Loss-of-function mutations in a glutathione S-transferase suppress the prune-Killer of prune lethal interaction.

Abstract:

:The prune gene of Drosophila melanogaster is predicted to encode a phosphodiesterase. Null alleles of prune are viable but cause an eye-color phenotype. The abnormal wing discs gene encodes a nucleoside diphosphate kinase. Killer of prune is a missense mutation in the abnormal wing discs gene. Although it has no phenotype by itself even when homozygous, Killer of prune when heterozygous causes lethality in the absence of prune gene function. A screen for suppressors of transgenic Killer of prune led to the recovery of three mutations, all of which are in the same gene. As heterozygotes these mutations are dominant suppressors of the prune-Killer of prune lethal interaction; as homozygotes these mutations cause early larval lethality and the absence of imaginal discs. These alleles are loss-of-function mutations in CG10065, a gene that is predicted to encode a protein with several zinc finger domains and glutathione S-transferase activity.

journal_name

Genetics

journal_title

Genetics

authors

Provost E,Hersperger G,Timmons L,Ho WQ,Hersperger E,Alcazar R,Shearn A

doi

10.1534/genetics.105.044669

keywords:

subject

Has Abstract

pub_date

2006-01-01 00:00:00

pages

207-19

issue

1

eissn

0016-6731

issn

1943-2631

pii

genetics.105.044669

journal_volume

172

pub_type

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