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Defective adgra2 (gpr124) splicing and function in zebrafish ouchless mutants.

Naguissa Bostaille¹, Anne Gauquier¹, Didier Y R Stainier²

¹Laboratory of Neurovascular Signaling, Department of Molecular Biology, ULB Neuroscience Institute, Université libre de Bruxelles (ULB), B-6041 Gosselies, Belgium.

Development (Cambridge, England)

|December 17, 2016

Summary

A zebrafish mutation causes defects in dorsal root ganglia formation by disrupting adgra2 (gpr124) gene splicing. This finding corrects previous research linking these phenotypes to sorbs3.

Keywords:

Blood–brain barrier Zebrafish adgra2 gpr124 ouchless reck sorbs3

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Area of Science:

Developmental biology
Genetics
Neuroscience

Background:

The ouchless zebrafish mutant exhibits defects in dorsal root ganglia (DRG) formation.
Previous studies suggested sorbs3 downregulation was responsible for the ouchless phenotype.

Discussion:

This study identifies a splice site mutation in the adgra2 (also known as gpr124) gene as the cause of ouchless phenotypes.
The mutation leads to aberrant splicing of adgra2, affecting its function in cerebrovascular development.

Key Insights:

The ouchless mutation is re-attributed to adgra2, not sorbs3.
Ouchless mutants fail to complement known adgra2 mutants, confirming the genetic link.
A specific mutation in adgra2 results in a receptor lacking a leucine-rich repeat (LRR).

Outlook:

Further investigation into the role of adgra2 and its LRR domain in DRG and vascular development is warranted.
Understanding this mutation's impact may provide insights into related human neurological and vascular disorders.