Affinage

CCDC73

Coiled-coil domain-containing protein 73 · UniProt Q6ZRK6

Length
1079 aa
Mass
124.2 kDa
Annotated
2026-04-28
4 papers in source corpus 2 papers cited in narrative 2 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CCDC73 is a component of the double-headed inner dynein arm f (IDAf) complex in cilia, where it physically interacts with DNAH10, CFAP57, and DYNLL1 to support proper IDAf assembly and ciliary motility; loss of DNAH10 leads to reduced CCDC73 expression and defective IDAf complex formation (PMID:40898283). Ccdc73 knockout mice show no detectable defects in spermatogenesis or male fertility under laboratory conditions, indicating that CCDC73 is dispensable for these processes (PMID:29563520).

Mechanistic history

Synthesis pass · year-by-year structured walk · 2 steps
  1. 2018 Medium

    Whether CCDC73 is required for spermatogenesis was unknown; CRISPR/Cas9 knockout in mice revealed that Ccdc73 is dispensable for sperm production and male fertility, narrowing the search for its essential function to other tissues or contexts.

    Evidence CRISPR/Cas9 knockout mouse with histological, sperm count, and fertility analyses

    PMID:29563520

    Open questions at the time
    • Single-lab study; independent replication in other mouse strains not reported
    • Ciliary motility and respiratory phenotypes were not assessed in these knockout mice
    • Compensatory mechanisms by paralogous proteins were not investigated
  2. 2025 Medium

    The molecular context of CCDC73 was resolved by showing it physically associates with DNAH10, CFAP57, and DYNLL1 within the IDAf complex, and that DNAH10 loss destabilizes CCDC73 expression and disrupts IDAf assembly, establishing CCDC73 as a structural component of this ciliary dynein arm.

    Evidence Reciprocal co-immunoprecipitation, immunostaining, proteomics, and Dnah10 knockout mouse model

    PMID:40898283

    Open questions at the time
    • Direct Ccdc73 knockout ciliary motility phenotype has not been characterized
    • No structural model of CCDC73 within the IDAf complex exists
    • Whether CCDC73 loss alone is sufficient to disrupt IDAf assembly remains untested

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unknown whether CCDC73 loss in ciliated epithelia (e.g., airway) causes primary ciliary dyskinesia-like phenotypes, and the precise structural role of CCDC73 within the IDAf complex is unresolved.
  • No human genetic studies linking CCDC73 mutations to disease
  • No in vitro reconstitution or cryo-EM structure of CCDC73-containing IDAf complex
  • Tissue-specific and conditional knockout phenotypes not explored

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005198 structural molecule activity 1
Localization
GO:0005929 cilium 1
Pathway
R-HSA-1852241 Organelle biogenesis and maintenance 1
Partners
CFAP57DNAH10DYNLL1
Complex memberships
IDAf (inner dynein arm f)

Evidence

Reading pass · 2 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2018 Ccdc73 knockout mice generated by CRISPR/Cas9 are fertile with no detectable difference in testis/body weight ratios, epididymal sperm counts, or testicular and epididymal histology compared to wild-type mice, indicating Ccdc73 is dispensable for spermatogenesis and male fertility in mice under laboratory conditions. CRISPR/Cas9 knockout mouse, histology, sperm count analysis Scientific reports Medium 29563520
2025 CCDC73 physically interacts with DNAH10, CFAP57, and DYNLL1, contributing to the assembly of the double-headed inner dynein arm f (IDAf) complex in cilia; loss of DNAH10 leads to reduced expression of CCDC73 and improper IDAf complex assembly and ciliary dysfunction. Co-immunoprecipitation (Co-IP), immunostaining, proteomic analysis, Dnah10 knockout mouse model Orphanet journal of rare diseases Medium 40898283

Source papers

Stage 0 corpus · 4 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2018 The evolutionarily conserved genes: Tex37, Ccdc73, Prss55 and Nxt2 are dispensable for fertility in mice. Scientific reports 41 29563520
2014 A novel Alu-mediated microdeletion at 11p13 removes WT1 in a patient with cryptorchidism and azoospermia. Reproductive biomedicine online 17 24912414
2026 Genomic analysis reveals convergent signatures of selection for milk traits in sheep and goats. Journal of animal science and biotechnology 0 41645336
2025 DNAH10 mutation cause primary ciliary dyskinesia with defects of IDAf complex assembly and lung fibrosis manifestation. Orphanet journal of rare diseases 0 40898283