ODAD3

outer dynein arm docking complex subunit 3

Ensembl:
ENSG00000198003
UniProt:
A5D8V7
OMIM:
615956
Synonyms:
CCDC151, MGC20983, ODA10

Cilia effects upon perturbation of ODAD3

Cilia number / % ciliated:
Unknown
Loss-of-function effect:
Longer cilia
Overexpression effect:
Unknown

Phenotypes

Mouse phenotype:
impaired glucose tolerance, preweaning lethality, incomplete penetrance, decreased bone mineral density, abnormal bone structure
Human ciliopathy phenotype:
primary ciliary dyskinesia

Ciliopathy associations

  • Primary Ciliary Dyskinesia

Subcellular localization

cilia

Functional category

  • Ciliary assembly/disassembly
  • Actin & cytoskeleton regulation
  • T cell biology
  • Reproduction & sperm
  • Cell migration & adhesion

Function

Ensures correct attachment of outer dynein arm (ODA) complexes to and is required for proper motile and non-motile functions, controls intraflagellar transport (IFT)- dependent dynein arm assembly and regulates primary cilia lenght in mammals. Required for the correct establishment of left-right asymmetry. When mutated causes PCD by disruption of the outer dynein arm docking complex formation (25192045 )

Model organism evidence

Xenopus (2 references)

Physical and functional interaction of the ciliopathy proteins Lrrc56 and Odad3 control deployment of axonemal dyneins in vertebrate multiciliated cells.

Physical and functional interaction of Lrrc56 and Odad3 controls deployment of axonemal dyneins in vertebrate multiciliated cells.

PMIDs: 41229303, 40631331

Mus musculus (1 reference)

Odad3 gene loss-of-function mutation leads to Primary Ciliary Dyskinesia (PCD), a disease caused by motile cilia dysfunction.

PMIDs: 38920681