Cilia act as motile or sensory devices on the surface of most eukaryotic cells, and cilia dysfunction results in a variety of severe human pathologies, now collectively termed ciliopathies. Phylogenetically conserved intraflagellar transport (IFT) machinery, which is composed of IFT-A and IFT-B subcomplexes, mediates the bidirectional movement of IFT cargos that are required for the biogenesis, maintenance, and signaling of cilia. However, how IFT particles assemble at cilia base and turnaround at cilia tip are poorly understood. From a mutagenesis screen searching for C. elegans mutants with defective IFT turnaround at the ciliary tip, we identified a new
dyf-2 allele,
dyf-2(
jhu616), which encodes a mutant DYF-2 with a G361R alteration in conserved WD40 domain. In contrast to the reported null
dyf-2 allele in which cilia are severely truncated,
dyf-2(
jhu616) mutants possess superficially normal cilia, and IFT-A and IFT-B move together anterogradely, suggested that this mutation itself doesn't affect the IFT-A and IFT-B complex integrity. However, IFT-B components and its associated OSM-3 motor, but not IFT-A components and its associated kinesin-II motor, accumulate at the ciliary tip. Kymograph analysis indicates that only IFT-A moves retrogradely in
dyf-2(
jhu616). Surprisingly, the BBSome are not found associating with moving IFT particles in
dyf-2(
jhu616). Furthermore,
bbs-1(
jhu598), which encodes a mutant BBS-1 altered at conserved G207 site (G207D), was characterized as the mutant that fully recapitulates the defective IFT turnaround phenotypes of
dyf-2(
jhu616) in our screen. Further analyses support a model that the BBSome controls IFT complex assembly at the ciliary base, and then associate with anterograde IFT particles in a DYF-2 dependent way to the ciliary tip to regulate IFT reassembly and turnaround. The absence of the BBSome at the ciliary tip impairs the IFT retrograde integrity.