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Somatic and axonal LIGHT signaling elicit degenerative and regenerative responses in motoneurons, respectively.

Otsmane B., Moumen A., Aebischer J., Coque E., Sar C., Sunyach C., Salsac C., Valmier J., Salinas S., Bowerman M., Raoul C.

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.

EMBO Rep. 15:540-547(2014) [PubMed] [Europe PMC]

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