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Updated: Mar 14, 2026

The Drosophila Imaginal Disc Tumor Model: Visualization and Quantification of Gene Expression and Tumor Invasiveness Using Genetic Mosaics
Published on: October 6, 2016
Coordinate redeployment of PRC1 proteins suppresses tumor formation during Drosophila development
Vincent Loubière1,2, Anna Delest1,2, Aubin Thomas1,2
1Institute of Human Genetics, UPR1142 CNRS, 141 Rue de la Cardonille, 34396, Montpellier Cedex 5, France.
Abstract:
Polycomb group proteins form two main complexes, PRC2 and PRC1, which generally coregulate their target genes. Here we show that PRC1 components act as neoplastic tumor suppressors independently of PRC2 function. By mapping the distribution of PRC1 components and trimethylation of histone H3 at Lys27 (H3K27me3) across the genome, we identify a large set of genes that acquire PRC1 in the absence of H3K27me3 in Drosophila larval tissues. These genes massively outnumber canonical targets and are mainly involved in the regulation of cell proliferation, signaling and polarity. Alterations in PRC1 components specifically deregulate this set of genes, whereas canonical targets are derepressed in both PRC1 and PRC2 mutants. In human embryonic stem cells, PRC1 components colocalize with H3K27me3 as in Drosophila embryos, whereas in differentiated cell types they are selectively recruited to a large set of proliferation and signaling-associated genes that lack H3K27me3, suggesting that the redeployment of PRC1 components during development is evolutionarily conserved.
Insights
Polycomb Repressive Complex 1 (PRC1) proteins function as tumor suppressors, regulating genes involved in cell growth independently of PRC2. This redeployment of PRC1 is conserved across species.
Area of Science:
- Epigenetics
- Developmental Biology
- Cancer Biology
Background:
- Polycomb group proteins, including PRC1 and PRC2, are crucial epigenetic regulators.
- These complexes typically coregulate target genes, playing roles in development and disease.
Purpose of the Study:
- To investigate the independent function of PRC1 components.
- To identify PRC1 targets independent of PRC2 and H3K27me3.
- To explore the evolutionary conservation of PRC1 function.
Main Methods:
- Genome-wide mapping of PRC1 components and H3K27me3 in Drosophila.
- Analysis of gene expression changes in PRC1 and PRC2 mutants.
- Comparative analysis in human embryonic stem cells and differentiated cells.
Main Results:
- PRC1 acts as a neoplastic tumor suppressor independently of PRC2.
- A large set of proliferation, signaling, and polarity genes are targeted by PRC1 in the absence of H3K27me3.
- These non-canonical PRC1 targets are specifically deregulated by PRC1 alterations.
Conclusions:
- PRC1 has functions independent of PRC2, particularly in tumor suppression.
- PRC1 is dynamically redeployed to regulate key cellular processes during development.
- This redeployment mechanism is evolutionarily conserved from Drosophila to humans.
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