Reovirus FAST proteins: virus-encoded cellular fusogens

Ciechonska, Marta; Duncan, Roy

doi:10.1016/j.tim.2014.08.005

Cited by 76 publications

(94 citation statements)

References 82 publications

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“…Indeed, fusion-associated small transmembrane (FAST) proteins are a class of nonenveloped viral proteins that induce syncytium formation31. Given that myomerger associates with membranes it is tempting to speculate that it functions to alter membrane dynamics that overcomes the thermodynamic barriers for fusion.…”

Section: Discussionmentioning

confidence: 99%

Myomerger induces fusion of non-fusogenic cells and is required for skeletal muscle development

et al. 2017

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Despite the importance of cell fusion for mammalian development and physiology, the factors critical for this process remain to be fully defined, which has severely limited our ability to reconstitute cell fusion. Myomaker (Tmem8c) is a muscle-specific protein required for myoblast fusion. Expression of myomaker in fibroblasts drives their fusion with myoblasts, but not with other myomaker-expressing fibroblasts, highlighting the requirement of additional myoblast-derived factors for fusion. Here we show that Gm7325, which we name myomerger, induces the fusion of myomaker-expressing fibroblasts. Thus, myomaker and myomerger together confer fusogenic activity to otherwise non-fusogenic cells. Myomerger is skeletal muscle-specific and genetic deletion in mice results in a paucity of muscle fibres demonstrating its requirement for normal muscle formation. Myomerger deficient myocytes differentiate and harbour organized sarcomeres but are fusion-incompetent. Our findings identify myomerger as a fundamental myoblast fusion protein and establish a system that begins to reconstitute mammalian cell fusion.

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Section: Discussionmentioning

confidence: 99%

Myomerger induces fusion of non-fusogenic cells and is required for skeletal muscle development

et al. 2017

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“…The reovirus small proteins that induce cell-cell, but not virus-cell fusion have been proposed to represent a fourth class of viral fusogens [8,9].…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of influenza viral membrane fusion

Blijleven

Boonstra

Onck

et al. 2016

Seminars in Cell & Developmental Biology

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Influenza viral particles are enveloped by a lipid bilayer. A major step in infection is fusion of the viral and host cellular membranes, a process with large kinetic barriers. Influenza membrane fusion is catalyzed by hemagglutinin (HA), a class I viral fusion protein activated by low pH. The exact nature of the HA conformational changes that deliver the energy required for fusion remains poorly understood. This review summarizes our current knowledge of HA structure and dynamics, describes recent single-particle experiments and modeling studies, and discusses their role in understanding how multiple HAs mediate fusion. These approaches provide a mechanistic picture in which HAs independently and stochastically insert into the target membrane, forming a cluster of HAs that is collectively able to overcome the barrier to membrane fusion. The new experimental and modeling approaches described in this review hold promise for a more complete understanding of other viral fusion systems and the protein systems responsible for cellular fusion. Disciplines Medicine and Health Sciences | Social and Behavioral Sciences Publication DetailsBlijleven, J. S., Boonstra, S., Onck, P. R., van AbstractInfluenza viral particles are enveloped by a lipid bilayer. A major step in infection is fusion of the viral and host cellular membranes, a process with large kinetic barriers. Influenza membrane fusion is catalyzed by hemagglutinin (HA), a class I viral fusion protein activated by low pH. The exact nature of the HA conformational changes that deliver the energy required for fusion remains poorly understood. This review summarizes our current knowledge of HA structure and dynamics, describes recent single-particle experiments and modeling studies, and discusses their role in understanding how multiple HAs mediate fusion. These approaches provide a mechanistic picture in which HAs independently and stochastically insert into the target membrane, forming a cluster of HAs that is collectively able to overcome the barrier to membrane fusion. The new experimental and modeling approaches described in this review hold promise for a more complete understanding of other viral fusion systems and the protein systems responsible for cellular fusion.

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“…For example, both bacteria and viruses have been shown to utilize host actin to move between host cells by inducing the uptake of a microbe-containing host cell protrusion into a neighboring cell, thereby avoiding contact with the extracellular space during dissemination 6 . Other pathogens avoid the extracellular space by coordinating the fusion of infected host cells with neighboring uninfected host cells to form syncytia 7, 8 . These studies highlight growth strategies that can be used by intracellular pathogens to expand their access to host space in vitro , although pathogen dissemination can involve alternative mechanisms in vivo 9 .…”

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confidence: 99%

Cell-to-cell spread of microsporidia causes Caenorhabditis elegans organs to form syncytia

et al. 2016

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The growth of pathogens is dictated by their interactions with the host environment1. Obligate intracellular pathogens undergo several cellular decisions as they progress through their life cycles inside of host cells2. We studied this process for microsporidian species in the genus Nematocida as they grew and developed inside their co-evolved animal host Caenorhabditis elegans3–5. We found that microsporidia can restructure multicellular host tissues into a single contiguous multinucleate cell. In particular, we found that all three Nematocida species we studied were able to spread across the cells of C. elegans tissues before forming spores, with two species causing syncytial formation in the intestine, and one species causing syncytial formation in the muscle. We also found that the decision to switch from replication to differentiation in N. parisii was altered by the density of infection, suggesting that environmental cues influence the dynamics of the pathogen life cycle. These findings show how microsporidia can maximize the use of host space for growth, and that environmental cues in the host can regulate a developmental switch in the pathogen.

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Reovirus FAST proteins: virus-encoded cellular fusogens

Cited by 76 publications

References 82 publications

Myomerger induces fusion of non-fusogenic cells and is required for skeletal muscle development

Myomerger induces fusion of non-fusogenic cells and is required for skeletal muscle development

Mechanisms of influenza viral membrane fusion

Cell-to-cell spread of microsporidia causes Caenorhabditis elegans organs to form syncytia

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