title: Investigating the function of follicular subpopulations during Drosophila oogenesis through hormone-dependent enhancer-targeted cell ablation.
abstract: Although it is known that the establishment of polarity during Drosophila oogenesis is initiated by signalling from the oocyte to the overlying follicle cells, much less is understood about the role of specific follicular subpopulations. One powerful approach for addressing this question, toxigenic cell ablation of specific subpopulations, has not previously been applicable to studying follicular subpopulations because many of the genes and Gal4 enhancer trap insertions that are expressed in the ovary are also expressed at earlier times in development. To overcome this problem, we have utilized a fusion protein between Gal4 and the human estrogen receptor to achieve hormone-dependent, tissue-specific gene expression of UAS-linked transgenes in flies. We used this system to study the role of the polar subpopulations of follicle cells during oogenesis by expressing within them a modified form of diphtheria toxin that causes cell death. Our results confirmed previous functions ascribed to these cells, and also demonstrated a previously undescribed role for the border cells in facilitating the migration of the anterior Fasciclin III-expressing polar pair cells to the edge of the oocyte.
authors.affiliation: Department of Developmental Biology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
authors.forename: D D
authors.initials: DD
authors.lastname: Han
authors.forename: D
authors.initials: D
authors.lastname: Stein
authors.forename: L M
authors.initials: LM
authors.lastname: Stevens
mesh_terms: D000818:Animals; D030801:Animals, Genetically Modified; D019521:Body Patterning; D015816:Cell Adhesion Molecules, Neuronal / Q000032:analysis; D016923:Cell Death / Q000187:drug effects; D004268:DNA-Binding Proteins; D004167:Diphtheria Toxin / Q000633:toxicity; D004330:Drosophila / Q000196:embryology* / Q000235:genetics*; D029721:Drosophila Proteins; D004742:Enhancer Elements, Genetic; D004958:Estradiol / Q000494:pharmacology; D005260:Female; D005656:Fungal Proteins / Q000235:genetics / Q000378:metabolism; D006801:Humans; D009865:Oocytes / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D009866:Oogenesis; D006080:Ovarian Follicle / Q000502:physiology*; D011960:Receptors, Estrogen / Q000235:genetics / Q000378:metabolism; D011993:Recombinant Fusion Proteins / Q000378:metabolism; D029701:Saccharomyces cerevisiae Proteins; D015398:Signal Transduction; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism; D001616:beta-Galactosidase / Q000235:genetics
chemical_list: D015816:Cell Adhesion Molecules, Neuronal; D004268:DNA-Binding Proteins; D004167:Diphtheria Toxin; D029721:Drosophila Proteins; C061565:Fas3 protein, Drosophila; D005656:Fungal Proteins; C052130:GAL4 protein, S cerevisiae; D011960:Receptors, Estrogen; D011993:Recombinant Fusion Proteins; D029701:Saccharomyces cerevisiae Proteins; D014157:Transcription Factors; D004958:Estradiol; D001616:beta-Galactosidase