Abstract

Cell competition was described in Drosophila as the loss from mosaic tissues of otherwise viable cells heterozygous for Ribosomal protein mutations ('Minutes'). Cell competition has now been described to occur between multiple other genotypes, such as cells differing in myc expression levels, or mutated for neoplastic tumor suppressors. Recent studies implicate innate immunity components, and possibly mechanical stress, compression and cell intercalation as a consequence of differential growth rates in competitive cell death. Competition to eliminate pre-neoplastic tumors makes use of signals and receptors also used in patterning the nervous system including Slit/Robo2 and Sas/PTP10D to recognize and extrude clones of mutant cells, at least where local epithelial cyto-architecture is favorable. Cell competition facilitates expansion of Drosophila tumors through host tissue, and in normal development may promote developmental robustness and longevity by selecting for optimal progenitor cells.

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