Apoptotic mechanisms during competition of ribosomal protein mutant cells: Roles of the initiator caspases Dronc and Dream/Strica

A. Kale, W. Li, C. H. Lee, N. E. Baker

Research output: Contribution to journalArticle

23 Scopus citations

Abstract

Heterozygosity for mutations in ribosomal protein genes frequently leads to a dominant phenotype of retarded growth and small adult bristles in Drosophila (the Minute phenotype). Cells with Minute genotypes are subject to cell competition, characterized by their selective apoptosis and removal in mosaic tissues that contain wild-type cells. Competitive apoptosis was found to depend on the pro-apoptotic reaper, grim and head involution defective genes but was independent of p53. Rp/+ cells are protected by anti-apoptotic baculovirus p35 expression but lacked the usual hallmarks of 'undead' cells. They lacked Dronc activity, and neither expression of dominant-negative Dronc nor dronc knockdown by dsRNA prevented competitive apoptosis, which also continued in dronc null mutant cells or in the absence of the initiator caspases dredd and dream/strica. Only simultaneous knockdown of dronc and dream/strica by dsRNA was sufficient to protect Rp/+ cells from competition. By contrast, Rp/Rp cells were also protected by baculovirus p35, but Rp/Rp death was dronc-dependent, and undead Rp/Rp cells exhibited typical dronc-dependent expression of Wingless. Independence of p53 and unusual dependence on Dream/Strica distinguish competitive cell death from noncompetitive apoptosis of Rp/Rp cells and from many other examples of cell death.

Original languageEnglish (US)
Pages (from-to)1300-1312
Number of pages13
JournalCell Death and Differentiation
Volume22
Issue number8
DOIs
StatePublished - Aug 7 2015

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

Fingerprint Dive into the research topics of 'Apoptotic mechanisms during competition of ribosomal protein mutant cells: Roles of the initiator caspases Dronc and Dream/Strica'. Together they form a unique fingerprint.

  • Cite this