scholarly journals Role of Bicaudal-D in patterning the Drosophila egg chamber in mid-oogenesis

Development ◽  
1996 ◽  
Vol 122 (11) ◽  
pp. 3577-3586 ◽  
Author(s):  
A. Swan ◽  
B. Suter
Keyword(s):  
Cell Migration ◽  
Nurse Cell ◽  
Germ Line ◽  
Follicle Cells ◽  
Oocyte Size ◽  
Hsp70 Promoter ◽  
Oocyte Growth ◽  
Drosophila Oogenesis ◽  
Specific Mrnas

The Bicaudal-D (Bic-D) gene is required early in Drosophila oogenesis for the differentiation of an oocyte from one of a cluster of 16 interconnected germarial cells. To analyze the role of Bic-D later in oogenesis, we have constructed Drosophila lines in which Bic-D expression is under the control of the hsp70 promoter. In these flies, Bic-D activity can be induced early in oogenesis, allowing an oocyte to be made. Then, by shifting females to non-inducing conditions, Bic-D levels are depleted for the remainder of oogenesis. Using this system, we find that Bic-D is indeed required in the later stages of oogenesis. In ovaries from mutant females, oocyte growth is reduced, apparently due to defects in nurse-cell-to-oocyte transport. Smaller oocyte size results in the misalignment of follicle cells and the underlying germ line, leading to ventralization of dorsal follicle cells and to defects in centripetal cell migration. In addition, we show that Bic-D is required for the localization of specific mRNAs at both the anterior and posterior of the oocyte.

The TGF-beta signaling pathway is essential for Drosophila oogenesis

Development ◽  
1996 ◽  
Vol 122 (5) ◽  
pp. 1555-1565 ◽  
Author(s):  
V. Twombly ◽  
R.K. Blackman ◽  
H. Jin ◽  
J.M. Graff ◽  
R.W. Padgett ◽  
...  
Keyword(s):  
Family Member ◽  
Signaling Pathway ◽  
Expression Pattern ◽  
Nurse Cell ◽  
Follicle Cells ◽  
Tgf Beta ◽  
Drosophila Oogenesis ◽  
Egg Chamber

We examine roles of signaling by secreted ligands of the TGF-beta family during Drosophila oogenesis. One family member, the DPP ligand encoded by the decapentaplegic (dpp) gene, is required for patterning of anterior eggshell structures. This requirement presumably reflects the expression pattern of dpp in an anterior subset of somatic follicle cells: the centripetally migrating and the nurse cell-associated follicle cells. Similar requirements are also revealed by mutations in the saxophone (sax)-encoded receptor, consistent with the idea that DPP signaling is, at least in part, mediated by the SAX receptor. A loss of germline sax function results in a block in oogenesis associated with egg chamber degeneration and a failure of the transfer of nurse cell contents to the oocyte, indicating that TGF-beta signaling is required for these events. Some phenotypes of sax mutations during oogenesis suggest that SAX responds to at least one other TGF-beta ligand as well in the posterior follicle cells.

scholarly journals DE-Cadherin Is Required for Intercellular Motility during Drosophila Oogenesis

1999 ◽  
Vol 144 (3) ◽  
pp. 533-547 ◽  
Author(s):  
Paulina Niewiadomska ◽  
Dorothea Godt ◽  
Ulrich Tepass
Keyword(s):  
Cell Migration ◽  
Follicle Cells ◽  
Epithelial Polarity ◽  
Border Cells ◽  
Drosophila Oogenesis ◽  
Animal Development ◽  
Border Cell ◽  
Germline Cells ◽  
Peripheral Cells ◽  
Homophilic Adhesion

Cadherins are involved in a variety of morphogenetic movements during animal development. However, it has been difficult to pinpoint the precise function of cadherins in morphogenetic processes due to the multifunctional nature of cadherin requirement. The data presented here indicate that homophilic adhesion promoted by Drosophila E-cadherin (DE-cadherin) mediates two cell migration events during Drosophila oogenesis. In Drosophila follicles, two groups of follicle cells, the border cells and the centripetal cells migrate on the surface of germline cells. We show that the border cells migrate as an epithelial patch in which two centrally located cells retain epithelial polarity and peripheral cells are partially depolarized. Both follicle cells and germline cells express DE-cadherin, and border cells and centripetal cells strongly upregulate the expression of DE-cadherin shortly before and during their migration. Removing DE-cadherin from either the follicle cells or the germline cells blocks migration of border cells and centripetal cells on the surface of germline cells. The function of DE-cadherin in border cells appears to be specific for migration as the formation of the border cell cluster and the adhesion between border cells are not disrupted in the absence of DE-cadherin. The speed of migration depends on the level of DE-cadherin expression, as border cells migrate more slowly when DE-cadherin activity is reduced. Finally, we show that the upregulation of DE-cadherin expression in border cells depends on the activity of the Drosophila C/EBP transcription factor that is essential for border cell migration.

scholarly journals GAGA Regulates Border Cell Migration in Drosophila

2020 ◽  
Vol 21 (20) ◽  
pp. 7468
Author(s):  
Anna A. Ogienko ◽  
Lyubov A. Yarinich ◽  
Elena V. Fedorova ◽  
Natalya V. Dorogova ◽  
Sergey I. Bayborodin ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Cell Migration ◽  
Target Genes ◽  
Genetic Interaction ◽  
Follicle Cells ◽  
Collective Cell Migration ◽  
Border Cells ◽  
Drosophila Oogenesis ◽  
Small Set ◽  
Multicellular Organisms

Collective cell migration is a complex process that happens during normal development of many multicellular organisms, as well as during oncological transformations. In Drosophila oogenesis, a small set of follicle cells originally located at the anterior tip of each egg chamber become motile and migrate as a cluster through nurse cells toward the oocyte. These specialized cells are referred to as border cells (BCs) and provide a simple and convenient model system to study collective cell migration. The process is known to be complexly regulated at different levels and the product of the slow border cells (slbo) gene, the C/EBP transcription factor, is one of the key elements in this process. However, little is known about the regulation of slbo expression. On the other hand, the ubiquitously expressed transcription factor GAGA, which is encoded by the Trithorax-like (Trl) gene was previously demonstrated to be important for Drosophila oogenesis. Here, we found that Trl mutations cause substantial defects in BC migration. Partially, these defects are explained by the reduced level of slbo expression in BCs. Additionally, a strong genetic interaction between Trl and slbo mutants, along with the presence of putative GAGA binding sites within the slbo promoter and enhancer, suggests the direct regulation of this gene by GAGA. This idea is supported by the reduction in the slbo-Gal4-driven GFP expression within BC clusters in Trl mutant background. However, the inability of slbo overexpression to compensate defects in BC migration caused by Trl mutations suggests that there are other GAGA target genes contributing to this process. Taken together, the results define GAGA as another important regulator of BC migration in Drosophila oogenesis.

Mutations in the Drosophila gene bullwinkle cause the formation of abnormal eggshell structures and bicaudal embryos

Development ◽  
1995 ◽  
Vol 121 (9) ◽  
pp. 3023-3033 ◽  
Author(s):  
K.R. Rittenhouse ◽  
C.A. Berg
Keyword(s):  
Cell Migration ◽  
Cell Fate ◽  
Germ Line ◽  
Follicle Cell ◽  
Posterior Pole ◽  
Mirror Image ◽  
Follicle Cells ◽  
Anterior Pole ◽  
Posterior Group ◽  
General Transport

Subcellular localization of gene products and cell migration are both critical for pattern formation during development. The bullwinkle gene is required in Drosophila for disparate aspects of these processes. In females mutant at the bullwinkle locus, the follicle cells that synthesize the dorsal eggshell filaments do not migrate properly, creating short, broad structures. Mosaic analyses demonstrate that wild-type BULLWINKLE function is required in the germ line for these migrations. Since the mRNA for gurken, the putative ligand that signals dorsal follicle cell fate, is correctly localized in bullwinkle mutants, we conclude that our bullwinkle alleles do not affect the dorsoventral polarity of the oocyte and thus must be affecting the follicle cell migrations in some other way. In addition, the embryos that develop from bullwinkle mothers are bicaudal. A KINESIN:beta-GALACTOSIDASE fusion protein is correctly localized to the posterior pole of bullwinkle oocytes during stage 9. Thus, the microtubule structure of the oocyte and general transport along it do not appear to be disrupted prior to cytoplasmic streaming. Unlike other bicaudal mutants, oskar mRNA is localized correctly to the posterior pole of the oocyte at stage 10. By early embryogenesis, however, some oskar mRNA is mislocalized to the anterior pole. Consistent with the mislocalization of oskar mRNA, a fraction of the VASA protein and nanos mRNA are also mislocalized to the anterior pole of bullwinkle embryos. Mislocalization of nanos mRNA to the anterior is dependent on functional VASA protein. Although the mirror-image segmentation defects appear to result from the action of the posterior group genes, germ cells are not formed at the anterior pole. The bicaudal phenotype is also germ-line dependent for bullwinkle. We suspect that BULLWINKLE interacts with the cytoskeleton and extracellular matrix and is necessary for gene product localization and cell migration during oogenesis after stage 10a.

Investigating the function of follicular subpopulations during Drosophila oogenesis through hormone-dependent enhancer-targeted cell ablation

Development ◽  
2000 ◽  
Vol 127 (3) ◽  
pp. 573-583 ◽  
Author(s):  
D.D. Han ◽  
D. Stein ◽  
L.M. Stevens
Keyword(s):  
Gene Expression ◽  
Diphtheria Toxin ◽  
Follicle Cells ◽  
Specific Gene ◽  
Border Cells ◽  
Drosophila Oogenesis ◽  
Cell Ablation ◽  
Powerful Approach ◽  
Human Estrogen Receptor

Although it is known that the establishment of polarity during Drosophila oogenesis is initiated by signalling from the oocyte to the overlying follicle cells, much less is understood about the role of specific follicular subpopulations. One powerful approach for addressing this question, toxigenic cell ablation of specific subpopulations, has not previously been applicable to studying follicular subpopulations because many of the genes and Gal4 enhancer trap insertions that are expressed in the ovary are also expressed at earlier times in development. To overcome this problem, we have utilized a fusion protein between Gal4 and the human estrogen receptor to achieve hormone-dependent, tissue-specific gene expression of UAS-linked transgenes in flies. We used this system to study the role of the polar subpopulations of follicle cells during oogenesis by expressing within them a modified form of diphtheria toxin that causes cell death. Our results confirmed previous functions ascribed to these cells, and also demonstrated a previously undescribed role for the border cells in facilitating the migration of the anterior Fasciclin III-expressing polar pair cells to the edge of the oocyte.

scholarly journals The GATOR complex regulates an essential response to meiotic double-stranded breaks in Drosophila

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Youheng Wei ◽  
Lucia Bettedi ◽  
Chun-Yuan Ting ◽  
Kuikwon Kim ◽  
Yingbiao Zhang ◽  
...  
Keyword(s):  
Metabolic Pathways ◽  
Oocyte Growth ◽  
Drosophila Oogenesis ◽  
Meiotic Progression ◽  
Delayed Repair ◽  
Meiotic Dsbs ◽  
Meiotic Entry

The TORC1 regulator GATOR1/SEACIT controls meiotic entry and early meiotic events in yeast. However, how metabolic pathways influence meiotic progression in metazoans remains poorly understood. Here we examine the role of the TORC1 regulators GATOR1 and GATOR2 in the response to meiotic double-stranded breaks (DSB) during Drosophila oogenesis. We find that in mutants of the GATOR2 component mio, meiotic DSBs trigger the constitutive downregulation of TORC1 activity and a permanent arrest in oocyte growth. Conversely, in GATOR1 mutants, high TORC1 activity results in the delayed repair of meiotic DSBs and the hyperactivation of p53. Unexpectedly, we found that GATOR1 inhibits retrotransposon expression in the presence of meiotic DSBs in a pathway that functions in parallel to p53. Thus, our studies have revealed a link between oocyte metabolism, the repair of meiotic DSBs and retrotransposon expression.

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