GAGA protein is required for multiple aspects of Drosophila oogenesis and female fertility

• Published in: Genesis (New York, N.Y. : 2000) N.Y. : 2000), 2019-02, Vol.57 (2), p.e23269-n/a
• Main Authors: Fedorova, Elena V., Dorogova, Natalya V., Bolobolova, Elena U., Fedorova, Svetlana A., Karagodin, Dmitry A., Ogienko, Anna A., Khruscheva, Asja S., Baricheva, Elina M.
• Format: Article
• Language: English
• Subjects: Abnormalities; Actin; Actin Cytoskeleton - metabolism; Animals; Cell adhesion & migration; Cell Death; Cell migration; Cell Movement; Cytoskeleton; Defects; Deoxyribonucleic acid; Depletion; DNA; DNA-Binding Proteins - genetics; DNA-Binding Proteins - metabolism; Drosophila; Drosophila egg chamber; Drosophila melanogaster; Drosophila Proteins - genetics; Drosophila Proteins - metabolism; Electron microscopy; Endoplasmic reticulum; Endoplasmic Reticulum - metabolism; Female; female sterility; Fertility; Filaments; Fluorescence; GAGA protein; Gene expression; Gene regulation; Germ cells; Insects; Mitochondria; Mutants; Mutation; Nurse cells; Oogenesis; Ovaries; Ovum - metabolism; Phenotypes; Proteins; Sterility; Transcription; Transcription Factors - genetics; Transcription Factors - metabolism; Trl mutant; Yolk
• ISSN: 1526-954X; 1526-968X; 1526-968X
• DOI: 10.1002/dvg.23269

Summary Investigation of Drosophila oogenesis provides the opportunity to understand conservative genetic mechanisms underlying fertile female gamete development. In this study, we showed that the Drosophila DNA‐binding protein GAGA factor (GAF) had a multifunctional role in oogenesis and it is involved in the regulation of this process genetic program. We studied the influence on Drosophila oogenesis of a number of mutations in the 5′ region of the Trl gene that encodes GAF. We found that our originally generated Trl mutations lead to a decrease in transcriptional gene activity and levels of GAF expression in both germline and follicular cells. Cytological (fluorescence and electron microscopy) analysis showed that GAF loss resulted in multiple oogenesis defects. Mutations affected the actin cytoskeleton, leading to decrease of cytoplasmic filaments in nurse cells and basal actin in follicular cells. GAF depletion also leads to abnormal follicular cells migration, both border and centripetal. In addition, mutant ovaries demonstrated abnormalities in germ cells, including mitochondria, endoplasmic reticulum, karyosome organization, yolk granule formation and selective transport. Loss of GAF also promoted excessive cell death and egg chamber degradation. In sum, these defects caused very high or full female sterility. Since one of the main GAF activities is regulation of transcription, the complex phenotypes of the Trl mutants might be the consequence of its multiple target genes misexpression.