As a component of the IFT complex A (IFT-A), a complex required for retrograde ciliary transport and entry into cilia of G protein-coupled receptors (GPCRs), it is required in ciliogenesis and ciliary protein trafficking (By similarity). Involved in cilia formation during neuronal patterning. Acts as a negative regulator of Shh signaling. Required to recruit TULP3 to primary cilia (PubMed:19000668, PubMed:21209331). Component of the IFT complex A (IFT-A) complex. IFT-A complex is divided into a core subcomplex composed of IFT122:IFT140:WDR19 which is associated with TULP3 and a peripheral subcomplex composed of IFT43:WDR35:TTC21B. Interacts with IFT43:WDR35; the interaction connects the 2 IFT-A subcomplexes. Interacts with IFTAP; the interaction associates IFTAP with IFT-A complex. Localizes to photoreceptor connecting cilia. Expression at least from 7.5 dpc onwards throughout embryonic development with lower levels at 7.5 dpc and 9.5 dpc. Ubiquitously expressed at 11.5 dpc. Forms the trimeric core subcomplex IFT122:IFT140:WDR19 via the C-terminal region, whereas it interacts with IFT43:WDR35 via the N-terminal region containing the WD repeats. Embryonic lethal (manifesting between 11.5 dpc and 13.5 dpc). Multiple developmental defects (exencephaly, situs viscerum inversus, delay in turning, hemorrhage and defects in limb development). In the node, primary cilia are absent or malformed in homozygous mutant and heterozygous embryos, respectively. The Shh signaling pathway is impaired in both neural tube patterning (expansion of motoneurons and rostro-caudal level-dependent contraction or expansion of the dorso-lateral interneurons) and limb patterning (ectrosyndactyly). The proteolytic processing of Gli3 is altered. Defects in Ift122 are the cause of the sister of open brain (sopb) phenotype, a mutant that induces embryonic lethality and generates primary cilia with features of defective retrograde intraflagellar transport. Extended N-terminus.