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Identifies Cmer-2 as a genetic factor controlling dwarf architecture in melon, suggesting new breeding avenues.
As a high-value horticultural crop, melon cultivation requires substantial labor input for plant architecture management. Dwarf architecture is a desirable trait for melon breeding, as it simplifies plant management and enables higher planting density. In this study, we identified a spontaneous dwarf mutant, HMN-d, derived from a cantalupensis melon HMN. Compared to HMN, HMN-d exhibited a 70% reduction in plant height with unchanged node number. BSA-seq mapped the mutation to a single 1.86 Mb interval on chromosome 7 containing CmER, a known regulator of melon height. A novel loss-of-function allele, Cmer-2, introducing a premature stop codon, was identified in this region of HMN-d. Linkage analysis using 1455 F2 individuals via KASP marker developed from the Cmer-2 variant revealed complete co-segregation with the dwarf phenotype. Allelism analysis further demonstrated that Cmer-2 is allelic to Cmer-1, a previously identified loss-of-function allele of CmER. CmER knockout lines generated by gene editing recapitulated the dwarf phenotype, directly confirming that loss of CmER function is sufficient to cause dwarfism. Collectively, these findings establish Cmer-2 as the causal variant underlying the dwarf phenotype and provide valuable genetic resources for melon plant architecture improvement and for dissecting the mechanisms of height regulation.
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Zhou et al. (2026) studied this question.
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