title: Hid arbitrates collective cell death in the Drosophila wing.
abstract: Elimination of cells and tissues by apoptosis is a highly conserved and tightly regulated process. In Drosophila, the entire wing epithelium is completely removed shortly after eclosion. The cells that make up this epithelium are collectively eliminated through a highly synchronized form of apoptotic cell death, involving canonical apoptosome genes. Here we present evidence that collective cell death does not require cell-cell contact and show that transcription of the IAP antagonist, head involution defective, is acutely induced in wing epithelial cells prior to this process. hid mRNAs accumulate to levels that exceed a component of the ribosome and likewise, Hid protein becomes highly abundant in these same cells. hid function is required for collective cell death, since loss of function mutants shows persisting wing epithelial cells and, furthermore, silencing of the hormone bursicon in the CNS produced collective cell death defective phenotypes manifested in the wing epithelium. Taken together, our observations suggest that acute induction of Hid primes wing epithelial cells for collective cell death and that Bursicon is a strong candidate to trigger this process, possibly by activating the abundant pool of Hid protein already present.
authors.affiliation: Department of Cell Biology, UT Southwestern Medical Center, Dallas, TX 75390-9039, United States.
authors.forename: Gianella
authors.initials: G
authors.lastname: Garcia-Hughes
authors.affiliation: Baylor College of Medicine, Houston, TX 77030, United States.
authors.forename: Nichole
authors.initials: N
authors.lastname: Link
authors.affiliation: Department of Cell Biology, UT Southwestern Medical Center, Dallas, TX 75390-9039, United States.
authors.forename: Anwesha B
authors.initials: AB
authors.lastname: Ghosh
authors.affiliation: Department of Cell Biology, UT Southwestern Medical Center, Dallas, TX 75390-9039, United States. Electronic address: John.Abrams@utsouthwestern.edu.
authors.forename: John M
authors.initials: JM
authors.lastname: Abrams
mesh_terms: D000818:Animals; D030801:Animals, Genetically Modified; D017209:Apoptosis / Q000235:genetics / Q000502:physiology*; D002448:Cell Adhesion; D002450:Cell Communication; D029721:Drosophila Proteins / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D004331:Drosophila melanogaster / Q000166:cytology* / Q000235:genetics / Q000254:growth & development*; D018507:Gene Expression Regulation, Developmental; D017344:Genes, Insect; D051034:Inhibitor of Apoptosis Proteins / Q000378:metabolism; D007447:Invertebrate Hormones / Q000037:antagonists & inhibitors / Q000235:genetics / Q000502:physiology; D009479:Neuropeptides / Q000235:genetics / Q000502:physiology*; D014921:Wings, Animal / Q000166:cytology* / Q000254:growth & development* / Q000378:metabolism
chemical_list: C111891:DIAP1 protein, Drosophila; D029721:Drosophila Proteins; C108880:HID protein, Drosophila; D051034:Inhibitor of Apoptosis Proteins; D007447:Invertebrate Hormones; D009479:Neuropeptides; C002295:bursicon
keywords: Apoptosis; Collective cell death; Development; Eclosion; Hormone