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RpS12-mediated induction of the Xrp1short isoform links ribosomal protein mutations to cell competition

ABSTRACT: Cell competition, the context-dependent cell elimination via short-range cell-cell interactions, was originally described in Drosophila, where heterozygous ribosomal protein (Rp+/-) mutant cells are outcompeted by wild-type neighbors. The transcription factor Xrp1 mediates most Rp+/- phenotypes, including reduced translation and competitiveness, yet how RpS12 induces Xrp1 has remained unclear. We show that RpS12 promotes a splice variant of Xrp1 encoding the short isoform Xrp1short, which defines the Rp+/- loser identity. RpS12 overexpression is sufficient to induce Xrp1short and a loser phenotype. Expression of either Xrp1 isoform alone can trigger competition, establishing Xrp1 as the central driver of the loser fate. When loser cells exceed a critical threshold, a quorum-like response supports their survival by post-transcriptionally downregulating Xrp1. We further identify the RNA-binding protein Syncrip, reduced in Rp+/- cells, as an Xrp1 suppressor whose depletion activates Xrp1-dependent competition. Thus, RpS12-dependent Xrp1short expression emerges as the primary Rp+/- signal driving cell competition.

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ORGANISM(S): Drosophila Melanogaster (fruit Fly)

TISSUE(S): Wing, Epithelial Cell

SUBMITTER: Martina Samiotaki

LAB HEAD: Marianthi Kiparaki

PROVIDER: PXD076715 | Pride | 2026-05-16

REPOSITORIES: Pride

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Project description:An analysis of the transcriptional profiles of weak genetic perturbations generated via P-elements measured as heterozygotes in wing imaginal discs of Drosophila melanogaster. Abstract: A major objective of genomics is to elucidate the mapping between genotypic and phenotypic space as a step toward understanding how small changes in gene function can lead to elaborate phenotypic changes. One approach that has been utilized is to examine overall patterns of co-variation between phenotypic variables of interest, such as morphology, physiology and behavior, and underlying aspects of gene activity, in particular transcript abundance on a genome wide scale. Numerous studies have demonstrated that such patterns of co-variation occur, although these are often between samples with large numbers of unknown genetic differences (different strains, or even species) or perturbations of large effect (sexual dimorphism, or strong loss of function mutations), that may represent physiological changes outside of the normal experiences of the organism. We used weak mutational perturbations in genes affecting wing development in Drosophila melanogaster, that influence wing shape relative to a co-isogenic wild-type. We profiled transcription of 1150 genes expressed during wing development in 27 heterozygous mutants, as well as their co-isogenic wild type and one additional wild-type strain. Despite finding clear evidence of expression differences between mutants and wild-type, transcriptional profiles did not co-vary strongly with shape, suggesting that information from transcriptional profiling may not generally be predictive of final phenotype. We discuss these results in the light of possible attractor states of gene expression, and how this would affect interpretation of co-variation between transcriptional profiles and other phenotypes. Total RNA was extracted from pools of wing imaginal discs for each mutant strain as well as for their co-isogenic wild-type, and one additional wild-type strain. RNA was extracted using a modified protocol using the Qiagen RNAeasy kit.

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RpS12-mediated induction of the Xrp1short isoform links ribosomal protein mutations to cell competition

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