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dc.contributor.authorField, Amanda
dc.contributor.authorXiang, Jie
dc.contributor.authorAnderson, W. Ray
dc.contributor.authorGraham, Patricia
dc.contributor.authorPick, Leslie
dc.date.accessioned2017-08-31T19:51:56Z
dc.date.available2017-08-31T19:51:56Z
dc.date.issued2016-10-10
dc.identifierhttps://doi.org/10.13016/M2M61BQ26
dc.identifier.citationField A, Xiang J, Anderson WR, Graham P, Pick L (2016) Activation of Ftz-F1-Responsive Genes through Ftz/Ftz-F1 Dependent Enhancers. PLoS ONE 11(10): e0163128. doi:10.1371/journal. pone.0163128en_US
dc.identifier.urihttp://hdl.handle.net/1903/19701
dc.descriptionPartial funding for Open Access provided by the UMD Libraries' Open Access Publishing Fund.en_US
dc.description.abstractThe orphan nuclear receptor Ftz-F1 is expressed in all somatic nuclei in Drosophila embryos, but mutations result in a pair-rule phenotype. This was explained by the interaction of Ftz-F1 with the homeodomain protein Ftz that is expressed in stripes in the primordia of segments missing in either ftz-f1 or ftz mutants. Ftz-F1 and Ftz were shown to physically interact and coordinately activate the expression of ftz itself and engrailed by synergistic binding to composite Ftz-F1/Ftz binding sites. However, attempts to identify additional target genes on the basis of Ftz-F1/ Ftz binding alone has met with only limited success. To discern rules for Ftz-F1 target site selection in vivo and to identify additional target genes, a microarray analysis was performed comparing wildtype and ftz-f1 mutant embryos. Ftz-F1-responsive genes most highly regulated included engrailed and nine additional genes expressed in patterns dependent on both ftz and ftz-f1. Candidate enhancers for these genes were identified by combining BDTNP Ftz ChIP-chip data with a computational search for Ftz-F1 binding sites. Of eight enhancer reporter genes tested in transgenic embryos, six generated expression patterns similar to the corresponding endogenous gene and expression was lost in ftz mutants. These studies identified a new set of Ftz-F1 targets, all of which are co-regulated by Ftz. Comparative analysis of enhancers containing Ftz/Ftz-F1 binding sites that were or were not bona fide targets in vivo suggested that GAF negatively regulates enhancers that contain Ftz/Ftz-F1 binding sites but are not actually utilized. These targets include other regulatory factors as well as genes involved directly in morphogenesis, providing insight into how pair-rule genes establish the body pattern.en_US
dc.language.isoen_USen_US
dc.publisherPLoS (Public Library of Science)en_US
dc.titleActivation of Ftz-F1-Responsive Genes through Ftz/Ftz-F1 Dependent Enhancersen_US
dc.typeArticleen_US
dc.relation.isAvailableAtDigital Repository at the University of Marylanden_us
dc.relation.isAvailableAtEntomologyen_us
dc.relation.isAvailableAtCollege of Computer, Mathematical & Natural Sciencesen_us
dc.relation.isAvailableAtUniversity of Maryland (College Park, MD)en_us


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