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Hunchback is counter-repressed to regulate even-skipped stripe 2 expression in Drosophila embryos.
- Source :
-
PLoS genetics [PLoS Genet] 2018 Sep 07; Vol. 14 (9), pp. e1007644. Date of Electronic Publication: 2018 Sep 07 (Print Publication: 2018). - Publication Year :
- 2018
-
Abstract
- Hunchback is a bifunctional transcription factor that can activate and repress gene expression in Drosophila development. We investigated the regulatory DNA sequence features that control Hunchback function by perturbing enhancers for one of its target genes, even-skipped (eve). While Hunchback directly represses the eve stripe 3+7 enhancer, we found that in the eve stripe 2+7 enhancer, Hunchback repression is prevented by nearby sequences-this phenomenon is called counter-repression. We also found evidence that Caudal binding sites are responsible for counter-repression, and that this interaction may be a conserved feature of eve stripe 2 enhancers. Our results alter the textbook view of eve stripe 2 regulation wherein Hb is described as a direct activator. Instead, to generate stripe 2, Hunchback repression must be counteracted. We discuss how counter-repression may influence eve stripe 2 regulation and evolution.<br />Competing Interests: The authors have declared that no competing interests exist.
- Subjects :
- Animals
Animals, Genetically Modified
Binding Sites genetics
DNA-Binding Proteins genetics
Drosophila melanogaster growth & development
Embryo, Nonmammalian
Enhancer Elements, Genetic genetics
Female
Homeodomain Proteins metabolism
Male
DNA-Binding Proteins metabolism
Drosophila Proteins genetics
Drosophila Proteins metabolism
Drosophila melanogaster genetics
Gene Expression Regulation, Developmental
Homeodomain Proteins genetics
Transcription Factors genetics
Transcription Factors metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1553-7404
- Volume :
- 14
- Issue :
- 9
- Database :
- MEDLINE
- Journal :
- PLoS genetics
- Publication Type :
- Academic Journal
- Accession number :
- 30192762
- Full Text :
- https://doi.org/10.1371/journal.pgen.1007644