Characterization of the molecular mechanism underlying the dwarfism of dsh mutant watermelon plants

Developing dwarf watermelon is a major objective among breeders. The dsh dwarf watermelon germplasm developed in our laboratory is genetically stable. We previously produced preliminary evidence that Cla010726, which encodes a gibberellin 20-oxidase-like protein, is the primary gene controlling dwarfism in watermelon. However, the underlying genetic mechanism was unknown. In this study, we characterized the spontaneous recessive mutant dsh, which is a gibberellin (GA)-deficient mutant. Many of the phenotypic traits of dsh plants are similar to those of known GA-deficient mutants. The dsh plants were sensitive to exogenous bioactive GAs, which increased seedling height. Moreover, a quantitative analysis of endogenous GA3 proved that the bioactive GA3 content was substantially lower than normal in dsh. Additionally, the T5 ClaGA20ox RNAi plants generally exhibited dwarfism, with short stems and internodes as well as small leaves and fruit. An examination of the transgenic plants carrying the ClaGA20ox1 promoter-GUS and mutant ClaGA20ox2 promoter-GUS constructs confirmed that two promoter sites are involved in the regulation of ClaGA20ox expression. Hence, mutations in the promoter of the GA20ox gene, which encodes a key enzyme involved in gibberellin biosynthesis, lead to the dwarfism of watermelon plants. The dsh mutant is a potentially useful germplasm resource for developing new watermelon varieties exhibiting dwarfism.