| Organism | Gene Name | Mutant Phenotypes | Key Findings | References |
|---|---|---|---|---|
| *Caenorhabditis elegans* | **dyf-3** (UniProt Q6I6D4; CLUAP1/IFT38 ortholog) | Fully penetrant dye-filling defects in amphid and phasmid neurons (0% dye fill reported for dyf-3 alleles), shortened/severely defective sensory cilia, abnormal accumulation of GFP::DLK-1 in ciliary regions, ivermectin resistance associated with amphid/cilia dysfunction (pqac-00000006, pqac-00000020, pqac-00000022, pqac-00000023) | dyf-3 encodes a conserved IFT-B complex component required for sensory cilium development and intraflagellar transport; it is regulated as a ciliary gene by DAF-19/RFX via an X-box motif and functions in ciliated sensory neurons (pqac-00000001, pqac-00000019, pqac-00000021, pqac-00000028, pqac-00000029) | Sun et al., 2025, G3, https://doi.org/10.1093/g3journal/jkaf004; Efimenko et al., 2006, Mol Biol Cell, https://doi.org/10.1091/mbc.e06-04-0260; Brinzer et al., 2021, bioRxiv, https://doi.org/10.1101/2021.10.22.465401 (pqac-00000001, pqac-00000006, pqac-00000020, pqac-00000022, pqac-00000028, pqac-00000029) |
| Zebrafish | **qilin** | Cilia degeneration/loss in pronephric duct, cystogenesis/polycystic kidney-like phenotype; morpholino knockdown produces more severe early cilia loss than some genetic mutants, consistent with maternal contribution masking early phenotypes (pqac-00000030, pqac-00000031, pqac-00000032) | qilin is the zebrafish ortholog of dyf-3/CLUAP1 and is required for cilia assembly and maintenance; zebrafish data support an evolutionarily conserved role in ciliogenesis and renal cilia integrity (pqac-00000030, pqac-00000031, pqac-00000034) | Pasek et al., 2012, *Cilia*, https://doi.org/10.1186/2046-2530-1-20 (summarizing prior zebrafish work) (pqac-00000030, pqac-00000031, pqac-00000034) |
| Mouse | **Cluap1** | Mid-gestation embryonic lethality; failure of embryonic turning; enlarged pericardial sac; neural tube defects/kinks; complete loss of primary cilia in examined tissues; repressed Sonic hedgehog signaling with reduced *Ptch1* and *Gli1* expression (pqac-00000014, pqac-00000015, pqac-00000016, pqac-00000018) | Cluap1 localizes to primary cilia/axoneme and is essential for ciliogenesis in vivo; mammalian loss causes severe developmental defects attributable to absent cilia and impaired Hedgehog signaling, establishing conserved IFT-B function (pqac-00000014, pqac-00000015, pqac-00000016, pqac-00000017) | Pasek et al., 2012, *Cilia*, https://doi.org/10.1186/2046-2530-1-20; Bangs & Anderson, 2017, Cold Spring Harb Perspect Biol, https://doi.org/10.1101/cshperspect.a028175 (pqac-00000014, pqac-00000015, pqac-00000016, pqac-00000018) |
| Human / human cell models | **CLUAP1 / IFT38** | In CRISPR-edited hTERT-RPE1 cells, CLUAP1 knockout causes loss of cilia, increased filamentous actin, and impaired cell migration; disease-association resources link IFT38 to Joubert syndrome, Leber congenital amaurosis, skeletal abnormalities, obesity disorder, and type 2 diabetes mellitus (pqac-00000013, pqac-00000035, pqac-00000036, pqac-00000038, pqac-00000000) | Human CLUAP1/IFT38 is an IFT-B2/peripheral IFT-B subunit with a calponin homology domain that binds IFT80 and forms a heterodimer with IFT57; it contributes structurally to IFT-B assembly and ciliogenesis, and may have separable roles in actin organization/cell migration (pqac-00000002, pqac-00000007, pqac-00000008, pqac-00000010, pqac-00000013, pqac-00000035) | Taschner et al., 2016, EMBO J, https://doi.org/10.15252/embj.201593164; Beyer et al., 2018, Mol Cell Proteomics, https://doi.org/10.1074/mcp.ra117.000487; Open Targets Platform association summary (pqac-00000000, pqac-00000002, pqac-00000007, pqac-00000010, pqac-00000013, pqac-00000035) |


*Table: This table compares the DYF-3/CLUAP1/IFT38 ortholog across worms, zebrafish, mouse, and human systems, summarizing mutation phenotypes, conserved biological roles, and representative references. It is useful for quickly linking the C. elegans gene to broader cilia biology and disease relevance.*