scholarly journals Erbb2 regulates neuromuscular synapse formation and is essential for muscle spindle development

Development ◽  
2003 ◽  
Vol 130 (11) ◽  
pp. 2291-2301 ◽  
Author(s):  
M. Leu
Keyword(s):  
Muscle Spindle ◽  
Synapse Formation ◽  
Neuromuscular Synapse ◽  
Spindle Development

scholarly journals GA-Binding Protein Is Dispensable for Neuromuscular Synapse Formation and Synapse-Specific Gene Expression

2007 ◽  
Vol 27 (13) ◽  
pp. 5040-5046 ◽  
Author(s):  
Alexander Jaworski ◽  
Cynthia L. Smith ◽  
Steven J. Burden
Keyword(s):  
Gene Expression ◽  
Synapse Formation ◽  
Binding Protein ◽  
Neuromuscular Synapse ◽  
Specific Gene ◽  
Promoter Regions ◽  
Specific Gene Expression ◽  
Muscle Gene Expression ◽  
Synaptic Region ◽  
Ga Binding Protein

ABSTRACT The mRNAs encoding postsynaptic components at the neuromuscular junction are concentrated in the synaptic region of muscle fibers. Accumulation of these RNAs in the synaptic region is mediated, at least in part, by selective transcription of the corresponding genes in synaptic myofiber nuclei. The transcriptional mechanisms that are responsible for synapse-specific gene expression are largely unknown, but an Ets site in the promoter regions of acetylcholine receptor (AChR) subunit genes and other “synaptic” genes is required for synapse-specific transcription. The Ets domain transcription factor GA-binding protein (GABP) has been implicated to mediate synapse-specific gene expression. Inactivation of GABPα, the DNA-binding subunit of GABP, leads to early embryonic lethality, preventing analysis of synapse formation in gabpα mutant mice. To study the role of GABP at neuromuscular synapses, we conditionally inactivated gabpα in skeletal muscle and studied synaptic differentiation and muscle gene expression. Although expression of rb, a target of GABP, is elevated in muscle tissue deficient in GABPα, clustering of synaptic AChRs at synapses and synapse-specific gene expression are normal in these mice. These data indicate that GABP is dispensable for synapse-specific transcription and maintenance of normal AChR expression at synapses.

scholarly journals New Dogs in the Dogma: Lrp4 and Tid1 in Neuromuscular Synapse Formation

Neuron ◽  
2008 ◽  
Vol 60 (4) ◽  
pp. 526-528 ◽  
Author(s):  
Yuanquan Song ◽  
Rita Balice-Gordon
Keyword(s):  
Synapse Formation ◽  
Neuromuscular Synapse

scholarly journals Nerve, Muscle, and Synaptogenesis

Cells ◽  
2019 ◽  
Vol 8 (11) ◽  
pp. 1448 ◽  
Author(s):  
Swenarchuk
Keyword(s):  
Experimental Validation ◽  
Synapse Formation ◽  
Current Model ◽  
Neuromuscular Synapse ◽  
Model System ◽  
Integrin Signaling ◽  
Neuromuscular Synapses ◽  
Nerve Muscle ◽  
Postsynaptic Differentiation ◽  
Pericellular Proteolysis

The vertebrate skeletal neuromuscular junction (NMJ) has long served as a model system for studying synapse structure, function, and development. Over the last several decades, a neuron-specific isoform of agrin, a heparan sulfate proteoglycan, has been identified as playing a central role in synapse formation at all vertebrate skeletal neuromuscular synapses. While agrin was initially postulated to be the inductive molecule that initiates synaptogenesis, this model has been modified in response to work showing that postsynaptic differentiation can develop in the absence of innervation, and that synapses can form in transgenic mice in which the agrin gene is ablated. In place of a unitary mechanism for neuromuscular synapse formation, studies in both mice and zebrafish have led to the proposal that two mechanisms mediate synaptogenesis, with some synapses being induced by nerve contact while others involve the incorporation of prepatterned postsynaptic structures. Moreover, the current model also proposes that agrin can serve two functions, to induce synaptogenesis and to stabilize new synapses, once these are formed. This review examines the evidence for these propositions, and concludes that it remains possible that a single molecular mechanism mediates synaptogenesis at all NMJs, and that agrin acts as a stabilizer, while its role as inducer is open to question. Moreover, if agrin does not act to initiate synaptogenesis, it follows that as yet uncharacterized molecular interactions are required to play this essential inductive role. Several alternatives to agrin for this function are suggested, including focal pericellular proteolysis and integrin signaling, but all require experimental validation.

scholarly journals Neuron–glia interactions: the roles of Schwann cells in neuromuscular synapse formation and function

2011 ◽  
Vol 31 (5) ◽  
pp. 295-302 ◽  
Author(s):  
Yoshie Sugiura ◽  
Weichun Lin
Keyword(s):  
Schwann Cells ◽  
Motor Neurons ◽  
Nerve Terminal ◽  
Synapse Formation ◽  
Neuromuscular Synapse ◽  
Synaptic Activity ◽  
Nerve Terminals ◽  
Presynaptic Nerve Terminal ◽  
Presynaptic Nerve Terminals ◽  
And Function

The NMJ (neuromuscular junction) serves as the ultimate output of the motor neurons. The NMJ is composed of a presynaptic nerve terminal, a postsynaptic muscle and perisynaptic glial cells. Emerging evidence has also demonstrated an existence of perisynaptic fibroblast-like cells at the NMJ. In this review, we discuss the importance of Schwann cells, the glial component of the NMJ, in the formation and function of the NMJ. During development, Schwann cells are closely associated with presynaptic nerve terminals and are required for the maintenance of the developing NMJ. After the establishment of the NMJ, Schwann cells actively modulate synaptic activity. Schwann cells also play critical roles in regeneration of the NMJ after nerve injury. Thus, Schwann cells are indispensable for formation and function of the NMJ. Further examination of the interplay among Schwann cells, the nerve and the muscle will provide insights into a better understanding of mechanisms underlying neuromuscular synapse formation and function.

scholarly journals Induction of multiple signaling loops by MuSK during neuromuscular synapse formation

2001 ◽  
Vol 98 (25) ◽  
pp. 14655-14660 ◽  
Author(s):  
C. Moore ◽  
M. Leu ◽  
U. Muller ◽  
H. R. Brenner
Keyword(s):  
Synapse Formation ◽  
Neuromuscular Synapse ◽  
Multiple Signaling

scholarly journals How prolonged expression of Hunchback, a temporal transcription factor, re-wires locomotor circuits

2019 ◽  
Author(s):  
Julia L. Meng ◽  
Zarion D. Marshall ◽  
Meike Lobb-Rabe ◽  
Ellie S. Heckscher
Keyword(s):  
Transcription Factor ◽  
Stem Cell ◽  
Motor Neuron ◽  
Motor Neurons ◽  
Synapse Formation ◽  
Target Selection ◽  
Neuromuscular Synapse ◽  
Biomedical Intervention ◽  
Neuronal Stem Cell ◽  
Dendrite Morphogenesis

Abstract:In many CNS regions, neuronal birth timing is associated with circuit membership. In Drosophila larvae, we show U motor neurons are a temporal cohort—a set of non-identical, contiguously-born neurons from a single neuronal stem cell that contribute to the same circuit. We prolong expression of a temporal transcription factor, Hunchback, to increase the number of U motor neurons with early-born molecular identities. On the circuit level, this expands and re-wires the U motor neuron temporal cohort. On the cell biological level, we find novel roles for Hunchback in motor neuron target selection, neuromuscular synapse formation, dendrite morphogenesis, and behavior. These data provide insight into the relationship between stem cell and circuit, show that Hunchback is a potent regulator of circuit assembly, and suggest that temporal transcription factors are molecules that could be altered during evolution or biomedical intervention for the generation of novel circuits.

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