title: An ancient defense system eliminates unfit cells from developing tissues during cell competition.
abstract: Developing tissues that contain mutant or compromised cells present risks to animal health. Accordingly, the appearance of a population of suboptimal cells in a tissue elicits cellular interactions that prevent their contribution to the adult. Here we report that this quality control process, cell competition, uses specific components of the evolutionarily ancient and conserved innate immune system to eliminate Drosophila cells perceived as unfit. We find that Toll-related receptors (TRRs) and the cytokine Spätzle (Spz) lead to NFκB-dependent apoptosis. Diverse "loser" cells require different TRRs and NFκB factors and activate distinct pro-death genes, implying that the particular response is stipulated by the competitive context. Our findings demonstrate a functional repurposing of components of TRRs and NFκB signaling modules in the surveillance of cell fitness during development.
authors.affiliation: Institute of Molecular Life Sciences, University of Zurich, Zurich, Switzerland.
authors.forename: S N
authors.initials: SN
authors.lastname: Meyer
authors.affiliation: Department of Genetics and Development, Columbia University, New York, NY 10032, USA.
authors.forename: M
authors.initials: M
authors.lastname: Amoyel
authors.affiliation: Department of Genetics and Development, Columbia University, New York, NY 10032, USA.
authors.forename: C
authors.initials: C
authors.lastname: Bergantiños
authors.affiliation: Department of Genetics and Development, Columbia University, New York, NY 10032, USA.
authors.forename: C
authors.initials: C
authors.lastname: de la Cova
authors.affiliation: Institute of Molecular Life Sciences, University of Zurich, Zurich, Switzerland.
authors.forename: C
authors.initials: C
authors.lastname: Schertel
authors.affiliation: Institute of Molecular Life Sciences, University of Zurich, Zurich, Switzerland. konrad.basler@imls.uzh.ch lj180@columbia.edu.
authors.forename: K
authors.initials: K
authors.lastname: Basler
authors.affiliation: Department of Genetics and Development, Columbia University, New York, NY 10032, USA. konrad.basler@imls.uzh.ch lj180@columbia.edu.
authors.forename: L A
authors.initials: LA
authors.lastname: Johnston
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000235:genetics / Q000276:immunology*; D002450:Cell Communication / Q000276:immunology*; D029721:Drosophila Proteins / Q000235:genetics / Q000378:metabolism; D004331:Drosophila melanogaster / Q000166:cytology / Q000235:genetics / Q000254:growth & development; D007113:Immunity, Innate / Q000235:genetics / Q000276:immunology*; D009154:Mutation; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism*; D009479:Neuropeptides / Q000235:genetics; D051193:Toll-Like Receptors / Q000235:genetics / Q000378:metabolism*; D014157:Transcription Factors / Q000378:metabolism; D014158:Transcription, Genetic
chemical_list: D029721:Drosophila Proteins; C108880:HID protein, Drosophila; D016328:NF-kappa B; D009479:Neuropeptides; C101626:Rel protein, Drosophila; D051193:Toll-Like Receptors; D014157:Transcription Factors; C086179:spz protein, Drosophila