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Originally published as Genetics Published Articles Ahead of Print on September 2, 2005.
Genetics, Vol. 172, 207-219, January 2006, Copyright © 2006
doi:10.1534/genetics.105.044669
Loss-of-Function Mutations in a Glutathione S-Transferase Suppress the prune-Killer of prune Lethal Interaction
Elayne Provost, Grafton Hersperger, Lisa Timmons, Wen Qi Ho, Evelyn Hersperger, Rosa Alcazar and Allen Shearn1
Department of Biology, Johns Hopkins University, Baltimore, Maryland 21218
1 Corresponding author: Department of Biology, Johns Hopkins University, 34th and Charles Sts., Baltimore, MD 21218.
E-mail: bio_cals{at}jhu.edu
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.
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