Eyes absent, a key repressor of polar cell fate during Drosophila oogenesis.

TitleEyes absent, a key repressor of polar cell fate during Drosophila oogenesis.
Publication TypeJournal Article
Year of Publication2002
AuthorsBai J, Montell D
JournalDevelopment
Volume129
Issue23
Pagination5377-88
Date Published2002 Dec
ISSN0950-1991
KeywordsAnimals, Cell Differentiation, Cell Lineage, DNA-Binding Proteins, Drosophila melanogaster, Drosophila Proteins, Epithelial Cells, Eye Proteins, Female, Gene Expression Regulation, Developmental, Green Fluorescent Proteins, Hedgehog Proteins, Kinesin, Luminescent Proteins, Membrane Proteins, Nuclear Proteins, Oogenesis, Ovary, Phenotype, Photoreceptor Cells, Invertebrate, Receptors, Cell Surface, Repressor Proteins, Signal Transduction, Transcription Factors
Abstract

<p>Throughout Drosophila oogenesis, specialized somatic follicle cells perform crucial functions in egg chamber formation and in signaling between somatic and germline cells. In the ovary, at least three types of somatic follicle cells, polar cells, stalk cells and main body epithelial follicle cells, can be distinguished when egg chambers bud from the germarium. Although specification of these three somatic cell types is important for normal oogenesis and subsequent embryogenesis, the molecular basis for establishment of their cell fates is not completely understood. Our studies reveal the gene eyes absent (eya) to be a key repressor of polar cell fate. EYA is a nuclear protein that is normally excluded from polar and stalk cells, and the absence of EYA is sufficient to cause epithelial follicle cells to develop as polar cells. Furthermore, ectopic expression of EYA is capable of suppressing normal polar cell fate and compromising the normal functions of polar cells, such as promotion of border cell migration. Finally, we show that ectopic Hedgehog signaling, which is known to cause ectopic polar cell formation, does so by repressing eya expression in epithelial follicle cells.</p>

DOI10.1242/dev.00115
Alternate JournalDevelopment
PubMed ID12403709
Grant ListR01 AG063907 / AG / NIA NIH HHS / United States