Functional analysis of novel GAP-43 phosphorylation sites in neuronal growth

2014 Fiscal Year Final Research Report

• Project/Area Number: 25870251
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Cell biology; Neurochemistry/Neuropharmacology
• Research Institution: Niigata University
• Principal Investigator: KAWASAKI Asami 新潟大学, 研究推進機構・超域学術院, 助教 (10609358)
• Project Period (FY): 2013-04-01 – 2015-03-31
• Keywords: 成長円錐 / JNK / GAP-43

Outline of Final Research Achievements

GAP-43 is thought to be involved in the mechanisms regulating the growth of neuronal processes during development and axon regeneration. However, its role for the molecular signaling is poorly understood. Recently, we performed a quantitative phosphoproteomic analysis of axonal growth cones and identified the novel phosphorylation sites of GAP-43 (Ser96 and Thr172), which are extensively highly phosphorylated in in vivo. Using specific antibodies of phospho-GAP-43 at these sites, we identified JNK was a major kinase responsible for these sites. In GAP-43 S96A knock-in mice, axonal growth of the primary cultured neurons was reduced by 50 %, compared with that of wild-type mice. These results suggest that JNK-dependent phosphorylation of GAP-43 is one of the important signaling involved in axonal generation and regeneration.

Free Research Field

細胞生物学