GONUTS has been updated to MW1.31 Most things seem to be working but be sure to report problems.

Have any questions? Please email us at ecoliwiki@gmail.com


Jump to: navigation, search


You don't have sufficient rights on this wiki to edit tables. Perhaps you need to log in. Changes you make in the Table editor will not be saved back to the wiki

See Help for Help on this wiki. See the documentation for how to use the table editor


Pearson, JC, Juarez, MT, Kim, M, Drivenes, Ø and McGinnis, W (2009) Multiple transcription factor codes activate epidermal wound-response genes in Drosophila. Proc. Natl. Acad. Sci. U.S.A. 106:2224-9


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.


PubMed PMC2630199 Online version:10.1073/pnas.0810219106


Animals; Binding Sites; Drosophila; Drosophila melanogaster; Enhancer Elements, Genetic; Epidermis/pathology; Gene Expression Regulation; Microscopy, Fluorescence; Models, Biological; Models, Genetic; Mutation; Time Factors; Transcription Factors/metabolism; Transcription, Genetic; Wound Healing