CEP97
centrosomal protein 97
- Ensembl:
- ENSG00000182504
- UniProt:
- Q8IW35
- OMIM:
- 615864
- Synonyms:
- FLJ23047, LRRIQ2
Cilia effects upon perturbation of CEP97
- Cilia number / % ciliated:
- Decreased cilia number
- Loss-of-function effect:
- Shorter cilia
Ciliogenesis screen results (2 screens)
- Wheway et al. 2015 (siRNA) [siRNA]: Ciliogenesis Defect (z=-8.88) PMID:26167766
- Breslow et al. 2018 (CRISPR) [CRISPR]: Positive Regulator (Hh signaling, casTLE effect=-0.98) PMID:29459680
Phenotypes
- Mouse phenotype:
- hemorrhage, edema, abnormal craniofacial morphology, cleft palate, spi bifida, bleb, preweaning lethality, complete penetrance
- Mouse ciliopathy phenotype:
- microphthalmia
Subcellular localization
basal body, centrosome
Functional category
- Ciliary assembly/disassembly
- Trafficking (BBSome, small GTPases, vesicular transport, ATPases)
- Actin & cytoskeleton regulation
Function
Recruitment and stabilisation of CP110 to centrosomes. Both CP110 and CEP97 complexes regulate basal body function, centrosome functions and inhibit cilia assembly (17719545). Loss of CEP97 causes premature cilia formation or abnormal centriole elongation (30375385). CEP97 ubiquitylation and degradation play a key role in the removal of the CEP97âCP110 complex from the mother centriole for initiating ciliary axoneme extension (30404837).
Model organism evidence
RNA sequencing of E18.5 kidneys from glucocorticoid receptor (GR) null mice identified significant reductions in key ciliogenesis-related genes including Ccp110, Cep97, Cep290 and Kif3a.
ENKD1 promotes CP110 removal through competing with CEP97 to initiate ciliogenesis.