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A Single Residue Mutation in the Gαq Subunit of the G Protein Complex Causes Blindness in Drosophila.

Published version
Peer-reviewed

Type

Article

Change log

Authors

Cao, Jinguo 
Bollepalli, Murali K 
Hu, Yuhui 
Zhang, Jin 
Li, Qiang 

Abstract

Heterotrimeric G proteins play central roles in many signaling pathways, including the phototransduction cascade in animals. However, the degree of involvement of the G protein subunit Gαq is not clear since animals with previously reported strong loss-of-function mutations remain responsive to light stimuli. We recovered a new allele of Gαq in Drosophila that abolishes light response in a conventional electroretinogram assay, and reduces sensitivity in whole-cell recordings of dissociated cells by at least five orders of magnitude. In addition, mutant eyes demonstrate a rapid rate of degeneration in the presence of light. Our new allele is likely the strongest hypomorph described to date. Interestingly, the mutant protein is produced in the eyes but carries a single amino acid change of a conserved hydrophobic residue that has been assigned to the interface of interaction between Gαq and its downstream effector, PLC. Our study has thus uncovered possibly the first point mutation that specifically affects this interaction in vivo.

Description

Keywords

ERG, G protein, Gα PLC interaction, Gαq, light-induced retinal degeneration, photoreceptor, phototransduction, Alleles, Animals, Drosophila Proteins, Drosophila melanogaster, Electroretinography, GTP-Binding Protein alpha Subunits, Gq-G11, Gene Expression Regulation, Light, Point Mutation, Protein Binding, Retina, Retinal Degeneration, Type C Phospholipases, Vision, Ocular

Journal Title

G3 (Bethesda)

Conference Name

Journal ISSN

2160-1836
2160-1836

Volume Title

8

Publisher

Oxford University Press (OUP)
Sponsorship
Biotechnology and Biological Sciences Research Council (BB/M007006/1)