Alleles of a wall‐associated kinase gene account for three of the major northern corn leaf blight resistance loci in maize

0301 basic medicine NCLB ZmWAK&#8208 Plant Science 580 Plants (Botany) Htn1 Genes, Plant Zea mays 1307 Cell Biology resistance 03 medical and health sciences 10126 Department of Plant and Microbial Biology 1311 Genetics Ascomycota 1110 Plant Science Genetics [SDV.BV]Life Sciences [q-bio]/Vegetal Biology 10211 Zurich-Basel Plant Science Center Alleles Disease Resistance Plant Diseases Plant Proteins 2. Zero hunger WAKs Phosphotransferases Chromosome Mapping Cell Biology ZmWAK-RLK1 Plant Leaves RLK1 Ht2 Ht3
DOI: 10.1111/tpj.15183 Publication Date: 2021-02-06T00:35:55Z
ABSTRACT
SUMMARYNorthern corn leaf blight, caused by the fungal pathogen Setosphaeria turcica (anamorph Exserohilum turcicum), is one of the most devastating foliar diseases of maize (Zea mays). Four genes Ht1, Ht2, Ht3 and Htn1 represent the major sources of genetic resistance against the hemibiotrophic fungus S. turcica. Differential maize lines containing these genes also form the basis to classify S. turcica races. Here, we show that Ht2 and Ht3 are identical and allelic to the previously cloned Htn1 gene. Using a map‐based cloning approach and Targeting Induced Local Lesions in Genomes (TILLING), we demonstrate that Ht2/Ht3 is an allele of the wall‐associated receptor‐like kinase gene ZmWAK‐RLK1. The ZmWAK‐RLK1 variants encoded by Htn1 and Ht2/Ht3 differ by multiple amino acid polymorphisms that particularly affect the putative extracellular domain. A diversity analysis in maize revealed the presence of dozens of ZmWAK‐RLK1 alleles. Ht2, Ht3 and Htn1 have been described over decades as independent resistance loci with different race spectra and resistance responses. Our work demonstrates that these three genes are allelic, which has major implications for northern corn leaf blight resistance breeding and nomenclature of S. turcica pathotypes. We hypothesize that genetic background effects have confounded the classical description of these disease resistance genes in the past.
SUPPLEMENTAL MATERIAL
Coming soon ....
REFERENCES (42)
CITATIONS (41)