Ribosomal Protein S12e Has a Distinct Function in Cell Competition

Abhijit Kale, Zhejun Ji, Marianthi Kiparaki, Jorge Blanco, Gerard Rimesso, Stephane Flibotte, Nicholas E. Baker

Research output: Contribution to journalArticle

7 Scopus citations

Abstract

Wild-type Drosophila cells can remove cells heterozygous for ribosomal protein mutations (known as “Minute” mutant cells) from genetic mosaics, a process termed cell competition. The ribosomal protein S12 was unusual because cells heterozygous for rpS12 mutations were not competed by wild-type, and a viable missense mutation in rpS12 protected Minute cells from cell competition with wild-type cells. Furthermore, cells with Minute mutations were induced to compete with one another by altering the gene dose of rpS12, eliminating cells with more rpS12 than their neighbors. Thus RpS12 has a special function in cell competition that defines the competitiveness of cells. We propose that cell competition between wild-type and Minute cells is initiated by a signal of ribosomal protein haploinsufficiency mediated by RpS12. Since competition between cells expressing different levels of Myc did not require RpS12, other kinds of cell competition may be initiated differently. Cells with mutations in ribosomal protein genes are eliminated from Drosophila tissues by cell competition, but how are mutations detected? Kale et al. show that ribosomal protein S12 is necessary for cell competition. The study suggests that S12 has a distinct signaling function that targets cells for competition.

Original languageEnglish (US)
Pages (from-to)42-55.e4
JournalDevelopmental Cell
Volume44
Issue number1
DOIs
StatePublished - Jan 8 2018

Keywords

  • cell competition
  • Drosophila development
  • ribosomal protein
  • RpS12
  • S12e

ASJC Scopus subject areas

  • Developmental Biology

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  • Cite this

    Kale, A., Ji, Z., Kiparaki, M., Blanco, J., Rimesso, G., Flibotte, S., & Baker, N. E. (2018). Ribosomal Protein S12e Has a Distinct Function in Cell Competition. Developmental Cell, 44(1), 42-55.e4. https://doi.org/10.1016/j.devcel.2017.12.007