Follicle cell development is partly independent of germ-line cell differentiation in Drosophila oogenesis

1989 ◽  
Vol 198 (4) ◽  
pp. 185-190 ◽  
Author(s):  
Herwig O. Gutzeit ◽  
Arthur Strau�
Keyword(s):  
Cell Differentiation ◽  
Germ Line ◽  
Follicle Cell ◽  
Cell Development ◽  
Germ Line Cell ◽  
Drosophila Oogenesis

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 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.

Testicular germ line cell identification, isolation, and transplantation in two North American catfish species

2018 ◽  
Vol 44 (2) ◽  
pp. 717-733 ◽  
Author(s):  
Mei Shang ◽  
Baofeng Su ◽  
Dayan A. Perera ◽  
Ahmed Alsaqufi ◽  
Elizabeth A. Lipke ◽  
...  
Keyword(s):  
North American ◽  
Germ Line ◽  
Germ Line Cell ◽  
Cell Identification

Intersection of regulatory pathways controlling hemostasis and hemochorial placentation

2021 ◽  
Vol 118 (50) ◽  
pp. e2111267118
Author(s):  
Masanaga Muto ◽  
Damayanti Chakraborty ◽  
Kaela M. Varberg ◽  
Ayelen Moreno-Irusta ◽  
Khursheed Iqbal ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Differentiation ◽  
Cell Invasion ◽  
Cell Development ◽  
Trophoblast Cell ◽  
Extravillous Trophoblast ◽  
Cell Phenotype ◽  
Trophoblast Cells ◽  
Rat Models ◽  
Endovascular Trophoblast

Hemochorial placentation is characterized by the development of trophoblast cells specialized to interact with the uterine vascular bed. We utilized trophoblast stem (TS) cell and mutant rat models to investigate regulatory mechanisms controlling trophoblast cell development. TS cell differentiation was characterized by acquisition of transcript signatures indicative of an endothelial cell-like phenotype, which was highlighted by the expression of anticoagulation factors including tissue factor pathway inhibitor (TFPI). TFPI localized to invasive endovascular trophoblast cells of the rat placentation site. Disruption of TFPI in rat TS cells interfered with development of the endothelial cell-like endovascular trophoblast cell phenotype. Similarly, TFPI was expressed in human invasive/extravillous trophoblast (EVT) cells situated within first-trimester human placental tissues and following differentiation of human TS cells. TFPI was required for human TS cell differentiation to EVT cells. We next investigated the physiological relevance of TFPI at the placentation site. Genome-edited global TFPI loss-of-function rat models revealed critical roles for TFPI in embryonic development, resulting in homogeneous midgestation lethality prohibiting analysis of the role of TFPI as a regulator of the late-gestation wave of intrauterine trophoblast cell invasion. In vivo trophoblast-specific TFPI knockdown was compatible with pregnancy but had profound effects at the uterine–placental interface, including restriction of the depth of intrauterine trophoblast cell invasion while leading to the accumulation of natural killer cells and increased fibrin deposition. Collectively, the experimentation implicates TFPI as a conserved regulator of invasive/EVT cell development, uterine spiral artery remodeling, and hemostasis at the maternal–fetal interface.

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.

scholarly journals The transcription factor ETS1 is an important regulator of human NK cell development and terminal differentiation

Blood ◽  
2020 ◽  
Author(s):  
Sylvie Taveirne ◽  
Sigrid Wahlen ◽  
Wouter Van Loocke ◽  
Laura Kiekens ◽  
Eva Persyn ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Cell Differentiation ◽  
Cell Biology ◽  
Nk Cell ◽  
Embryonic Stem ◽  
Terminal Differentiation ◽  
Cell Development ◽  
Immune Defense ◽  
Nk Cell Differentiation ◽  
Important Regulator

Natural killer (NK) cells are important in the immune defense against tumor cells and pathogens, and regulate other immune cells by cytokine secretion. Whereas murine NK cell biology has been extensively studied, knowledge about transcriptional circuitries controlling human NK cell development and maturation is limited. By generating ETS1-deficient human embryonic stem cells (hESC) and by expressing the dominant-negative ETS1 p27 isoform in cord blood (CB) hematopoietic progenitor cells (HPCs), we show that the transcription factor ETS1 is critically required for human NK cell differentiation. Genome-wide transcriptome analysis determined by RNA-sequencing combined with chromatin immunoprecipitation-sequencing (ChIP-seq) analysis reveals that human ETS1 directly induces expression of key transcription factors that control NK cell differentiation, i.e. E4BP4, TXNIP, TBET, GATA3, HOBIT and BLIMP1. In addition, ETS1 regulates expression of genes involved in apoptosis and NK cell activation. Our study provides important molecular insights into the role of ETS1 as an important regulator of human NK cell development and terminal differentiation.

scholarly journals A Critical E-box in Barhl1 3′ Enhancer Is Essential for Auditory Hair Cell Differentiation

Cells ◽  
2019 ◽  
Vol 8 (5) ◽  
pp. 458 ◽  
Author(s):  
Kun Hou ◽  
Hui Jiang ◽  
Md. Rezaul Karim ◽  
Chao Zhong ◽  
Zhouwen Xu ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Hair Cell ◽  
Hair Cells ◽  
Embryonic Stem ◽  
Cell Development ◽  
Homologous Gene ◽  
Auditory Hair Cells ◽  
E Box ◽  
Hair Cell Differentiation

Barhl1, a mouse homologous gene of Drosophila BarH class homeobox genes, is highly expressed within the inner ear and crucial for the long-term maintenance of auditory hair cells that mediate hearing and balance, yet little is known about the molecular events underlying Barhl1 regulation and function in hair cells. In this study, through data mining and in vitro report assay, we firstly identified Barhl1 as a direct target gene of Atoh1 and one E-box (E3) in Barhl1 3’ enhancer is crucial for Atoh1-mediated Barhl1 activation. Then we generated a mouse embryonic stem cell (mESC) line carrying disruptions on this E3 site E-box (CAGCTG) using CRISPR/Cas9 technology and this E3 mutated mESC line is further subjected to an efficient stepwise hair cell differentiation strategy in vitro. Disruptions on this E3 site caused dramatic loss of Barhl1 expression and significantly reduced the number of induced hair cell-like cells, while no affections on the differentiation toward early primitive ectoderm-like cells and otic progenitors. Finally, through RNA-seq profiling and gene ontology (GO) enrichment analysis, we found that this E3 box was indispensable for Barhl1 expression to maintain hair cell development and normal functions. We also compared the transcriptional profiles of induced cells from CDS mutated and E3 mutated mESCs, respectively, and got very consistent results except the Barhl1 transcript itself. These observations indicated that Atoh1-mediated Barhl1 expression could have important roles during auditory hair cell development. In brief, our findings delineate the detail molecular mechanism of Barhl1 expression regulation in auditory hair cell differentiation.

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