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Southern leaf blight (SLB) is a foliar disease caused by the fungus Cochliobolus heterostrophus infecting maize plants in humid, warm weather conditions. SLB causes production losses to corn producers in different regions of the world such as Latin America, Europe, India, and Africa. In this paper, we demonstrate a non-destructive method to quantify the signs of fungal infection in SLB-infected corn plants using a deep UV (DUV) fluorescence spectrometer, with a 248.6 nm excitation wavelength, to acquire the emission spectra of healthy and SLB-infected corn leaves. Fluorescence emission spectra of healthy and diseased leaves were used to train an Autoencoder (AE) anomaly detection algorithm—an unsupervised machine learning model—to quantify the phenotype associated with SLB-infected leaves. For all samples, the signature of corn leaves consisted of two prominent peaks around 450 nm and 325 nm. However, SLB-infected leaves showed a higher response at 325 nm compared to healthy leaves, which was correlated to the presence of C. heterostrophus based on disease severity ratings from Visual Scores (VS). Specifically, we observed a linear inverse relationship between the AE error and the VS (R2 = 0.94 and RMSE = 0.935). With improved hardware, this method may enable improved quantification of SLB infection versus visual scoring based on e.g., fungal spore concentration per unit area and spatial localization. [ABSTRACT FROM AUTHOR]

These papers cover established and emerging viral tools for functional genomics in maize, a genomic study of maize resistance genes, and the identification and detailed characterization of maize genes involved in pathogen resistance and microbial genes involved in pathogenicity. The first identification of a plant disease resistance gene, I Hm1 i (Johal & Briggs, [12]), and of a plant disease susceptibility gene, I T-urf13 i (Dewey et al., [7]), occurred in maize. Thatcher, Jung et al. ([35], this issue) took advantage of the recent availability of a set of diverse maize genome sequences to characterize the diversity of NLR genes in maize as well as the maize relative I Zea luxurians i . Maize ( I Zea mays i ) is an annual grass belonging to the tribe Andropogoneae of the family Gramineae. [Extracted from the article]

Summary: Southern leaf blight (SLB), caused by the necrotrophic fungal pathogen Cochliobolus heterostrophus (anamorph Bipolaris maydis), is a major foliar disease which causes significant yield losses in maize worldwide. A major quantitative trait locus, qSLB3.04, conferring recessive resistance to SLB was previously mapped on maize chromosome 3.Using a combination of map‐based cloning, association analysis, ethyl methanesulfonate and transposon mutagenesis, and CRISPR‐Cas9 editing, we demonstrate that a leucine‐rich repeat receptor‐like kinase gene which we have called ChSK1 (Cochliobolus heterostrophus Susceptibility Kinase 1) at qSLB3.04 causes increased susceptibility to SLB. Genes of this type have generally been associated with the defense response.We present evidence that ChSK1 may be associated with suppression of the basal immune response.These findings contribute to our understanding of plant disease susceptibility genes and the potential to use them for engineering durable disease resistance. [ABSTRACT FROM AUTHOR]

Summary: Plant genotype strongly affects disease resistance, and also influences the composition of the leaf microbiome. However, these processes have not been studied and linked in the microevolutionary context of breeding for improved disease resistance. We hypothesised that broad‐spectrum disease resistance alleles also affect colonisation by nonpathogenic symbionts.Quantitative trait loci (QTL) conferring resistance to multiple fungal pathogens were introgressed into a disease‐susceptible maize inbred line. Bacterial and fungal leaf microbiomes of the resulting near‐isogenic lines were compared with the microbiome of the disease‐susceptible parent line at two time points in multiple fields.Introgression of QTL from disease‐resistant lines strongly shifted the relative abundance of diverse fungal and bacterial taxa in both 3‐wk‐old and 7‐wk‐old plants. Nevertheless, the effects on overall community structure and diversity were minor and varied among fields and years. Contrary to our expectations, host genotype effects were not any stronger in fields with high disease pressure than in uninfected fields, and microbiome succession over time was similar in heavily infected and uninfected plants.These results show that introgressed QTL can greatly improve broad‐spectrum disease resistance while having only limited and inconsistent pleiotropic effects on the leaf microbiome in maize. [ABSTRACT FROM AUTHOR]

Southern leaf blight ([SLB], causal agent Cochliobolus heterostrophus) is an important fungal disease of maize (Zea mays L.). Teosinte (Z. mays ssp. parviglumis), the wild progenitor of maize, offers a novel source of resistance alleles that may have been lost during domestication. The aims of this study were to identify teosinte alleles that, when present in a temperate maize background, confer a significant level of resistance to SLB. Ten populations of BC4S2 near isogenic lines (NILs), developed by crossing 10 different teosinte accessions to the maize inbred B73, comprising 774 lines in total, were screened for SLB resistance. Quantitative trait locus (QTL) analysis identified four significant QTL associated with SLB in bins 2.04, 3.04, 3.05, and 8.05. Sixteen individual NILs which were significantly different to the susceptible recurrent parent, B73 and which were carrying at least one of the teosinte-derived resistance alleles were used to develop F2:3 populations by crossing each to B73 followed by two rounds of self-pollination. These F2:3 populations were evaluated for SLB resistance and genotyped at the loci of interest. In 13 of 19 cases single marker analysis validated allelic substitution effects predicted from the original NIL population analysis, while in five cases we were not able to validate the effects and in one case a significant effect was detected in the opposite to the predicted direction. An allele at the QTL in bin 2.04 was shown to confer resistance to both SLB and a second maize foliar disease, gray leaf spot (GLS). [ABSTRACT FROM AUTHOR]

Plant disease resistance is often mediated by nucleotide binding-leucine rich repeat (NLR) proteins which remain auto-inhibited until recognition of specific pathogen-derived molecules causes their activation, triggering a rapid, localized cell death called a hypersensitive response (HR). Three domains are recognized in one of the major classes of NLR proteins: a coiled-coil (CC), a nucleotide binding (NB-ARC) and a leucine rich repeat (LRR) domains. The maize NLR gene Rp1-D21 derives from an intergenic recombination event between two NLR genes, Rp1-D and Rp1-dp2 and confers an autoactive HR. We report systematic structural and functional analyses of Rp1 proteins in maize and N. benthamiana to characterize the molecular mechanism of NLR activation/auto-inhibition. We derive a model comprising the following three main features: Rp1 proteins appear to self-associate to become competent for activity. The CC domain is signaling-competent and is sufficient to induce HR. This can be suppressed by the NB-ARC domain through direct interaction. In autoactive proteins, the interaction of the LRR domain with the NB-ARC domain causes de-repression and thus disrupts the inhibition of HR. Further, we identify specific amino acids and combinations thereof that are important for the auto-inhibition/activity of Rp1 proteins. We also provide evidence for the function of MHD2, a previously uncharacterized, though widely conserved NLR motif. This work reports several novel insights into the precise structural requirement for NLR function and informs efforts towards utilizing these proteins for engineering disease resistance. [ABSTRACT FROM AUTHOR]

Maize inbred lines NC292 and NC330 were derived by repeated backcrossing of an elite source of southern leaf blight (SLB) resistance (NC250P) to the SLB-susceptible line B73, with selection for SLB resistance among and within backcross families at each generation. Consequently, while B73 is very SLB susceptible, its sister lines NC292 and NC330 are both SLB resistant. Previously, we identified the 12 introgressions from NC250P that differentiate NC292 and NC330 from B73. The goals of this study were to determine the effects of each introgression on resistance to SLB and to two other foliar fungal diseases of maize, northern leaf blight and gray leaf spot. This was achieved by generating and testing a set of near isogenic lines carry single or combinations of just two or three introgressions in a B73 background. Introgressions 3B, 6A, and 9B (bins 3.03-3.04, 6.01, and 9.02-9.03) all conferred significant levels of SLB resistance in the field. Introgression 6A was the only introgression that had a significant effect on juvenile plant resistance to SLB. Introgressions 6A and 9B conferred resistance to multiple diseases. [ABSTRACT FROM AUTHOR]

Southern leaf blight (SLB) is a foliar necrotrophic disease of maize (Zea mays L.) caused by the ascomycete fungus Cochliobolus heterostrophus (Drechs.) Drechs. It is particularly important in warm humid parts of the world where maize is cultivated, such as the southern Atlantic coast area of the United States and parts of India, Africa, and Western Europe. Quantitative trait loci (QTL) for resistance to SLB disease caused by C. heterostrophus race O were identified in three maize recombinant inbred populations assessed in two environments: Clayton, NC, in the summer and Homestead, FL, in the winter. The three populations were derived from the crosses B73 × CML254, CML254 × B97, and B97 × Ki14. Each of these populations was derived from a cross between a temperate maize line (B73 or B97) and a tropical maize line (Ki14 or CML254). Quantitative trait loci were identified by separate analysis of each population and by joint connected and disconnected analyses of all the populations. The most significant QTL identified were on chromosomes 3, 8, 9, and 10. Joint analysis led to more precise position estimates than separate analysis in each case. Results are discussed in the context of previous SLB QTL analysis studies and a recent flowering time QTL study that used the same populations. The chromosome 8 and 9 QTL colocalized with previously identified flowering time QTL, which suggested that the perceived effect on SLB resistance at these QTL may have been mediated through an effect on flowering time. [ABSTRACT FROM AUTHOR]

Nested association mapping (NAM) offers power to resolve complex, quantitative traits to their causal loci. The maize NAM population, consisting of 5,000 recombinant inbred lines (RILs) from 25 families representing the global diversity of maize, was evaluated for resistance to southern leaf blight (SLB) disease. Joint-linkage analysis identified 32 quantitative trait loci (QTLs) with predominantly small, additive effects on SLB resistance. Genome-wide association tests of maize HapMap SNPs were conducted by imputing founder SNP genotypes onto the NAM RILs. SNPs both within and outside of QTL intervals were associated with variation for SLB resistance. Many of these SNPs were within or near sequences homologous to genes previously shown to be involved in plant disease resistance. Limited linkage disequilibrium was observed around some SNPs associated with SLB resistance, indicating that the maize NAM population enables high-resolution mapping of some genome regions. [ABSTRACT FROM AUTHOR]

Fifty publications on the mapping of maize disease resistance loci were synthesized. These papers reported the locations of 437 quantitative trait loci (QTL) for disease (dQTL), 17 resistance genes (R-genes), and 25 R-gene analogs. A set of rules was devised to enable the placement of these loci on a single consensus map, permitting analysis of the distribution of resistance loci identified across a variety of maize germplasm for a number of different diseases. The confidence intervals of the dQTL were distributed over all 10 chromosomes and covered 89% of the genetic map to which the data were anchored. Visual inspection indicated the presence of clusters of dQTL for multiple diseases. Clustering of dQTL was supported by statistical tests that took into account genome-wide variations in gene density. Several novel clusters of resistance loci were identified. Evidence was also found for the association of dQTL with maturity-related QTL. It was evident from the distinct dQTL distributions for the different diseases that certain breeding schemes may be more suitable for certain diseases. This review provides an up-to-date synthesis of reports on the locations of resistance loci in maize. [ABSTRACT FROM AUTHOR]

Southern leaf blight (SLB), gray leaf spot (GLS), and northern leaf blight (NLB) are all important foliar diseases impacting maize production. The objectives of this study were to identify quantitative trait loci (QTL) for resistance to these diseases in a maize recombinant inbred line (RIL) population derived from a cross between maize lines Ki14 and B73, and to evaluate the evidence for the presence genes or loci conferring multiple disease resistance (MDR). Each disease was scored in multiple separate trials. Highly significant correlations between the resistances and the three diseases were found. The highest correlation was identified between SLB and GLS resistance (r = 0.62). Correlations between resistance to each of the diseases and time to flowering were also highly significant. Nine, eight, and six QTL were identified for SLB, GLS, and NLB resistance, respectively. QTL for all three diseases colocalized in bin 1.06, while QTL colocalizing for two of the three diseases were identified in bins 1.08 to 1.09, 2.02/2.03, 3.04/3.05, 8.05, and 10.05. QTL for time to flowering were also identified at four of these six loci (bins 1.06, 3.04/3.05, 8.05, and 10.05). No disease resistance QTL was identified at the largest-effect QTL for flowering time in bin 10.03. [ABSTRACT FROM AUTHOR]