Abstract
The zig-1 mutant of Arabidopsis lacking Qb-SNARE VTI11 shows abnormal shoot gravitropism and morphological defects. VTI11 functions in vesicular trafficking between trans-Golgi network and vacuoles. To understand the molecular basis of vesicle transport involved in physiological function of higher plants, we have analyzed zig suppressor(zip) mutants that can suppress defects of zig-1.
The zig suppresor4 is recessive mutant that partially suppresses defects of zig-1. Based on the map position, a mutation was found in splicing acceptor site of the gene encoding homolog of adaptor protein complex-3(AP-3) μ3 subunit. AP complexes have been known as coat proteins of transport vesicles in yeast and animal cells.
T-DNA insertion mutants of this gene also suppressed defects zig-1 as well as zip4. Finally, we identified ZIP4 as AP-3μ3 by complementation analysis. These results indicate that loss of function mutation of AP-3 μ3 acts as suppressor of zig-1.
