Cell–cell fusion

Chen, Elizabeth H.; Grote, Eric; Mohler, William A.; Vignery, Agnès

doi:10.1016/j.febslet.2007.03.033

Cited by 239 publications

(210 citation statements)

References 116 publications

(139 reference statements)

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“…The current understanding of myoblast fusion in mammals is largely derived from experiments with myoblast cell culture systems wherein the fusion step can be recapitulated in vitro. In contrast, myoblast fusion is a biological process prone to genetic analysis in Drosophila, and research over the last decade has suggested several candidate genes whose functions might be conserved in mammals (5). Surprisingly, none of these candidates have been confirmed thus far in mouse models.…”

Section: Dock1mentioning

confidence: 99%

“…Proper regulation of these various fusion events controls muscle fiber diameter and is central for appropriate contractile strength and muscle function (4). At the cellular level, myoblast fusion is divided into steps of cell-cell adhesion, alignment of cell membranes, and formation of membrane prefusion compartments, and the fusion is ultimately completed by the union of the two membranes (5). The molecular mechanisms regulating myoblast fusion in higher vertebrates remain poorly understood (6).…”

Section: Dock1mentioning

confidence: 99%

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The atypical Rac activator Dock180 (Dock1) regulates myoblast fusion in vivo

Laurin

Fradet

Blangy

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

151

163

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Dock1(also known as Dock180) is a prototypical member of a new family of atypical Rho GTPase activators. Genetic studies in Drosophila and Caenorhabditis elegans have demonstrated that Dock1 orthologues in these organisms have a crucial role in activating Rac GTPase signaling. We generated mutant alleles of the closely related Dock1 and Dock5 genes to study their function in mammals. We report that while Dock5 is dispensable for normal mouse embryogenesis, Dock1 has an essential role in embryonic development. A dramatic reduction of all skeletal muscle tissues is observed in Dock1-null embryos. Mechanistically, this embryonic defect is attributed to a strong deficiency in myoblast fusion, which is detectable both in vitro and in vivo. Furthermore, we have uncovered a contribution of Dock5 toward myofiber development. These studies identify Dock1 and Dock5 as critical regulators of the fusion step during primary myogenesis in mammals and demonstrate that a specific component of the myoblast fusion machinery identified in Drosophila plays an evolutionarily conserved role in higher vertebrates. Dock5 ͉ mouse model ͉ myogenesis ͉ Myoblast City

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Section: Dock1mentioning

confidence: 99%

Section: Dock1mentioning

confidence: 99%

The atypical Rac activator Dock180 (Dock1) regulates myoblast fusion in vivo

Laurin

Fradet

Blangy

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

151

163

View full text Add to dashboard Cite

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“…Membrane fusion events triggered by specialized proteins are not only essential for intracellular trafficking, viral infection, and neurotransmitter release, but also play a pivotal role in embryogenesis, i.e., tissue formation and pathogenesis (1,2). Generally, fusion of two adjacent membranes requires lowering of the free energy barrier by concerted action of proteins in the context of an overall exergonic reaction.…”

Section: Introductionmentioning

confidence: 99%

Geometry of the Contact Zone between Fused Membrane-Coated Beads Mimicking Cell-Cell Fusion

Savić

Kliesch

Verbeek

et al. 2016

Biophysical Journal

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The fusion of lipid membranes is a key process in biology. It enables cells and organelles to exchange molecules with their surroundings, which otherwise could not cross the membrane barrier. To study such complex processes we use simplified artificial model systems, i.e., an optical fusion assay based on membrane-coated glass spheres. We present a technique to analyze membrane-membrane interactions in a large ensemble of particles. Detailed information on the geometry of the fusion stalk of fully fused membranes is obtained by studying the diffusional lipid dynamics with fluorescence recovery after photobleaching experiments. A small contact zone is a strong obstruction for the particle exchange across the fusion spot. With the aid of computer simulations, fluorescence-recovery-after-photobleaching recovery times of both fused and single-membrane-coated beads allow us to estimate the size of the contact zones between two membrane-coated beads. Minimizing delamination and bending energy leads to minimal angles close to those geometrically allowed.

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“…M ultinucleate osteoclasts originate from the fusion of macrophages and play a major role in the resorption of bone (1)(2)(3)(4). Osteoclasts are essential for both the development and remodeling of bone, and increases in the number and/or activity of osteoclasts lead to diseases associated with generalized bone loss, such as osteoporosis, and others associated with localized bone loss, such as rheumatoid arthritis and periodontal disease.…”

mentioning

confidence: 99%

CD200 and its receptor, CD200R, modulate bone mass via the differentiation of osteoclasts

Cui

Cuartas

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

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Fusion of macrophages is an essential step in the differentiation of osteoclasts, which play a central role in the development and remodeling of bone. Osteoclasts are important mediators of bone loss, which leads, for example, to osteoporosis. Macrophage fusion receptor/signal regulatory protein ␣ (MFR/SIRP␣) and its ligand CD47, which are members of the Ig superfamily (IgSF), have been implicated in the fusion of macrophages. We show that CD200, which is not expressed in cells that belong to the myeloid lineage, is strongly expressed in macrophages at the onset of fusion. By contrast, the CD200 receptor (CD200R), which, like CD200, belongs to the IgSF, is expressed only in cells that belong to the myeloid lineage, including osteoclasts, and in CD4 ؉ T cells. Osteoclasts from CD200 ؊/؊ mice differentiated at a reduced rate. Activation of the NF-B and MAP kinase signaling pathways downstream of RANK, a receptor that plays a central role in the differentiation of osteoclasts, was depressed in these cells. A soluble recombinant protein that included the extracellular domain of CD200 rescued the fusion of CD200 ؊/؊ macrophages and their activation downstream of RANK. Conversely, addition of a soluble recombinant protein that included the extracellular domain of CD200R or short-hairpin RNA-mediated silencing of the expression of CD200R prevented fusion. Thus CD200 engagement of the CD200R at the initiation of macrophage fusion regulated further differentiation to osteoclasts. Consistent with in vitro observations, CD200 ؊/؊ mice contained fewer osteoclasts and accumulated more bone than CD200 ؉/؉ mice. The CD200-CD200R axis is therefore a putative regulator of bone mass, via the formation of osteoclasts.fusion ͉ macrophage ͉ RANK ͉ MAPK

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Cell–cell fusion

Cited by 239 publications

References 116 publications

The atypical Rac activator Dock180 (Dock1) regulates myoblast fusion in vivo

The atypical Rac activator Dock180 (Dock1) regulates myoblast fusion in vivo

Geometry of the Contact Zone between Fused Membrane-Coated Beads Mimicking Cell-Cell Fusion

CD200 and its receptor, CD200R, modulate bone mass via the differentiation of osteoclasts

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