A major QTL conferring tolerance to radish (Raphanus sativus) root cracking was mapped for the first time and two calcium regulatory genes were identified that positively associated with the cracking phenomenon. Root cracking is a severe physiological disorder that significantly decreases the yield and commercial value of radish. The genetic and physiological mechanisms underlying this root cracking disorder have not been characterized. In this study, quantitative trait loci (QTLs) putatively associated with radish root cracking were mapped. Ten QTLs were distributed in six linkage groups, among these QTLs, 'RCr1' in LG1 was detected over 3 consecutive years and was considered to be a major QTL for root cracking. The QTL 'RCr1' was responsible for 4.47-18.11% of variance in the root cracking phenotype. We subsequently identified two candidate genes, RsANNAT and RsCDPK. Both genes encode proteins involved in calcium binding, ion transport, and Ca2+ signal transduction, which are important for regulating plant development and adaptations to the environment. These genes were co-localized to the major QTL region. Additionally, we analyzed physiological changes (i.e., root firmness, cell wall content, and cell-wall-bound calcium content) in two parental lines during different developmental stages. Moreover, we observed that the RsANNAT and RsCDPK expression levels are positively correlated with Ca2+ contents in the roots of the cracking-tolerant '835' cultivar. Thus, these genes may influence root cracking. The data provided herein may support the useful information to understand root cracking behavior in radish and may enable breeders to develop new cultivars exhibiting increased tolerance to root and fruit cracking.
Keywords: Calcium; Calmodulin-dependent protein kinase (CDPK); Cell wall; Quantitative trait loci (QTLs); Radish; Root cracking.