{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,3]],"date-time":"2026-11-03T17:19:59Z","timestamp":1793726399238,"version":"4.6.1"},"reference-count":35,"publisher":"Society for Neuroscience","issue":"4","license":[{"start":{"date-parts":[[2014,7,22]],"date-time":"2014-07-22T00:00:00Z","timestamp":1405987200000},"content-version":"vor","delay-in-days":181,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-sa\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J. Neurosci."],"published-print":{"date-parts":[[2014,1,22]]},"abstract":"<jats:p>Formation of proper neuromuscular connections is a process coordinated by both motoneuron-intrinsic and target-dependent programs. Under these programs, motoneurons innervate target muscles, escape programmed cell death during fetal development, and form neuromuscular junctions (NMJ). Although a number of studies have revealed molecules involved in axon guidance to target muscles and NMJ formation, little is known about the molecular mechanisms linking intramuscular innervation and target-derived trophic factor-dependent prevention of motoneuron apoptosis. Here we studied the physiological function of CLAC-P\/collagen XXV, a transmembrane-type collagen originally identified as a component of senile plaque amyloid of Alzheimer's disease brains, by means of generating<jats:italic>Col25a1<\/jats:italic>-deficient (KO) mice.<jats:italic>Col25a1<\/jats:italic>KO mice died immediately after birth of respiratory failure. In<jats:italic>Col25a1<\/jats:italic>KO mice, motor axons projected properly toward the target muscles but failed to elongate and branch within the muscle, followed by degeneration of axons. Failure of muscular innervation in<jats:italic>Col25a1<\/jats:italic>KO mice led to excessive apoptosis during development, resulting in almost complete and exclusive loss of spinal motoneurons and immaturity in skeletal muscle development.<jats:italic>Bax<\/jats:italic>deletion in<jats:italic>Col25a1<\/jats:italic>KO mice rescued motoneurons from apoptosis, although motor axons remained halted around the muscle entry site. Furthermore, these motoneurons were positive for phosphorylated c-Jun, an indicator of insufficient supply of target-derived survival signals. Together, these observations indicate that CLAC-P\/collagen XXV is a novel essential factor that regulates the initial phase of intramuscular motor innervation, which is required for subsequent target-dependent motoneuron survival and NMJ formation during development.<\/jats:p>","DOI":"10.1523\/jneurosci.2440-13.2014","type":"journal-article","created":{"date-parts":[[2014,1,22]],"date-time":"2014-01-22T18:10:59Z","timestamp":1390414259000},"page":"1370-1379","source":"Crossref","is-referenced-by-count":59,"title":["CLAC-P\/Collagen Type XXV Is Required for the Intramuscular Innervation of Motoneurons during Neuromuscular 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