FGF signaling supports Drosophila fertility by regulating development of ovarian muscle tissues
The thisbe (ths) gene encodes a Drosophila fibroblast growth factor (FGF), and mutant females are viable but sterile suggesting a link between FGF signaling and fertility. Ovaries exhibit abnormal morphology including lack of epithelial sheaths and muscle tissues that surround ovarioles. Here we investigated how FGF influences Drosophila ovary morphogenesis and identified several roles. Heartless (Htl) FGF receptor was found to be expressed within somatic cells at the larval and pupal stages, and phenotypes were uncovered using RNAi. Differentiation of terminal filament cells was affected, but this effect did not alter the ovariole number. In addition, proliferation of epithelial sheath progenitors and the apical cells was decreased in both htl and ths mutants, while ectopic expression of the Ths ligand led to these cells' over-proliferation suggesting that FGF signaling supports ovarian muscle sheath formation by controlling apical cell number in the developing gonad. Additionally, live imaging of adult ovaries was used to show that htl RNAi mutants and hypomorphic mutants, in which epithelial sheaths are present, exhibit abnormal muscle contractions. Collectively, our results demonstrate that proper formation of ovarian muscle tissues is regulated by FGF signaling in the larval and pupal stages through control of apical cell proliferation and is required to support fertility.
© 2015 Elsevier Inc. Received 23 April 2015, Accepted 28 April 2015, Available online 6 May 2015. We thank Leslie Dunipace and Ha Vu for generating fly stocks used in this study including htl.mCherry and pyr.GAL4s and Va Si for initiating study of the FGF mutant sterility phenotype. We also are grateful to D. Godt and M. Leptin for sending antibodies and many Drosophila researchers for sharing published fly stocks. This study was supported by a Grant to A.S. from the NIH/NIGMS R01GM104838 as well as support of J.I. from CIRM Bridges to Stem Cell Research Program Grant (Cal Poly and Cal State Los Angeles) TB1-01176 and NIH/NRSA training Grant (Caltech) 5T32GM07616.
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