ABSTRACT Dwarf mutants are valuable materials for investigating plant gene function and developing new crop varieties. In the present study, dwarf mutant (D-CK) and wild-type (W-CK) Sophora davidii (Franch.) Skeels plants foliarly sprayed with distilled water were used as controls, and dwarf mutants were treated with different concentrations of gibberellin A3 (GA3; 20, 40 and 60 mg L-1), brassinosteroid (BR; 12.5, 25 and 50 mg L-1); and auxin indole-3-acetic acid (IAA; 12.5, 25 and 50 mg L-1) to study the changes in plant height at 20, 40 and 60 d after exogenous hormone spraying. The changes in endogenous contents of IAA, GA3, BR, abscisic acid (ABA), jasmonic acid (JA), and salicylic acid (SA) and IAA:ABA ratio in the dwarf mutant plants were also measured at 20, 40 and 60 d after exogenous hormone application. The dwarf mutants reverted to the W-CK height phenotype after 60 d of exogenous spraying with different concentrations of GA3 and BR (except 50 mg·L-1), but after exogenous spraying with IAA, dwarf mutants did not revert to the W-CK height phenotype. Compared with D-CK plants, endogenous GA3, BR and IAA contents in dwarf mutant plants increased to some extent with exogenous spraying of GA3, BR and IAA. The results indicated that exogenous spraying of different concentrations of GA3 and BR regulated S. davidii plant height by promoting the secretion of endogenous GA3, BR, IAA and SA and inhibiting endogenous ABA secretion in dwarf mutant. The height of mutants was sensitive to exogenous GA3 and BR but not to exogenous IAA.

OBJECTIVE: The aim of this study was to evaluate the prevalence and spectrum of Nkx2.5 mutations associated with idiopathic atrial fibrillation (AF). METHODS: A cohort of 136 unrelated patients with idiopathic atrial fibrillation and 200 unrelated, ethnically matched healthy controls were enrolled. The coding exons and splice junctions of the Nkx2.5 gene were sequenced in 136 atrial fibrillation patients, and the available relatives of mutation carriers and 200 controls were subsequently genotyped for the identified mutations. The functional characteristics of the mutated Nkx2.5 gene were analyzed using a dual-luciferase reporter assay system. RESULTS: Two novel heterozygous Nkx2.5 mutations (p.N19D and p.F186S) were identified in 2 of the 136 unrelated atrial fibrillation cases, with a mutational prevalence of approximately 1.47%. These missense mutations co-segregated with atrial fibrillation in the families and were absent in the 400 control chromosomes. Notably, 2 mutation carriers also had congenital atrial septal defects and atrioventricular block. Multiple alignments of the Nkx2.5 protein sequences across various species revealed that the altered amino acids were completely conserved evolutionarily. Functional analysis demonstrated that the mutant Nkx2.5 proteins were associated with significantly reduced transcriptional activity compared to their wild-type counterpart. CONCLUSION: These findings associate the Nkx2.5 loss-of-function mutation with atrial fibrillation and atrioventricular block and provide novel insights into the molecular mechanism involved in the pathogenesis of atrial fibrillation. These results also have potential implications for early prophylaxis and allele-specific therapy of this common arrhythmia.