IFT122
intraflagellar transport 122
- Ensembl:
- ENSG00000163913
- UniProt:
- Q9HBG6
- OMIM:
- 606045
- Synonyms:
- CFAP80, FAP80, SPG, WDR10, WDR10P
Cilia effects upon perturbation of IFT122
- Cilia number / % ciliated:
- Decreased cilia number
- Loss-of-function effect:
- Shorter cilia
- Overexpression effect:
- No effect
Ciliogenesis screen results (3 screens)
- Wheway et al. 2015 (siRNA) [siRNA]: Ciliogenesis Defect (z=-6.53) PMID:26167766
- Breslow et al. 2018 (CRISPR) [CRISPR]: Positive Regulator (Hh signaling, casTLE effect=-3.39) PMID:29459680
- Roosing et al. 2015 (siRNA) [siRNA]: No effect PMID:26595381
Phenotypes
- Mouse phenotype:
- abnormal behavior, long tibia, decreased locomotor activity, preweaning lethality, complete penetrance, increased mean corpuscular volume
- Mouse ciliopathy phenotype:
- increased circulating aspartate transamise level
Ciliopathy associations
- Cranioectodermal Dysplasia (Sensenbrenner)
- Skeletal Ciliopathy
- Weyers Acrofacial Dysostosis
Subcellular localization
basal body, cilia
Functional category
- Ciliary assembly/disassembly
- Actin & cytoskeleton regulation
- Signaling (Hedgehog, GPCRs, ion channels)
- Transition zone
- Transcription regulation
Function
Negative regulator of the Shh pathway, controlling the ciliary localization of Shh pathway activators and repressors. Loss of IFT122 causes accumulation of Gli2 and Gli3 at cilia tips. Function in retrograde intraflagellar transport (ITF) that facilitates complex A stability (21209331). Required for transport of opsin, and the distal elongation of outer segments (27681595). IFT122 connects the core and peripheral subcomplexes of the IFT-A (29220510).
Model organism evidence
Loss of NSUN7 altered the abundance of proteins essential for dynein arm assembly (PIH1D3, CCDC103, CCDC40), intraflagellar transport (IFT122), and fibrous sheath organization (AKAP3, AKAP4, ROPN1L).
IFT122 Regulates Proliferation of mEPMCs Through the Shh Signaling Pathway by Primary Cilia.
Here, we applied DIFFRAC to investigate the consequences of genetic loss of Ift122, a subunit of the intraflagellar transport-A (IFT-A) protein complex that plays a vital role in the formation and function of cilia and flagella, on the proteome of Tetrahymena thermophila.
Here, we applied DIFFRAC to investigate the consequences of genetic loss of Ift122, a subunit of the intraflagellar transport-A (IFT-A) protein complex that plays a vital role in the formation and function of cilia and flagella, on the proteome of Tetrahymena thermophila .