GAGA protein is required for multiple aspects of Drosophila oogenesis and female fertility. / Fedorova, Elena V.; Dorogova, Natalya V.; Bolobolova, Elena U. et al.
In: Genesis, Vol. 57, No. 2, e23269, 01.02.2019.Research output: Contribution to journal › Article › peer-review
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TY - JOUR
T1 - GAGA protein is required for multiple aspects of Drosophila oogenesis and female fertility
AU - Fedorova, Elena V.
AU - Dorogova, Natalya V.
AU - Bolobolova, Elena U.
AU - Fedorova, Svetlana A.
AU - Karagodin, Dmitry A.
AU - Ogienko, Anna A.
AU - Khruscheva, Asja S.
AU - Baricheva, Elina M.
N1 - Publisher Copyright: © 2018 Wiley Periodicals, Inc.
PY - 2019/2/1
Y1 - 2019/2/1
N2 - 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.
AB - 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.
KW - Drosophila egg chamber
KW - female sterility
KW - Trl mutant
KW - Actin Cytoskeleton/metabolism
KW - Drosophila Proteins/genetics
KW - Male
KW - Transcription Factors/genetics
KW - Oogenesis
KW - Animals
KW - DNA-Binding Proteins/genetics
KW - Fertility
KW - Cell Death
KW - Female
KW - Drosophila melanogaster
KW - Endoplasmic Reticulum/metabolism
KW - Cell Movement
KW - Ovum/metabolism
KW - ENCODES
KW - ORGANIZATION
KW - EPITHELIAL MORPHOGENESIS
KW - GENE-EXPRESSION
KW - CHROMATIN
KW - HOMOLOG
KW - CHROMOSOME
KW - CELL-MIGRATION
KW - EGG CHAMBER
KW - MELANOGASTER
UR - http://www.scopus.com/inward/record.url?scp=85059005566&partnerID=8YFLogxK
U2 - 10.1002/dvg.23269
DO - 10.1002/dvg.23269
M3 - Article
C2 - 30537428
AN - SCOPUS:85059005566
VL - 57
JO - Genesis
JF - Genesis
SN - 1526-954X
IS - 2
M1 - e23269
ER -
ID: 25439155