LPAR1

Ciliogenesis screen results (3 screens)

• Wheway et al. 2015 (siRNA) [siRNA]: Ciliogenesis Defect (z=-6.46) PMID:26167766
• Breslow et al. 2018 (CRISPR) [CRISPR]: No Significant Effect PMID:29459680
• Elliott et al. 2025 (CRISPRa) [CRISPRa]: Disassembly Trigger (casTLE Effect=-4.05) PMID:41160700

Phenotypes

Mouse phenotype:

increased fasting circulating glucose level, preweaning lethality, complete penetrance, improved glucose tolerance

Subcellular localization

cilia

References: PMID:29321663, doi:10.1101/2025.05.11.653368

Functional category

• Ciliary assembly/disassembly
• Trafficking (BBSome, small GTPases, vesicular transport, ATPases)
• Actin & cytoskeleton regulation
• Signaling (Hedgehog, GPCRs, ion channels)

Function

LPA-LPAR1-driven mitogenic signaling was restricted in cells with primary cilium due to compartmentalization of LPAR1 and its downstream effectors, Gα12 and Gαq, in cilia and in cytoplasm, respectively. LPAR1 was redistributed to the plasma membrane upon loss of primary cilium, thus e bling its binding to Gα12 and Gαq, and therefore suggesting that redistribution of LPAR1 is a key mechanism driving proliferation in a cilia-dependent manner(29321663). Detected in primary cilia of human hypothalamic neurons by proximity proteomics (Macarelli et al., 2025, bioRxiv, doi 10.1101/2025.05.11.653368).