title: Somatic and axonal LIGHT signaling elicit degenerative and regenerative responses in motoneurons, respectively.
abstract: A receptor-ligand interaction can evoke a broad range of biological activities in different cell types depending on receptor identity and cell type-specific post-receptor signaling intermediates. Here, we show that the TNF family member LIGHT, known to act as a death-triggering factor in motoneurons through LT-βR, can also promote axon outgrowth and branching in motoneurons through the same receptor. LIGHT-induced axonal elongation and branching require ERK and caspase-9 pathways. This distinct response involves a compartment-specific activation of LIGHT signals, with somatic activation-inducing death, while axonal stimulation promotes axon elongation and branching in motoneurons. Following peripheral nerve damage, LIGHT increases at the lesion site through expression by invading B lymphocytes, and genetic deletion of Light significantly delays functional recovery. We propose that a central and peripheral activation of the LIGHT pathway elicits different functional responses in motoneurons.
authors.affiliation: The Mediterranean Institute of Neurobiology, Inmed, Marseille, France.
authors.forename: Belkacem
authors.initials: B
authors.lastname: Otsmane
authors.forename: Anice
authors.initials: A
authors.lastname: Moumen
authors.forename: Julianne
authors.initials: J
authors.lastname: Aebischer
authors.forename: Emmanuelle
authors.initials: E
authors.lastname: Coque
authors.forename: Chamroeun
authors.initials: C
authors.lastname: Sar
authors.forename: Claire
authors.initials: C
authors.lastname: Sunyach
authors.forename: Céline
authors.initials: C
authors.lastname: Salsac
authors.forename: Jean
authors.initials: J
authors.lastname: Valmier
authors.forename: Sara
authors.initials: S
authors.lastname: Salinas
authors.forename: Melissa
authors.initials: M
authors.lastname: Bowerman
authors.forename: Cédric
authors.initials: C
authors.lastname: Raoul
mesh_terms: D000818:Animals; D001369:Axons / Q000502:physiology*; D001402:B-Lymphocytes / Q000276:immunology; D002070:Butadienes / Q000494:pharmacology; D053453:Caspase 9 / Q000378:metabolism; D061945:Caspase Inhibitors / Q000494:pharmacology; D049109:Cell Proliferation; D048049:Extracellular Signal-Regulated MAP Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism; D005419:Flavonoids / Q000494:pharmacology; D053259:Lymphotoxin beta Receptor / Q000037:antagonists & inhibitors / Q000378:metabolism; D051379:Mice; D018345:Mice, Knockout; D009046:Motor Neurons / Q000378:metabolism*; D009570:Nitriles / Q000494:pharmacology; D047428:Protein Kinase Inhibitors / Q000494:pharmacology; D011994:Recombinant Proteins / Q000235:genetics / Q000494:pharmacology; D012584:Sciatic Nerve / Q000293:injuries / Q000473:pathology; D053326:Tumor Necrosis Factor Ligand Superfamily Member 14 / Q000096:biosynthesis / Q000235:genetics* / Q000378:metabolism*
chemical_list: D002070:Butadienes; D061945:Caspase Inhibitors; D005419:Flavonoids; D053259:Lymphotoxin beta Receptor; D009570:Nitriles; D047428:Protein Kinase Inhibitors; D011994:Recombinant Proteins; C505915:Tnfsf14 protein, mouse; D053326:Tumor Necrosis Factor Ligand Superfamily Member 14; C113580:U 0126; D048049:Extracellular Signal-Regulated MAP Kinases; D053453:Caspase 9; C093973:2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one