Abstract
Key message
A novel locus was discovered on chromosome 7 associated with a lesion mimic in maize; this lesion mimic had a quantitative and heritable phenotype and was predicted better via subset genomic markers than whole genome markers across diverse environments.
Abstract
Lesion mimics are a phenotype of leaf micro-spotting in maize (Zea mays L.), which can be early signs of biotic or abiotic stresses. Dissecting its inheritance is helpful to understand how these loci behave across different genetic backgrounds. Here, 538 maize recombinant inbred lines (RILs) segregating for a novel lesion mimic were quantitatively phenotyped in Georgia, Texas, and Wisconsin. These RILs were derived from three bi-parental crosses using a tropical pollinator (Tx773) as the common parent crossed with three inbreds (LH195, LH82, and PB80). While this lesion mimic was heritable across three environments based on phenotypic (\({H}_{\mathrm{p}}\) = 0.68) and genomic (\({H}_{\mathrm{g}}\) = 0.91) data, transgressive segregation was observed. A genome-wide association study identified a single novel locus on chromosome 7 (at 70.6 Mb) also covered by a quantitative trait locus interval (69.3–71.0 Mb), explaining 11–15% of the variation, depending on the environment. One candidate gene identified in this region, Zm00001eb308070, is related to the abscisic acid pathway involving in cell death. Genomic predictions were applied to genome-wide markers (39,611 markers) contrasted with a marker subset (51 markers). Population structure explained more variation than environment in genomic prediction, but other substantial genetic background effects were additionally detected. Subset markers explained substantially less genetic variation (24.9%) for the lesion mimic than whole genome markers (55.4%) in the model, yet predicted the lesion mimic better (0.56–0.66 vs. 0.26–0.29). These results indicate this lesion mimic phenotype was less affected by environment than by epistasis and genetic background effects, which explain its transgressive segregation.
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The datasets generated during and/or analyzed during the current study are available from the corresponding author on reasonable request.
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Funding
Texas Corn Producers Board supported this study. USDA-NIFA-AFRI project Award Nos. 2020-68013-32371 and 2021-67013-33915), Texas A&M AgriLife Research, USDA-NIFA-HATCH, the Eugene Butler Endowed Chair and USDA grant (1024073) in WI and GA. We appreciate the help of WI and GA crews as well as graduate students, staff, and undergraduate and high school employees of the Texas A&M Quantitative Genetics and Maize Breeding Program for their hard work and effort in maintaining this experiment, Dustin Eilert and Marina Borsecnik at University of Wisconsin, Madison, and Naomi Rodman at the University of Georgia.
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All authors contributed to the study conception and design. Material preparation, data collection, genomic sequencing, growing materials in diverse environments and analysis were performed by AA, SCM, CIC, VI, JW, JIV, NS, TI, J-MA, JW, NDL, MAS, MB, JH, CDJ. The first draft of the manuscript was written by Alper Adak, and all authors commented on previous versions of the manuscript. All authors read and approved the final manuscript.
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Communicated by Jiankang Wang.
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Adak, A., Murray, S.C., Calderón, C.I. et al. Genetic mapping and prediction for novel lesion mimic in maize demonstrates quantitative effects from genetic background, environment and epistasis. Theor Appl Genet 136, 155 (2023). https://doi.org/10.1007/s00122-023-04394-y
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DOI: https://doi.org/10.1007/s00122-023-04394-y