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  Adhesion G protein-coupled receptor Gpr126/Adgrg6 is essential for placental development

Torregrosa-Carrion, R., Pineiro-Sabaris, R., Siguero-Alvarez, M., Grego-Bessa, J., Luna-Zurita, L., Samuel Fernandes, V., et al. (2021). Adhesion G protein-coupled receptor Gpr126/Adgrg6 is essential for placental development. SCIENCE ADVANCES, 7(46): eabj5445. doi:10.1126/sciadv.abj5445.

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 Creators:
Torregrosa-Carrion, Rebeca, Author
Pineiro-Sabaris, Rebeca, Author
Siguero-Alvarez, Marcos, Author
Grego-Bessa, Joaquim, Author
Luna-Zurita, Luis, Author
Samuel Fernandes, Vitor, Author
MacGrogan, Donal, Author
Stainier, Didier Y. R.1, Author              
Luis de la Pompa, Jose, Author
Affiliations:
1Developmental Genetics, Max Planck Institute for Heart and Lung Research, Max Planck Society, ou_2591697              

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 Abstract: Mutations in the G protein-coupled receptor GPR126/ADGRG6 cause human diseases, including defective peripheral nervous system (PNS) myelination. To study GPR126 function, we generated new genetic mice and zebrafish models. Murine Gpr126 is expressed in developing heart endocardium, and global Gpr126 inactivation is embryonically lethal, with mutants having thin-walled ventricles but unaffected heart patterning or maturation. Endocardial-specific Gpr126 deletion does not affect heart development or function, and transgenic endocardial GPR126 expression fails to rescue lethality in Gpr126-null mice. Zebrafish gpr126 mutants display unaffected heart development. Gpr126 is also expressed in placental trophoblast giant cells. Gpr126-null mice with a heterozygous placenta survive but exhibit GPR126-defective PNS phenotype. In contrast, Gpr126-null embryos with homozygous mutant placenta die but are rescued by placental GPR126 expression. Gpr126-deficient placentas display down-regulation of preeclampsia markers Mmp9, Cts7, and Cts8. We propose that the placenta-heart axis accounts for heart abnormalities secondary to placental defects in Gpr126 mutants.

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 Dates: 2021-11-12
 Publication Status: Published online
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 Rev. Type: -
 Identifiers: ISI: 000720344200012
DOI: 10.1126/sciadv.abj5445
PMID: 34767447
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Title: SCIENCE ADVANCES
Source Genre: Journal
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Pages: - Volume / Issue: 7 (46) Sequence Number: eabj5445 Start / End Page: - Identifier: ISSN: 2375-2548