Abstract
The Arabidopsis zigzag (zig) is a loss-of-function mutant of Qb-SNARE VTI11, which is involved in vesicle trafficking pathway from trans-Golgi network (TGN) to prevacuolar compartment (PVC)/vacuole. zig mutant exhibits abnormality in shoot gravitropism and morphological defects in leaves and stems. To investigate molecular genetic network of the post-Golgi trafficking in Arabidopsis, we have analyzed the suppressor mutants of zig. zip (zigzag suppressor) 3, which is a loss of function mutation of AtVPS35b, partially suppressed phenotype of zig. Considering homology to yeast Vps35p, it is thought that AtVPS35 is involved in PVC-TGN retrograde transport as a component of the retromer complex together with AtVPS29 and AtVPS26. We found that zig phenotype is also suppressed both by T-DNA insertion mutation of AtVPS26b and by maigo1-1 mutation that causes reduced expression of AtVPS29. The results suggest that impairment in PVC-TGN retrograde transport suppresses functional defects of VTI11.
