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Published on: October 28, 2021
Identification of race 2 anthracnose resistance Quantitative Trait Loci using biparental and association panel of
Bed Prakash Bhatta1,2,3, Lakhvir Kaur1,2, Edgar Correa1,2,4
1Department of Horticultural Sciences, Texas A&M University, College Station, TX, 77843, USA.
Abstract:
Anthracnose is an important fungal disease in cucurbits, caused by the pathogen Colletotrichum orbiculare, which negatively affects all the aboveground parts of the plant. Race 2 anthracnose causes severe economic damage in watermelon. The objective of the study was to identify race 2 anthracnose resistance QTL in a biparental mapping population and association mapping panel. For the F2 biparental population (N = 188), resistant and susceptible parents were PI 189225 (C. amarus) and 'New Hampshire Midget' (C. lanatus), respectively. The association mapping panel consisted of 1,008 watermelon germplasm accessions (C. amarus (N = 72), C. lanatus (N = 894), and C. mucosospermus (N = 42)). The biparental mapping population identified a significant QTL for race 2 anthracnose resistance, Qar2-3 (LOD = 4.53), on chromosome 3 from the resistant parent, PI 189225. In the association mapping panel, MLM and BLINK models identified a significant marker S06_9279285 and S08_ 28493121 (LOD > 5) on chromosomes 6, Qar2-6, and 8, Qar2-8, respectively, conferring resistance to anthracnose race 2. Three receptor kinase genes (CaUC03G056690, CaUC03G056730, and CaUC03G056740) were close to the Qar2-3. Similarly, leucine-rich receptor-like protein kinase family protein (ClCG06G007520) and serine/threonine protein kinase (ClCG08G016080) genes were close to the Qar2-6 and Qar2-8, respectively. Inconsistent results on QTL locations between the biparental and association mapping populations could be due to various factors including selected germplasm, minor allele frequency, linkage disequilibrium (LD), LD decay, and genotyping. Future research should focus on identifying and understanding the roles of LRR-RLKs genes in governing resistance.
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