John P. Wing

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The gene cul-1 (formerly lin-19) is a negative regulator of the cell cycle in C. elegans. Null mutations cause hyperplasia of all tissues. cul-1 is required for developmentally programmed transitions from the G1 phase of the cell cycle to the GO phase or the apoptotic pathway. Moreover, the mutant phenotype suggests that G1-to-S phase progression is(More)
In Drosophila melanogaster, apoptosis is controlled by the integrated actions of the Grim-Reaper (Grim-Rpr) and Drosophila Inhibitor of Apoptosis (DIAP) proteins (reviewed in refs 1 4). The anti-apoptotic DIAPs bind to caspases and inhibit their proteolytic activities. DIAPs also bind to Grim-Rpr proteins, an interaction that promotes caspase activity and(More)
The Drosophila reaper, head involution defective (hid), and grim genes play key roles in regulating the activation of programmed cell death. Two useful systems for studying the functions of these genes are the embryonic CNS midline and adult eye. In this study we use the Gal4/UAS targeted gene expression system to demonstrate that unlike reaper or hid,(More)
Members of the ICE/ced-3 gene family have been implicated as components of the cell death pathway. Based on similarities with the structural prototype interleukin-1 beta-converting enzyme (ICE), family members are synthesized as proenzymes that are proteolytically processed to form active heterodimeric enzymes. In this report, we describe a novel member of(More)
Reaper, Hid, and Grim are three Drosophila cell death activators that each contain a conserved NH(2)-terminal Reaper, Hid, Grim (RHG) motif. We have analyzed the importance of the RHG motifs in Reaper and Grim for their different abilities to activate cell death during development. Analysis of chimeric R/Grim and G/Reaper proteins indicated that the Reaper(More)
The Drosophila genes reaper, head involution defective (hid), and grim all reside at 75C on chromosome three and encode related proteins that have crucial functions in programmed cell death (reviewed in ). In this report, we describe a novel grim-reaper gene, termed sickle, that resides adjacent to reaper. The sickle gene, like reaper and grim, encodes a(More)
Recombination-deficient (Ret-) mutants of Salmonella typhitn&um were used to study special transduction by phage P22 in the absence of the usual background of general transduction. Retstrains could not be transduced for any marker with a lysate arising by infection. When the same strains were infected with a lysate obtained by induction, low but significant(More)
A recombination-deficient (Rec(-)) ultraviolet-sensitive mutant of Salmonella typhimurium was isolated. The mutant grows more slowly than the wild-type strain and degrades its deoxyribonucleic acid extensively both during normal growth and after ultraviolet irradiation. Evidence is presented that a growing Rec(-) population consists of two types of cells,(More)
Phage P22 can integrate as prophage into a recombination-deficient (Rec(-)) strain of Salmonella typhimurium. At 37 C, the integration efficiency is only 10% that in Rec(+) infection, but at 25 C the efficiencies in Rec(-) and Rec(+) hosts are similar. Rec(-) lysogens cannot be induced by ultraviolet irradiation or by treatments with the chemical inducing(More)