Regenerative neurogenic response from glia requires insulin driven neuron-glia communication

摘要: ABSTRACT Some animals can regenerate their central nervous system (CNS) after injury by inducing de novo neurogenesis: discovering the underlying mechanisms would help promote regeneration in damaged human CNS. Glial cells could be source of regenerative neurogenesis, but this is debated. The glia transmembrane protein Neuron-Glia antigen-2 (NG2) may have a key role sensing injury-induced neuronal signals, however these not been identified. Here, we used Drosophila genetics to search for functional partners NG2 homologue kon-tiki (kon), and identified Islet Antigen-2 (Ia-2), required neurons insulin secretion. Alterations Ia-2 function induced neural stem cell fate, increased ia-2 expression ectopic cells. Using genetic epistasis analysis lineage tracing, demonstrate that functions with Kon regulate insulin-like peptide 6 (Dilp-6) which turn generates both more glial from glia. Ectopic divide, limited neurogenesis traced back Altogether, Dilp-6 drive neuron-glia relay restores glia, reprograms into CNS regeneration.