LRRK2
leucine rich repeat kinase 2
- Ensembl:
- ENSG00000188906
- UniProt:
- Q5S007
- OMIM:
- 609007
- Synonyms:
- DKFZP434H2111, FLJ45829, PARK8, RIPK7, ROCO2
Cilia effects upon perturbation of LRRK2
- Cilia number / % ciliated:
- Decreased cilia number
- Loss-of-function effect:
- Decreased cilia number
Ciliogenesis screen results (4 screens)
- Kim2016: Not Reported
- Wheway et al. 2015 (siRNA) [siRNA]: No effect PMID:26167766
- Breslow et al. 2018 (CRISPR) [CRISPR]: No Significant Effect PMID:29459680
- Roosing et al. 2015 (siRNA) [siRNA]: No effect PMID:26595381
Subcellular localization
basal body, cytosol, microtubules
Functional category
- Ciliary assembly/disassembly
- Trafficking (BBSome, small GTPases, vesicular transport, ATPases)
- Actin & cytoskeleton regulation
- Protein processing & maturation
- Cell migration & adhesion
- Signaling (Hedgehog, GPCRs, ion channels)
- Cilia length regulation
Function
Phosphorylates Rab8A, Rab10 and Rab12, mutations interferer with primary cilia formation by generating pRab10 that binds endogenous RILPL1 and blocks cilia formation. Regulates intracellular vesicular traffic during ciliogenesis (30398148, 29125462). RAB12-LRRK2 complex suppresses primary ciliogenesis … the ciliated cell percentage, cilia length, and cilia volume were quantified in astrocytes …(39343966) Activating LRRK2 mutations cause Parkinson’s and block primary cilia formation in specific cells in the mouse brain. (39088390) Some data suggest LRRK2 kinase activity may not directly regulate ciliogenesis depending on cell type. (30398148) (34230223)
Model organism evidence
To date, LRRK2 has at least two major cellular roles: it promotes exocytosis of lysosome-related organelles-particularly under conditions of lysosome stress in macrophages and microglia-and it regulates the formation and stabilization of primary cilia in neurons and astrocytes.
Previously, we showed that pathogenic LRRK2 mutations inhibit primary cilia formation in rare interneurons and astrocytes of the mouse and human dorsal striatum.