Multiple transcription factor codes activate epidermal wound-response genes in Drosophila

Wounds in Drosophila and mouse embryos induce similar genetic pathways to repair epidermal barriers. However, the transcription factors that transduce wound signals to repair epidermal barriers are largely unknown. We characterize the transcriptional regulatory enhancers of 4 genes--Ddc, ple, msn, a...

Full description

Saved in:
Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 2009-02, Vol.106 (7), p.2224-2229
Main Authors: Pearson, Joseph C, Juarez, Michelle T, Kim, Myungjin, McGinnis, William
Format: Article
Language:English
Subjects:
animal injuries
Animals
Binding Sites
Biological Sciences
DNA
DNA repair
Drosophila
Drosophila melanogaster
embryo (animal)
Embryos
enhancer elements
Enhancer Elements, Genetic
Epidermal cells
Epidermis
epidermis (animal)
Epidermis - pathology
Gene Expression Regulation
Genes
Genetic mutation
Genetics
Insects
larvae
Microscopy, Fluorescence
Models, Biological
Models, Genetic
Mutation
Rodents
Signal transduction
Time Factors
tissue repair
transcription (genetics)
Transcription factors
Transcription Factors - metabolism
Transcription, Genetic
transcriptional regulatory enhancers
Wound Healing
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Wounds in Drosophila and mouse embryos induce similar genetic pathways to repair epidermal barriers. However, the transcription factors that transduce wound signals to repair epidermal barriers are largely unknown. We characterize the transcriptional regulatory enhancers of 4 genes--Ddc, ple, msn, and kkv--that are rapidly activated in epidermal cells surrounding wounds in late Drosophila embryos and early larvae. These epidermal wound enhancers all contain evolutionarily conserved sequences matching binding sites for JUN/FOS and GRH transcription factors, but vary widely in trans- and cis-requirements for these inputs and their binding sites. We propose that the combination of GRH and FOS is part of an ancient wound-response pathway still used in vertebrates and invertebrates, but that other mechanisms have evolved that result in similar transcriptional output. A common, but largely untested assumption of bioinformatic analyses of gene regulatory networks is that transcription units activated in the same spatial and temporal patterns will require the same cis-regulatory codes. Our results indicate that this is an overly simplistic view.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.0810219106