| Gene name | Protein name | Organism | Protein family | Key domains | Primary function | Subcellular localization | Interacting partners / complex context | Mutant phenotypes in *C. elegans* | Disease relevance / human ortholog |
|---|---|---|---|---|---|---|---|---|---|
| **bbs-4** | BBS-4; BBSome complex member bbs-4; Bardet-Biedl syndrome 4 protein homolog | *Caenorhabditis elegans* | BBS4 family; BBSome subunit | TPR-like helical domain superfamily; tetratricopeptide repeats (TPRs), consistent with a TPR α-solenoid/adaptor architecture (pqac-00000011, pqac-00000012, pqac-00000015) | Non-enzymatic trafficking adaptor subunit of the BBSome. Helps organize ciliary membrane protein trafficking, especially removal/degradative sorting of sensory receptors, and contributes to IFT particle assembly/turnaround through the BBSome rather than catalyzing a chemical reaction (pqac-00000001, pqac-00000002, pqac-00000020, pqac-00000029) | Localizes to cilia and the ciliary base in worms; in dyf-2 mutants accumulates around the ciliary base and loses normal ciliary localization. In broader BBS literature, BBS4/BBSome also associates with basal body, centrosomal/pericentriolar regions and centriolar satellites (pqac-00000010, pqac-00000021, pqac-00000024, pqac-00000009) | Directly interacts with **BBS-5** in worms; structurally connected within the BBSome to BBS1, BBS8, BBS9, and BBS18; assembled late into the BBSome after the BBS2-BBS7-BBS9 core and after incorporation of BBS1/BBS5/BBS8 in assembly models (pqac-00000002, pqac-00000015, pqac-00000016, pqac-00000036, pqac-00000037) | **Single mutants:** often normal in dye-filling/ciliogenesis assays but show defects in polycystin signaling. **bbs-4;bbs-5 double mutants:** strong ciliary dysfunction, IFT-A/IFT-B dissociation with altered velocities, receptor accumulation in cilia (e.g., PKD-2, OSM-9, ODR-10), and defective sensory/ciliary homeostasis (pqac-00000019, pqac-00000001, pqac-00000003, pqac-00000018) | Human ortholog **BBS4** is a Bardet-Biedl syndrome gene. Disease associations include Bardet-Biedl syndrome / Bardet-Biedl syndrome 4, retinitis pigmentosa, and polydactyly, supporting evolutionary conservation of BBS4-dependent ciliary trafficking (pqac-00000000) |


*Table: This table summarizes the core molecular and functional properties of *C. elegans* bbs-4/BBS-4, emphasizing its role as a TPR-containing BBSome subunit involved in ciliary trafficking and IFT-related processes. It also links worm findings to conserved human BBS4 disease relevance.*