scholarly journals DRP1-dependent mitochondrial fission initiates follicle cell differentiation during Drosophila oogenesis

2012 ◽  
Vol 197 (4) ◽  
pp. 487-497 ◽  
Author(s):  
Kasturi Mitra ◽  
Richa Rikhy ◽  
Mary Lilly ◽  
Jennifer Lippincott-Schwartz
Keyword(s):  
Cell Cycle ◽  
Cell Differentiation ◽  
Cell Layer ◽  
Mitochondrial Fission ◽  
Follicle Cell ◽  
Follicle Cells ◽  
Developmental Defects ◽  
Drosophila Oogenesis ◽  
Regulated Expression ◽  
Regulatory Link

Exit from the cell cycle is essential for cells to initiate a terminal differentiation program during development, but what controls this transition is incompletely understood. In this paper, we demonstrate a regulatory link between mitochondrial fission activity and cell cycle exit in follicle cell layer development during Drosophila melanogaster oogenesis. Posterior-localized clonal cells in the follicle cell layer of developing ovarioles with down-regulated expression of the major mitochondrial fission protein DRP1 had mitochondrial elements extensively fused instead of being dispersed. These cells did not exit the cell cycle. Instead, they excessively proliferated, failed to activate Notch for differentiation, and exhibited downstream developmental defects. Reintroduction of mitochondrial fission activity or inhibition of the mitochondrial fusion protein Marf-1 in posterior-localized DRP1-null clones reversed the block in Notch-dependent differentiation. When DRP1-driven mitochondrial fission activity was unopposed by fusion activity in Marf-1–depleted clones, premature cell differentiation of follicle cells occurred in mitotic stages. Thus, DRP1-dependent mitochondrial fission activity is a novel regulator of the onset of follicle cell differentiation during Drosophila oogenesis.

Patterning of the follicle cell epithelium along the anterior-posterior axis during Drosophila oogenesis

Development ◽  
1998 ◽  
Vol 125 (15) ◽  
pp. 2837-2846 ◽  
Author(s):  
A. Gonzalez-Reyes ◽  
D. St Johnston
Keyword(s):  
Follicle Cell ◽  
Cell Types ◽  
Follicle Cells ◽  
Follicular Epithelium ◽  
Axis Formation ◽  
Main Body ◽  
Drosophila Oogenesis ◽  
Egfr Mutant ◽  
Anterior Posterior ◽  
Anterior Posterior Axis

Gurken signals from the oocyte to the adjacent follicle cells twice during Drosophila oogenesis; first to induce posterior fate, thereby polarising the anterior-posterior axis of the future embryo and then to induce dorsal fate and polarise the dorsal-ventral axis. Here we show that Gurken induces two different follicle cell fates because the follicle cells at the termini of the egg chamber differ in their competence to respond to Gurken from the main-body follicle cells in between. By removing the putative Gurken receptor, Egfr, in clones of cells, we show that Gurken signals directly to induce posterior fate in about 200 cells, defining a terminal competence domain that extends 10–11 cell diameters from the pole. Furthermore, small clones of Egfr mutant cells at the posterior interpret their position with respect to the pole and differentiate as the appropriate anterior cell type. Thus, the two terminal follicle cell populations contain a symmetric prepattern that is independent of Gurken signalling. These results suggest a three-step model for the anterior-posterior patterning of the follicular epithelium that subdivides this axis into at least five distinct cell types. Finally, we show that Notch plays a role in both the specification and patterning of the terminal follicle cells, providing a possible explanation for the defect in anterior-posterior axis formation caused by Notch and Delta mutants.

Role of Notch pathway in terminal follicle cell differentiation during Drosophila oogenesis

1999 ◽  
Vol 209 (5) ◽  
pp. 301-311 ◽  
Author(s):  
Michele Keller Larkin ◽  
W.-M. Deng ◽  
Kristen Holder ◽  
Michael Tworoger ◽  
Nigel Clegg ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Notch Pathway ◽  
Follicle Cell ◽  
Drosophila Oogenesis

scholarly journals Transcriptional Repressor Functions of Drosophila E2F1 and E2F2 Cooperate To Inhibit Genomic DNA Synthesis in Ovarian Follicle Cells

2003 ◽  
Vol 23 (6) ◽  
pp. 2123-2134 ◽  
Author(s):  
Pelin Cayirlioglu ◽  
William O. Ward ◽  
S. Catherine Silver Key ◽  
Robert J. Duronio
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Dna Synthesis ◽  
Gene Amplification ◽  
Cell Cycle Progression ◽  
Ovarian Follicle ◽  
Cell Cycle Control ◽  
Control Cell ◽  
Follicle Cell ◽  
Follicle Cells

ABSTRACT Individual members of the E2F/DP protein family control cell cycle progression by acting predominantly as an activator or repressor of transcription. In Drosophila melanogaster the E2f1, E2f2, Dp, and Rbf1 genes all contribute to replication control in ovarian follicle cells, which become 16C polyploid and subsequently undergo chorion gene amplification late in oogenesis. Mutation of E2f2, Dp, or Rbf1 causes ectopic DNA replication throughout the follicle cell genome during gene amplification cycles. Here we show by both reverse transcription-PCR and DNA microarray analysis that the transcripts of prereplication complex (pre-RC) genes are elevated compared to the wild type in E2f2, Dp, and Rbf1 mutant follicle cells. For some genes the magnitude of this transcriptional derepression is greater in Rbf1 than in E2f2 mutants. These differences correlate with differences in the magnitude of the replication defects in follicle cells, which attain an inappropriate 32C DNA content in both Rbf1 and Dp mutants but not in E2f2 mutants. The ectopic genomic replication of E2f2 mutant follicle cells can be suppressed by reducing the Orc2, Orc5, or Mcm2 gene dose by half, indicating that small changes in pre-RC gene expression can affect DNA synthesis in these cells. We conclude that RBF1 forms complexes with both E2F1/DP and E2F2/DP that cooperate to repress the expression of pre-RC genes, which helps confine DNA synthesis to sites of gene amplification. In contrast, E2F1 and E2F2 repressors function redundantly for some genes in the embryo. Thus, the relative functional contributions of E2F1 and E2F2 to gene expression and cell cycle control depends on the developmental context.

scholarly journals Nuclear receptor Ftz-f1 promotes follicle maturation and ovulation partly via bHLH/PAS transcription factor Sim

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Elizabeth M Knapp ◽  
Wei Li ◽  
Vijender Singh ◽  
Jianjun Sun
Keyword(s):  
Transcription Factor ◽  
Cell Differentiation ◽  
Nuclear Receptors ◽  
Follicle Cell ◽  
Follicle Cells ◽  
Maturation Stage ◽  
Steroidogenic Factor 1 ◽  
Final Maturation ◽  
And Function ◽  
Follicle Maturation

The NR5A-family nuclear receptors are highly conserved and function within the somatic follicle cells of the ovary to regulate folliculogenesis and ovulation in mammals; however, their roles in Drosophila ovaries are largely unknown. Here, we discover that Ftz-f1, one of the NR5A nuclear receptors in Drosophila, is transiently induced in follicle cells in late stages of oogenesis via ecdysteroid signaling. Genetic disruption of Ftz-f1 expression prevents follicle cell differentiation into the final maturation stage, which leads to anovulation. In addition, we demonstrate that the bHLH/PAS transcription factor Single-minded (Sim) acts as a direct target of Ftz-f1 to promote follicle cell differentiation/maturation and that Ftz-f1’s role in regulating Sim expression and follicle cell differentiation can be replaced by its mouse homolog steroidogenic factor 1 (mSF-1). Our work provides new insight into the regulation of follicle maturation in Drosophila and the conserved role of NR5A nuclear receptors in regulating folliculogenesis and ovulation.

scholarly journals A large-scale in vivo RNAi screen to identify genes involved in Notch-mediated follicle cell differentiation and cell cycle switches

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Dongyu Jia ◽  
Muhammed Soylemez ◽  
Gabriel Calvin ◽  
Randy Bornmann ◽  
Jamal Bryant ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Differentiation ◽  
Large Scale ◽  
Follicle Cell ◽  
Rnai Screen

Notch-Delta signaling induces a transition from mitotic cell cycle to endocycle inDrosophilafollicle cells

Development ◽  
2001 ◽  
Vol 128 (23) ◽  
pp. 4737-4746 ◽  
Author(s):  
Wu-Min Deng ◽  
Cassandra Althauser ◽  
Hannele Ruohola-Baker
Keyword(s):  
Cell Cycle ◽  
Mitotic Cycle ◽  
Notch Pathway ◽  
Follicle Cell ◽  
Delta Function ◽  
Mitotic Cell ◽  
Follicle Cells ◽  
Transcriptional Level ◽  
M Cell ◽  
Normal Transition

In many developmental processes, polyploid cells are generated by a variation of the normal cell cycle called the endocycle in which cells increase their genomic content without dividing. How the transition from the normal mitotic cycle to endocycle is regulated is poorly understood. We show that the transition from mitotic cycle to endocycle in the Drosophila follicle cell epithelium is regulated by the Notch pathway. Loss of Notch function in follicle cells or its ligand Delta function in the underlying germline disrupts the normal transition of the follicle cells from mitotic cycle to endocycle, mitotic cycling continues, leading to overproliferation of these cells. The regulation is at the transcriptional level, as Su(H), a downstream transcription factor in the pathway, is also required cell autonomously in follicle cells for proper transitioning to the endocycle. One target of Notch and Su(H) is likely to be the G2/M cell cycle regulator String, a phosphatase that activates Cdc2 by dephosphorylation. String is normally repressed in the follicle cells just before the endocycle transition, but is expressed when Notch is inactivated. Analysis of the activity of String enhancer elements in follicle cells reveals the presence of an element that promotes expression of String until just before the onset of polyploidy in wild-type follicle cells but well beyond this stage in Notch mutant follicle cells. This suggests that it may be the target of the endocycle promoting activity of the Notch pathway. A second element that is insensitive to Notch regulation promotes String expression earlier in follicle cell development, which explains why Notch, while active at both stages, represses String only at the mitotic cycle-endocycle transition.

scholarly journals hold up Is Required for Establishment of Oocyte Positioning, Follicle Cell Fate and Egg Polarity and Cooperates with Egfr during Drosophila Oogenesis

Genetics ◽  
1998 ◽  
Vol 148 (2) ◽  
pp. 767-773
Author(s):  
Deborah Rotoli ◽  
Silvia Andone ◽  
Claudia Tortiglione ◽  
Andrea Manzi ◽  
Carla Malva ◽  
...  
Keyword(s):  
Cell Fate ◽  
Cell Layer ◽  
Growth Factor Receptor ◽  
Follicle Cell ◽  
Follicle Cells ◽  
Early Event ◽  
Parallel Pathway ◽  
Egg Chambers ◽  
Molecular Machinery ◽  
Epidermal Growth

Abstract In Drosophila the posterior positioning of the oocyte within the germline cluster defines the initial asymmetry during oogenesis. From this early event, specification of both body axes is controlled through reciprocal signaling between germline and soma. Here it is shown that the mutation hold up (hup) affects oocyte positioning in the egg chamber, follicle cell fate and localization of different markers in the growing oocytes. This occurs not only in dicephalic egg chambers, but also in oocytes normally located at the posterior. Generation of mosaic egg chambers indicates that hup has to be at least somatically required. Possible interactions of hup with Egfr, the Drosophila epidermal growth factor receptor homolog, have been investigated in homozygous double mutants constructed by recombination. Stronger new ovarian phenotypes have been obtained, the most striking being accumulation of follicle cells in multiple layers posteriorly to the oocyte. It is proposed that the hup gene product is a component of the molecular machinery that leads to the establishment of polarity both in follicle cell layer and oocyte, acting in the same or in a parallel pathway of Egfr.

Cell Cycle Influence of Stem Cell Differentiation in Culture.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 4194-4194
Author(s):  
Toska J. Zomorodian ◽  
Mehrdad Abedi ◽  
Gerri Dooner ◽  
Debbie Greer ◽  
Kevin Johnson ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Stem Cells ◽  
Stem Cell ◽  
Cell Differentiation ◽  
Stromal Cell ◽  
Cultured Cells ◽  
Cell Layer ◽  
Stem Cell Differentiation ◽  
S Phase ◽  
Time Point

Abstract Hierarchical models of hematopoiesis suppose an ordered system in which stem cells and progenitors with specific fixed differentiation potentials exist. We show that the potential of marrow stem cells to differentiate changes reversibly with cytokine-induced cell cycle transit. To address whether the cell cycle plays a role in the differentiation of stem cells, we co-cultured murine bone marrow Lin- Sca-1+ cells, at different points in their cycle, with the OP9-DL1 system. OP9-DL1 stromal cell layer has been transduced to allow T-cell differentiation in culture. We first induced cell cycle synchrony by exposing the isolated cells to a cytokine cocktail of TPO, Flt-3 and Stem Cell Factor. The cells were exposed to this primary culture for 0, 6, 24, 32 and 40 hours and were subsequently cultured on an OP9-DL1 stromal cell layer grown in 6-well plates. Cells were co-cultured for 8 days and 21 days, in the presence of IL-7 and Flt-3. Cultured cells were evaluated for CD4, CD8, B220, CD19, NK1.1, and Mac-1 surface markers, using flow cytometry. On Day 8, we found a significant hotspot at 32-hours (early-S phase) for B220+ cells (34.3 %), while Mac-1 positive cells demonstrated a 24-hour hotspot (18.1 %). As expected, terminal T and B-cell differentiation (CD 4, CD8, and CD19) was undetectable at 8 days. Three separate short-term (8 day) experiments have confirmed these data. Cells in culture for 21 days similarly show variation in differentiation outcome. CD4 cells demonstrate a peak at the 40 hour time point (mid-S phase) (69.9%), while CD8 positive cells were significantly increased at the 32 hour time point (34.4%). These data indicate both B and T cells show reversible differentiation fluxes linked to cell cycle. This work supports previous evidence that marrow hematopoiesis at the stem cell level is regulated on a continuum and that stem cells have reversible, cycle-related differentiation capacity.

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