title: Genes that induce apoptosis: transcriptional regulation in identified, doomed neurons of the Drosophila CNS.
abstract: Hormones and trophic factors provide cues that control neuronal death during development. These developmental cues in some way regulate activation of apoptosis, the mechanism by which most, if not all, developmentally programmed cell deaths occur. In Drosophila, apoptosis can be induced by the expression of the genes reaper, grim, or head involution defective. We demonstrate that prior to the death of a set of identifiable doomed neurons, these neurons accumulate transcripts of the reaper and grim genes, but do not accumulate transcripts of the head involution defective gene. Death of these doomed neurons can be suppressed by two manipulations: by increasing the levels of the steroid hormone 20-hydroxyecdysone or by decapitation. We have investigated the impact that these two manipulations have on reaper expression. Steroid treatment prevents the accumulation of reaper transcripts, whereas decapitation results in the accumulation of lower levels of reaper transcripts that are not sufficient to activate apoptosis. These data demonstrate that in vivo, reaper, and grim transcripts accumulate coordinately in a set of identified doomed neurons prior to the onset of apoptosis. These observations raise the possibility that products of the reaper and grim genes act in concert in postembryonic neurons to induce apoptosis. That reaper transcript accumulation is regulated by the steroid hormone titer and by the presence of the head is evidence that developmental factors control programmed cell death by regulating the expression of genes that induce apoptosis.
authors.affiliation: Department of Zoology, University of Hawaii, 2538 The Mall, Honolulu, Hawaii 96822, USA.
authors.forename: S
authors.initials: S
authors.lastname: Robinow
authors.forename: T A
authors.initials: TA
authors.lastname: Draizen
authors.forename: J W
authors.initials: JW
authors.lastname: Truman
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000235:genetics*; D002450:Cell Communication; D004330:Drosophila / Q000196:embryology* / Q000235:genetics; D029721:Drosophila Proteins; D004441:Ecdysterone / Q000494:pharmacology; D015870:Gene Expression / Q000187:drug effects; D018507:Gene Expression Regulation, Developmental; D017344:Genes, Insect; D006257:Head / Q000601:surgery; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D007301:Insect Hormones / Q000494:pharmacology; D009420:Nervous System / Q000166:cytology / Q000196:embryology*; D009474:Neurons / Q000502:physiology*; D009479:Neuropeptides / Q000096:biosynthesis / Q000235:genetics; D010455:Peptides / Q000235:genetics; D012333:RNA, Messenger / Q000096:biosynthesis; D014158:Transcription, Genetic
chemical_list: D029721:Drosophila Proteins; C108880:HID protein, Drosophila; D007301:Insect Hormones; D009479:Neuropeptides; D010455:Peptides; D012333:RNA, Messenger; C108881:grim protein, Drosophila; C086973:rpr protein, Drosophila; D004441:Ecdysterone