A promoter polymorphism defines distinct roles in anther development for Col‐0 and Ler‐0 alleles of Arabidopsis ACYL‐COA BINDING PROTEIN3

Abstract

Summary Acyl‐CoA‐Binding Proteins (ACBPs) bind acyl‐CoA esters and function in lipid metabolism. Although acbp3‐1, the ACBP3 mutant in Arabidopsis thaliana ecotype Col‐0, displays normal floral development, the acbp3‐2 mutant from ecotype Ler‐0 characterized herein exhibits defective adaxial anther lobes and improper sporocyte formation. To understand these differences and identify the role of ERECTA in ACBP3 function, the acbp3 mutants and acbp3‐erecta (er) lines were analyzed by microscopy for anther morphology and high‐performance liquid chromatography for lipid composition. Defects in Landsberg anther development were related to the ERECTA‐mediated pathway because the progenies of acbp3‐2 × La‐0 and acbp3‐1 × er‐1 in Col‐0 showed normal anthers, contrasting to that of acbp3‐2 in Ler‐0. Polymorphism in the regulatory region of ACBP3 enabled its function in anther development in Ler‐0 but not Col‐0 which harbored an AT‐repeat insertion. ACBP3 expression and anther development in acbp3‐2 were restored using ACBP3pro (Ler)::ACBP3 not ACBP3pro (Col)::ACBP3. SPOROCYTELESS (SPL), a sporocyte formation regulator activated ACBP3 transcription in Ler‐0 but not Col‐0. For anther development, the ERECTA‐related role of ACBP3 is required in Ler‐0, but not Col‐0. The disrupted promoter regulatory region for SPL binding in Col‐0 eliminates the role of ACBP3 in anther development.