ArticlePloS one2014
Orphan G-protein coupled receptor 22 (Gpr22) regulates cilia length and structure in the zebrafish Kupffer's vesicle.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Functions of cilia in cardiac development and disease.Annals of human genetics · 2024Review
- Emerging principles of primary cilia dynamics in controlling tissue organization and function.The EMBO journal · 2023Review
- An SNN retrocopy insertion upstream of GPR22 is associated with dark red coat color in Poodles.G3 (Bethesda, Md.) · 2022Article
- Patterns of cilia gene dysregulations in major psychiatric disorders.Progress in neuro-psychopharmacology & biological psychiatry · 2021Article
- Chronic Voluntary Ethanol Drinking in Cynomolgus Macaques Elicits Gene Expression Changes in Prefrontal Cortical Area 46.Alcoholism, clinical and experimental research · 2020Article
- The role of GPCRs in bone diseases and dysfunctions.Bone research · 2019Review
- A Reduced Transcriptome Approach to Assess Environmental Toxicants Using Zebrafish Embryo Test.Environmental science & technology · 2018Article
- Primary Cilium-Dependent Signaling Mechanisms.International journal of molecular sciences · 2017Review
- Cystinosis (ctns) zebrafish mutant shows pronephric glomerular and tubular dysfunction.Scientific reports · 2017Article
- Dopaminergic signaling within the primary cilia in the renovascular system.Frontiers in physiology · 2015Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
GPR22 is an orphan G protein-coupled receptor (GPCR). Since the ligand of the receptor is currently unknown, its biological function has not been investigated in depth. Many GPCRs and their intracellular effectors are targeted to cilia. Cilia are highly conserved eukaryotic microtubule-based organelles that protrude from the membrane of most mammalian cells. They are involved in a large variety of physiological processes and diseases. However, the details of the downstream pathways and mechanisms that maintain cilia length and structure are poorly understood. We show that morpholino knock down or overexpression of gpr22 led to defective left-right (LR) axis formation in the zebrafish embryo. Specifically, defective LR patterning included randomization of the left-specific lateral plate mesodermal genes (LPM) (lefty1, lefty2, southpaw and pitx2a), resulting in randomized cardiac looping. Furthermore, gpr22 inactivation in the Kupffer's vesicle (KV) alone was still able to generate the phenotype, indicating that Gpr22 mainly regulates LR asymmetry through the KV. Analysis of the KV cilia by immunofluorescence and transmission electron microscopy (TEM), revealed that gpr22 knock down or overexpression resulted in changes of cilia length and structure. Further, we found that Gpr22 does not act upstream of the two cilia master regulators, Foxj1a and Rfx2. To conclude, our study characterized a novel player in the field of ciliogenesis.
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