β1 integrins in muscle, but not in motor neurons, are required for skeletal muscle innervation

Martin Schwander, Ryuichi Shirasaki, Samuel L. Pfaff, Ulrich Müller

Research output: Contribution to journalArticle

Abstract

In vitro studies have provided evidence that β1 integrins in motor neurons promote neurite outgrowth, whereas β1 integrins in myotubes regulate acetylcholine receptor (AChR) clustering. Surprisingly, using genetic studies in mice, we show here that motor axon outgrowth and neuromuscular junction (NMJ) formation in large part are unaffected when the integrin β1 gene (Itgb1) is inactivated in motor neurons. In the absence of Itgb1 expression in skeletal muscle, interactions between motor neurons and muscle are defective, preventing normal presynaptic differentiation. Motor neurons fail to terminate their growth at the muscle midline, branch excessively, and develop abnormal nerve terminals. These defects resemble the phenotype of agrin-null mice, suggesting that signaling molecules such as agrin, which coordinate presynaptic and postsynaptic differentiation, are not presented properly to nerve terminals. We conclude that Itgb1 expression in muscle, but not in motor neurons, is critical for NMJ development.

Original languageEnglish (US)
Pages (from-to)8181-8191
Number of pages11
JournalJournal of Neuroscience
Volume24
Issue number37
DOIs
StatePublished - Sep 15 2004

Keywords

  • Agrin
  • Axon outgrowth
  • Integrin
  • Motor neuron
  • Muscle
  • Synapse formation

ASJC Scopus subject areas

  • Neuroscience(all)

Fingerprint Dive into the research topics of 'β1 integrins in muscle, but not in motor neurons, are required for skeletal muscle innervation'. Together they form a unique fingerprint.

  • Cite this