[대학원 생명과학과 금요세미나 안내]
연사 : 신정은 박사(서울대학교 기초과학연구원)
연제 : Neuronal responses to axon injury – Axon degeneration, regeneration and beyond
일시 : 2016년 5월 27일 (금) 오후 4시
장소 : 하나과학관 A동 109호
초청교수 : 조용철 교수
Abstract
The goal of our study is to understand neuron-intrinsic factors that control axon regeneration and degeneration. We have previously reported the role of the dual leucine zipper kinase (DLK) for axonal injury responses after peripheral nerve injury. DLK is a MAP3K that can activate cJun N-terminal kinase (JNK) stress-responsive pathway. We found that DLK-JNK pathway promotes axon degeneration by regulating axonal levels of SCG10 that controls microtubule stability. DLK is also required for the retrograde transport of injury signaling molecules from the sciatic nerve lesion and the subsequent activation of transcription factors in the nucleus of dorsal root ganglia (DRG) neurons. Consistently, genetic deletion of DLK delays axon regeneration after sciatic nerve injury and abolishes the preconditioning effect by which a DRG neuron exposed to a prior lesion displays improved regeneration after a second injury. Currently, we are testing a hypothesis that the DLK pathway is required for transcriptional changes that support axon regeneration. To identify injury-induced, DLK-dependent transcriptional changes in DRG neurons, we have performed an RNA-seq experiment to compare gene expression profiles between wild type and DLK knockout mice with or without sciatic nerve injury. We found that the injury-dependent transcriptional changes are largely dependent on DLK. As DLK is required for the preconditioning effect, the DLK-dependent gene list provides us candidate regulators of the intrinsic signaling that controls dorsal column and sciatic nerve regeneration.