Damage-responsive elements in Drosophila regeneration
- Elena Vizcaya-Molina1,5,
- Cecilia C. Klein1,2,5,
- Florenci Serras1,
- Rakesh K. Mishra3,
- Roderic Guigó2,4 and
- Montserrat Corominas1
- 1Departament de Genètica, Microbiologia i Estadística, Facultat de Biologia and Institut de Biomedicina (IBUB), Universitat de Barcelona, Barcelona 08028, Catalonia, Spain;
- 2Centre for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Barcelona 08003, Catalonia, Spain;
- 3The Centre for Cellular and Molecular Biology (CCMB), Hyderabad 500007, India;
- 4Universitat Pompeu Fabra (UPF), Barcelona 08003, Catalonia, Spain
-
↵5 These authors contributed equally to this work.
Abstract
One of the most important questions in regenerative biology is to unveil how and when genes change expression and trigger regeneration programs. The resetting of gene expression patterns during response to injury is governed by coordinated actions of genomic regions that control the activity of multiple sequence-specific DNA binding proteins. Using genome-wide approaches to interrogate chromatin function, we here identify the elements that regulate tissue recovery in Drosophila imaginal discs, which show a high regenerative capacity after genetically induced cell death. Our findings indicate there is global coregulation of gene expression as well as a regeneration program driven by different types of regulatory elements. Novel enhancers acting exclusively within damaged tissue cooperate with enhancers co-opted from other tissues and other developmental stages, as well as with endogenous enhancers that show increased activity after injury. Together, these enhancers host binding sites for regulatory proteins that include a core set of conserved transcription factors that control regeneration across metazoans.
Footnotes
-
[Supplemental material is available for this article.]
-
Article published online before print. Article, supplemental material, and publication date are at http://www.genome.org/cgi/doi/10.1101/gr.233098.117.
-
Freely available online through the Genome Research Open Access option.
- Received December 4, 2017.
- Accepted October 10, 2018.
This article, published in Genome Research, is available under a Creative Commons License (Attribution 4.0 International), as described at http://creativecommons.org/licenses/by/4.0/.
