The breathless FGF receptor homolog, a downstream target of Drosophila C/EBP in the developmental control of cell migration.

TitleThe breathless FGF receptor homolog, a downstream target of Drosophila C/EBP in the developmental control of cell migration.
Publication TypeJournal Article
Year of Publication1995
AuthorsMurphy AM, Lee T, Andrews CM, Shilo BZ, Montell DJ
JournalDevelopment
Volume121
Issue8
Pagination2255-63
Date Published1995 Aug
ISSN0950-1991
KeywordsAnimals, Base Sequence, Binding Sites, CCAAT-Enhancer-Binding Proteins, Cell Movement, DNA, DNA-Binding Proteins, Drosophila, Drosophila Proteins, Female, Gene Expression Regulation, Developmental, Genes, Insect, Genes, Lethal, Molecular Sequence Data, Mutation, Nuclear Proteins, Ovary, Promoter Regions, Genetic, Protein-Tyrosine Kinases, Receptors, Fibroblast Growth Factor, Transcription Factors
Abstract

<p>To investigate the molecular mechanisms responsible for the temporal and spatial control of cell movements during development, we have been studying the migration of a small group of follicle cells, called the border cells, in the Drosophila ovary. Timely initiation of border cell migration requires the product of the slow border cells (slbo) locus, which encodes the Drosophila homolog of the transcription factor C/EBP. Here we report evidence that one target of C/EBP in the control of border cell migration is the FGF receptor homolog encoded by the breathless (btl) locus. btl expression in the ovary was border cell-specific, beginning just prior to the migration, and this expression was reduced in slbo mutants. btl mutations dominantly enhanced the border cell migration defects found in weak slbo alleles. Furthermore, C/EBP-independent btl expression was able to rescue the migration defects of hypomorphic slbo alleles. Purified Drosophila C/EBP bound eight sites in the btl 5' flanking region by DNAse I footprinting. Taken together these results suggest that btl is a key, direct target for C/EBP in the regulation of border cell migration.</p>

Alternate JournalDevelopment
PubMed ID7671793
Grant ListR01 AG063907 / AG / NIA NIH HHS / United States
R29GM464 / GM / NIGMS NIH HHS / United States