scholarly journals Dynamin and endocytosis are required for the fusion of osteoclasts and myoblasts

2014 ◽  
Vol 207 (1) ◽  
pp. 73-89 ◽  
Author(s):  
Nah-Young Shin ◽  
Hyewon Choi ◽  
Lynn Neff ◽  
Yumei Wu ◽  
Hiroaki Saito ◽  
...  
Keyword(s):  
Cell Fusion ◽  
Knockout Mouse ◽  
Cell Types ◽  
Cytoskeletal Reorganization ◽  
Knockout Mouse Model ◽  
Osteoclast Precursors ◽  
Evolutionarily Conserved ◽  
Myoblast Cell ◽  
Cell Cell

Cell–cell fusion is an evolutionarily conserved process that leads to the formation of multinucleated myofibers, syncytiotrophoblasts and osteoclasts, allowing their respective functions. Although cell–cell fusion requires the presence of fusogenic membrane proteins and actin-dependent cytoskeletal reorganization, the precise machinery allowing cells to fuse is still poorly understood. Using an inducible knockout mouse model to generate dynamin 1– and 2–deficient primary osteoclast precursors and myoblasts, we found that fusion of both cell types requires dynamin. Osteoclast and myoblast cell–cell fusion involves the formation of actin-rich protrusions closely associated with clathrin-mediated endocytosis in the apposed cell. Furthermore, impairing endocytosis independently of dynamin also prevented cell–cell fusion. Since dynamin is involved in both the formation of actin-rich structures and in endocytosis, our results indicate that dynamin function is central to the osteoclast precursors and myoblasts fusion process, and point to an important role of endocytosis in cell–cell fusion.

Spalt modifies EGFR-mediated induction of chordotonal precursors in the embryonic PNS of Drosophila promoting the development of oenocytes

Development ◽  
2001 ◽  
Vol 128 (5) ◽  
pp. 711-722 ◽  
Author(s):  
T.E. Rusten ◽  
R. Cantera ◽  
J. Urban ◽  
G. Technau ◽  
F.C. Kafatos ◽  
...  
Keyword(s):  
Nervous System ◽  
Cell Fate ◽  
System Development ◽  
Cell Types ◽  
Nervous System Development ◽  
Dual Function ◽  
Evolutionarily Conserved ◽  
A Cell ◽  
And Migration

Genes of the spalt family encode nuclear zinc finger proteins. In Drosophila melanogaster, they are necessary for the establishment of head/trunk identity, correct tracheal migration and patterning of the wing imaginal disc. Spalt proteins display a predominant pattern of expression in the nervous system, not only in Drosophila but also in species of fish, mouse, frog and human, suggesting an evolutionarily conserved role for these proteins in nervous system development. Here we show that Spalt works as a cell fate switch between two EGFR-induced cell types, the oenocytes and the precursors of the pentascolopodial organ in the embryonic peripheral nervous system. We show that removal of spalt increases the number of scolopodia, as a result of extra secondary recruitment of precursor cells at the expense of the oenocytes. In addition, the absence of spalt causes defects in the normal migration of the pentascolopodial organ. The dual function of spalt in the development of this organ, recruitment of precursors and migration, is reminiscent of its role in tracheal formation and of the role of a spalt homologue, sem-4, in the Caenorhabditis elegans nervous system.

The role of cell swelling and haemolysis in Sendai virus-induced cell fusion and in the diffusion of incorporated viral antigens

1980 ◽  
Vol 42 (1) ◽  
pp. 153-167
Author(s):  
S. Knutton ◽  
T. Bachi
Keyword(s):  
Cell Fusion ◽  
Erythrocyte Membrane ◽  
Sendai Virus ◽  
Viral Envelope ◽  
Cell Swelling ◽  
Haemolytic Activity ◽  
Erythrocyte Ghosts ◽  
Viral Antigens ◽  
Cell Cell

The role of the haemolytic activity of Sendai virus in cell-cell fusion has been examined in monolayers of human erythrocytes and erythrocyte ghosts fused with either haemolytic or non-haemolytic virus. Morphological observations indicate that cell swelling and haemolysis is a distinct event in cell-cell fusion irrespective of whether it is virally induced or, in the case of non-haemolytic virus, experimentally induced. Osmotic swelling appears to be the driving force by which cells which have established sites of membrane fusion expand such sites to form poly-erythrocytes. Immunofluorescent labelling of viral antigens incorporated into the erythrocyte membrane as a result of viral envelope-cell fusion indicates that diffusion of antigens in the plane of the membrane is restricted in intact erythrocytes and resealed erythrocyte ghosts but not in haemolysed erythrocytes or unsealed ghosts. A perturbation of the erythrocyte membrane resulting from osmotic lysis appears to form a prerequisite for the lateral diffusion of viral elements.

scholarly journals Nckβ Adapter Controls Neuritogenesis by Maintaining the Cellular Paxillin Level

2007 ◽  
Vol 27 (17) ◽  
pp. 6001-6011 ◽  
Author(s):  
Shengxi Guan ◽  
Mei Chen ◽  
David Woodley ◽  
Wei Li
Keyword(s):  
Pc12 Cells ◽  
Cortical Neurons ◽  
State Level ◽  
Cell Types ◽  
Steady State Level ◽  
Down Regulation ◽  
Evolutionarily Conserved ◽  
Rat Cortical Neurons ◽  
Interfering Rna

ABSTRACT The SH2/SH3 adapter Nck has an evolutionarily conserved role in neurons, linking the cell surface signals to actin cytoskeleton-mediated responses. The mechanism, however, remains poorly understood. We have investigated the role of Nck/Nckα/Nck1 versus Grb4/Nckβ/Nck2 side-by-side in the process of mammalian neuritogenesis. Here we show that permanent genetic silencing of Nckβ, but not Nckα, completely blocked nerve growth factor-induced neurite outgrowth in PC12 cells and dramatically disrupted the axon and dendrite tree in primary rat cortical neurons. By screening for changes among the components reportedly present in complex with Nck, we found that the steady-state level of paxillin was significantly reduced in Nckβ knockdown, but not Nckα knockdown, neurons. Interestingly, Nckβ knockdown did not affect the paxillin level in glial cells and several other cell types of various tissue origins. Genetic silencing of paxillin blocked neuritogenesis, just like Nckβ knockdown. Reintroducing a nondegradable Nckβ into Nckβ short interfering RNA-expressing PC12 cells rescued paxillin from down-regulation and allowed the resumption of neuritogenesis. Forced expression of paxillin in Nckβ knockdown PC12 also rescued its capacity for neuritogenesis. Finally, Nckβ, but not Nckα, binds strongly to paxillin and treatment of the neurons with proteosome inhibitors prevented paxillin down-regulation in Nckβ knockdown neurons. Thus, Nckβ maintains paxillin stability during neuritogenesis.

scholarly journals Drosophila Myoblast Fusion: Invasion and Resistance for the Ultimate Union

2019 ◽  
Vol 53 (1) ◽  
pp. 67-91 ◽  
Author(s):  
Donghoon M. Lee ◽  
Elizabeth H. Chen
Keyword(s):  
Cell Fusion ◽  
Genetic Model ◽  
Myoblast Fusion ◽  
Cellular Mechanism ◽  
Fundamental Question ◽  
Cellular Invasion ◽  
The Past ◽  
Evolutionarily Conserved ◽  
Cell Cell

Cell–cell fusion is indispensable for creating life and building syncytial tissues and organs. Ever since the discovery of cell–cell fusion, how cells join together to form zygotes and multinucleated syncytia has remained a fundamental question in cell and developmental biology. In the past two decades, Drosophila myoblast fusion has been used as a powerful genetic model to unravel mechanisms underlying cell–cell fusion in vivo. Many evolutionarily conserved fusion-promoting factors have been identified and so has a surprising and conserved cellular mechanism. In this review, we revisit key findings in Drosophila myoblast fusion and highlight the critical roles of cellular invasion and resistance in driving cell membrane fusion.

scholarly journals Functional Analysis of Hepatitis C Virus Envelope Proteins, Using a Cell-Cell Fusion Assay

2006 ◽  
Vol 80 (4) ◽  
pp. 1817-1825 ◽  
Author(s):  
Mariko Kobayashi ◽  
Michael C. Bennett ◽  
Theodore Bercot ◽  
Ila R. Singh
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Cell Fusion ◽  
Viral Entry ◽  
Antiviral Agents ◽  
Cell Types ◽  
Envelope Proteins ◽  
Virus Envelope ◽  
Host Cell Membrane ◽  
Cell Cell

ABSTRACT Hepatitis C virus (HCV) envelope proteins mediate the entry of virus into cells by binding to cellular receptors, resulting in fusion of the viral membrane with the host cell membrane and permitting the viral genome to enter the cytoplasm. We report the development of a robust and reproducible cell-cell fusion assay using envelope proteins from commonly occurring genotypes of HCV. The assay scored HCV envelope protein-mediated fusion by the production of fluorescent green syncytia and allowed us to elucidate many aspects of HCV fusion, including the pH of fusion, cell types that permit viral entry, and the conformation of envelope proteins essential for fusion. We found that fusion could be specifically inhibited by anti-HCV antibodies and by at least one peptide. We also generated a number of insertional mutations in the envelope proteins and tested nine of these using the fusion assay. We demonstrate that this fusion assay is a powerful tool for understanding the mechanism of HCV-mediated fusion, elucidating mutant function, and testing antiviral agents.

Ablation of adipose-HO-1 expression increases white fat over beige fat through inhibition of mitochondrial fusion and of PGC1α in female mice

2017 ◽  
Vol 31 (1) ◽  
Author(s):  
Shailendra P. Singh ◽  
Ilana Grant ◽  
Aliza Meissner ◽  
Attallah Kappas ◽  
Nader G. Abraham
Keyword(s):  
Adipose Tissue ◽  
Knockout Mouse ◽  
Potential Role ◽  
Mitochondrial Quality Control ◽  
Knockout Mouse Model ◽  
Genetic Ablation ◽  
Beige Fat ◽  
And Function ◽  
White Fat

AbstractBackgroundHmox1 plays an important role in the regulation of mitochondrial bioenergetics and function by regulating cellular heme-derived CO and bilirubin. Previous studies have demonstrated that global disruption of HO-1 in humans and mice resulted in severe organ dysfunction.MethodsWe investigated the potential role of adipose-specific-HO-1 genetic ablation on adipose tissue function, mitochondrial quality control and energy expenditure by generating an adipo-HO-1 knockout mouse model (Adipo-HO-1ResultsAdipo-HO-1ConclusionAblation of adipose tissue-HO-1 abridged PGC1 expression promoted mitochondrial dysfunction and contributed to an increase of pro-inflammatory visceral fat and abrogated beige-cell like phenotype.

scholarly journals Tribbles in normal and malignant haematopoiesis

2015 ◽  
Vol 43 (5) ◽  
pp. 1112-1115 ◽  
Author(s):  
Sarah J. Stein ◽  
Ethan A. Mack ◽  
Kelly S. Rome ◽  
Warren S. Pear
Keyword(s):  
E3 Ligase ◽  
Cell Types ◽  
Protein Family ◽  
Conserved Motifs ◽  
Tissue Specific ◽  
Cellular Events ◽  
Haematopoietic Cells ◽  
Evolutionarily Conserved ◽  
Multiple Cell

The tribbles protein family, an evolutionarily conserved group of pseudokinases, have been shown to regulate multiple cellular events including those involved in normal and malignant haematopoiesis. The three mammalian Tribbles homologues, Trib1, Trib2 and Trib3 are characterized by conserved motifs, including a pseudokinase domain and a C-terminal E3 ligase-binding domain. In this review, we focus on the role of Trib (mammalian Tribbles homologues) proteins in mammalian haematopoiesis and leukaemia. The Trib proteins show divergent expression in haematopoietic cells, probably indicating cell-specific functions. The roles of the Trib proteins in oncogenesis are also varied and appear to be tissue-specific. Finally, we discuss the potential mechanisms by which the Trib proteins preferentially regulate these processes in multiple cell types.

scholarly journals Current Understanding of Autophagy in Pregnancy

2019 ◽  
Vol 20 (9) ◽  
pp. 2342 ◽  
Author(s):  
Akitoshi Nakashima ◽  
Sayaka Tsuda ◽  
Tae Kusabiraki ◽  
Aiko Aoki ◽  
Akemi Ushijima ◽  
...  
Keyword(s):  
Protein Quality ◽  
Autophagy Flux ◽  
Knockout Mouse Model ◽  
Model Studies ◽  
Evolutionarily Conserved ◽  
Autophagy Inhibition ◽  
Extravillous Trophoblasts ◽  
Wrong Interpretation ◽  
In Pregnancy

Autophagy is an evolutionarily conserved process in eukaryotes to maintain cellular homeostasis under environmental stress. Intracellular control is exerted to produce energy or maintain intracellular protein quality controls. Autophagy plays an important role in embryogenesis, implantation, and maintenance of pregnancy. This role includes supporting extravillous trophoblasts (EVTs) that invade the decidua (endometrium) until the first third of uterine myometrium and migrate along the lumina of spiral arterioles under hypoxic and low-nutrient conditions in early pregnancy. In addition, autophagy inhibition has been linked to poor placentation—a feature of preeclamptic placentas—in a placenta-specific autophagy knockout mouse model. Studies of autophagy in human placentas have revealed controversial results, especially with regard to preeclampsia and gestational diabetes mellitus (GDM). Without precise estimation of autophagy flux, wrong interpretation would lead to fixed tissues. This paper presents a review of the role of autophagy in pregnancy and elaborates on the interpretation of autophagy in human placental tissues.

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