The Arabidopsis zigzgag (zig) is a loss-of-function mutant of Qb-SNARE VTI11 which is involved in vesicle trafficking between the trans-Golgi network (TGN) and vacuoles. zig-1 exhibits abnormality in both shoot gravitropism and morphology. To elucidate the molecular network of the post-Golgi membrane trafficking in plant cells, we have isolated the suppressor mutants of zig. Here we report zig suppressor 2 (zip2) and zip4 that are recessive mutants and partially suppress abnormality in both gravitropism and morphology. ZIP2 encodes AtVPS41/AtVAM2 protein that is thought to be an Arabidopsis ortholog of yeast Vps41p/Vam2p, which is involved in protein sorting to vacuoles as a subunit of the tethering complex HOPS. Yeast Vps41p is also proposed to function in budding of adaptor protein (AP)-3-coated vesicles from the Golgi. The zip2 mutation is a missense mutation in a conserved amino acid of a putative clathrin heavy chain repeat (CHCR) domain. AtVPS41 is a single-copy gene in the Arabidopsis genome and the T-DNA insertion mutant appears to be lethal, whereas the zip2 single mutant showed no obvious phenotype. On the other hand, zip4 is a loss-of-function mutant of a putative ortholog of the yeast AP-3 mu subunit. In addition, loss-of-function mutants of other subunits of AP-3, ap-3beta and ap-3delta, also exhibit a suppressive effect on the zig-1 phenotype. Although these genes are also single-copy genes in the genome, the loss-of-function mutants of AP-3 grow normally. Our results suggest that AtVPS41 and AP-3 play roles in the proper function of the post-Golgi trafficking network and support membrane trafficking to vacuoles.