The Drosophila G-protein-coupled receptor kinase homologue Gprk2 is required for egg morphogenesis

Lynne E. Schneider, Allan C. Spradling

Research output: Contribution to journalArticle

Abstract

G protein signaling is a widely utilized form of extracellular communication that is mediated by a family of serpentine receptors containing seven transmembrane domains. In sensory neurons, cardiac muscle and other tissues, G protein-coupled receptors are desensitized through phosphorylation by a family of kinases, the G protein-coupled receptor kinases (GRKs). Desensitization allows a cell to decrease its response to a given signal, in the continued presence of that signal. We have identified a Drosophila mutant, gprk26936 that disrupts expression of a putative member of the GRK family, the G protein-coupled receptor kinase 2 gene (Gprk2). This mutation affects Gprk2 gene expression in the ovaries and renders mutant females sterile. The mutant eggs contain defects in several anterior eggshell structures that are produced by specific subsets of migratory follicle cells. In addition, rare eggs that become fertilized display gross defects in embryogenesis. These observations suggest that developmental signals transduced by G protein-coupled receptors are regulated by receptor phosphorylation. Based on the known functions of G protein-coupled receptor kinases, we speculate that receptor desensitization assists cells that are migrating or undergoing shape changes to respond rapidly to changing external signals.

Original languageEnglish (US)
Pages (from-to)2591-2602
Number of pages12
JournalDevelopment
Volume124
Issue number13
StatePublished - Jul 1997
Externally publishedYes

Keywords

  • Cell signaling
  • Drosophila
  • G protein signaling
  • Gprk2
  • Ovarian development

ASJC Scopus subject areas

  • Anatomy
  • Cell Biology

Fingerprint Dive into the research topics of 'The Drosophila G-protein-coupled receptor kinase homologue Gprk2 is required for egg morphogenesis'. Together they form a unique fingerprint.

  • Cite this