Abstract
The Small Acidic Protein 1 (SMAP1) gene is responsible for the anti-auxin resistant mutation, aar1, and encodes a factor that mediates the synthetic auxin 2,4-D response. SMAP1 functions upstream of the AUX/IAA degradation step in auxin signaling and physically interacts to COP9 signalosome (CSN) in Arabidopsis extract. To investigate genetic relationship between CSN and SMAP1, the aar1 mutant was crossed with a weak csn mutant, csn5a-1. The double mutant aar1-1 csn5a-1 shows extremely short hypocotyls and slower root growth than the single mutants. The double mutant also showed relatively more auxin resistant than its parent lines and extremely dwarf phenotype in adult stage. The introduction 35S:SMAP1-GFP gene to the aar1-1 csn5a-1 background restored hypocotyl length and dwarf phenotype, suggesting that the luck of the SMAP1 gene results to the morphological defects of the double mutant. Although the aar1 mutant is morphologically indistinguishable to wild type except showing long hypocotyl, the phenotype of the double mutants unveiled the significance of SMAP1 for plant growth and development when CSN function is diminished.
