Damage-responsive, maturity-silenced enhancers regulate multiple genes that direct regeneration in Drosophila

Like tissues of many organisms, imaginal discs lose the ability to regenerate as they mature. This loss of regenerative capacity coincides with reduced damage-responsive expression of multiple genes needed for regeneration. We previously showed that two such genes, and , are regulated by a single da...

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Bibliographic Details
Published in:eLife 2020-06, Vol.9
Main Authors: Harris, Robin E, Stinchfield, Michael J, Nystrom, Spencer L, McKay, Daniel J, Hariharan, Iswar K
Format: Article
Language:English
Subjects:
Ablation
Animals
Binding sites
Chromatin
Deoxyribonucleic acid
Developmental Biology
DNA
Drosophila
Drosophila melanogaster - genetics
Drosophila melanogaster - growth & development
Drosophila melanogaster - physiology
Drosophila Proteins - genetics
Drosophila Proteins - metabolism
Enhancer Elements, Genetic
Enhancers
epigenetic
Epigenetics
Gene expression
Gene Expression Regulation, Developmental
Gene Silencing
Genes
Genetic aspects
Genetic engineering
Genomes
Imaginal discs
Imaginal Discs - growth & development
Imaginal Discs - metabolism
Insects
Polycomb group proteins
Regeneration
Research Advance
silencing
Stem Cells and Regenerative Medicine
Transcription factors
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Summary:Like tissues of many organisms, imaginal discs lose the ability to regenerate as they mature. This loss of regenerative capacity coincides with reduced damage-responsive expression of multiple genes needed for regeneration. We previously showed that two such genes, and , are regulated by a single damage-responsive enhancer that becomes progressively inactivated via Polycomb-mediated silencing as discs mature (Harris et al., 2016). Here we explore the generality of this mechanism and identify additional damage-responsive, maturity-silenced (DRMS) enhancers, some near genes known to be required for regeneration such as , and others near genes that we now show function in regeneration. Using a novel GAL4-independent ablation system we characterize two DRMS-associated genes, ( ), which curtails regeneration and CG9752/ , which promotes it. This mechanism of suppressing regeneration by silencing damage-responsive enhancers at multiple loci can be partially overcome by reducing activity of the chromatin regulator ( ).
ISSN:2050-084X
2050-084X
DOI:10.7554/eLife.58305