A mutation in the brassinosteroid biosynthesis gene disrupts vegetative and reproductive development and the salt stress response in squash ().

A mutant with multiple defects in growth and development has been identified and characterized. The mutant displayed a dwarf phenotype with dark green and shrinking leaves, shortened internodes and petioles, shorter but thicker roots and greater root biomass, and reduced fertility. The causal mutation of the phenotype was found to disrupt gene , the squash orthologue of the brassinosteroid (BR) biosynthesis gene , encoding for 7-dehydrocholesterol reductase. A single nucleotide transition (G > A) causes a splicing defect in intron 6 that leads to a premature stop codon and a truncated CpDWF5 protein. The mutation co-segregated with the dwarf phenotype in a large BCS segregating population. The reduced expression of and brassinolide (BL) content in most mutant organs, and partial rescue of the mutant phenotype by exogenous application of BL, showed that the primary cause of the dwarfism in is a BR deficiency. The results showed that in , is not only a positive growth regulator of different plant organs but also a negative regulator of salt tolerance. During germination and the early stages of seedling development, the dwarf mutant was less affected by salt stress than the wild type, concomitantly with a greater upregulation of genes associated with salt tolerance, including those involved in abscisic acid (ABA) biosynthesis, ABA and Ca signaling, and those coding for cation exchangers and transporters.