved performance of a hybrid compared with its parents, can be caused by nonadditive gene action and is fundamental to the breeding of several crops including maize. In the backcross populations and a diverse set of maize hybrids, we find heterosis for resistance in many cases and that the degree of heterosis appears to be dependent on both hybrid genotype and disease. 

The southern corn leaf blight epidemic of 1970 caused estimated losses of about 16% for the U.S. corn crop, equivalent to about $8 billion in current terms. The epidemic was caused by the prevalence of Texas male sterile cytoplasm ( cms-T), used to produce most of the hybrid corn seed planted that year, combined with the emergence of a novel race of the fungus Cochliobolus heterostrophus that was exquisitely virulent on cms-T corn. Remarkably, the epidemic lasted just a single year. This episode has often been portrayed in the literature and textbooks over the last 50 years as a catastrophic mistake perpetrated by corn breeders and seed companies of the time who did not understand or account for the dangers of crop genetic uniformity. In this perspective article, we aim to present an alternative interpretation of these events. First, we contend that, rather than being caused by a grievous error on the part of the corn breeding and seed industry, this epidemic was a particularly unfortunate, unusual, and unlucky consequence of a technological advancement intended to improve the efficiency of corn seed production for America's farmers. Second, we tell the story of the resolution of the epidemic as an example of timely, meticulously applied research in the public sector for the public good. 

{"Abstract":["Data and code from the submitted manuscript "The interaction between abiotic and biotic soil factors modulates heterosis expression in maize". Descriptions of each file can be found in the README.txt file. The raw sequence data associated with this work is available in the NCBI Sequence Read Archive under BioProject PRJNA1235732."],"Other":["This work was supported by the United States National Science Foundation (award #IOS-2033621 to M.R.W., P.B.K., and M.K.) and the United States Department of Agriculture (#2022-67013-36672 to K.M.C.). The University of Kansas Medical Center Genomics Core is supported by the Kansas Intellectual and Developmental Disabilities Research Center (NIH U54 HD090216), the NIH S10 High End Instrumentation Grant (NIH S10 OD036343) and the Frontiers CTSA Grant (UL1TR002366)."]} 

SUMMARY In this study, we characterized a panel of 1264 maize near‐isogenic lines (NILs), developed from crosses between 18 diverse inbred lines and the recurrent parent B73, referred to as nested NILs (nNILs). In this study, 888 of the nNILs were genotyped using genotyping‐by‐sequencing (GBS). Subsequently, 24 of these nNILs, and all the parental lines, were re‐genotyped using a high‐density single nucleotide polymorphism (SNP) chip. A novel pipeline for calling introgressions, which does not rely on knowing the donor parent of each nNIL, was developed based on a hidden Markov model (HMM) algorithm. By comparing the introgressions detected using GBS data with those identified using chip data, we optimized the HMM parameters for analyzing the entire nNIL population. A total of 2969 introgressions were identified across the 888 nNILs. Individual introgression blocks ranged from 21 bp to 204 Mbp, with an average size of 17 Mbp. By comparing SNP genotypes within introgressed segments to the known genotypes of the donor lines, we determined that in about one third of the lines, the identity of the donors did not match expectation based on their pedigrees. We characterized the entire nNIL population for three foliar diseases. Using these data, we mapped a number of quantitative trait loci (QTL) for disease resistance in the nNIL population and observed extensive variation in effects among the alleles from different donor parents at most QTL identified. This population will be of significant utility for dissecting complex agronomic traits and allelic series in maize.