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 -