MAP1B Shapes Radial Glial Cells and Promotes Postinjury Neural Recovery

Microtubule-associated protein 1B (MAP1B) is a crucial cytoskeletal regulator essential for microtubule dynamics during neurite elongation and is active in growth cones. While its functions in neuronal development are well-documented, its specific role in glial cells remains largely unexplored. Here, we investigate Map1b’s function in radial glia and its potential for facilitating neural repair in zebrafish. We found that knockdown of map1b disrupted the morphology of radial glial processes and impaired the development of spinal motor neurons, leading to aberrant swimming behavior. Using transgenic zebrafish models including Tg(gfap:eGFP) and Tg(mnx1:eGFP), we found that map1b depletion significantly shortened both radial glial processes and motor neuron axons. Specific depletion of map1b expression in radial glia caused abnormalities in motor neurons. Mechanistically, we identify that MAP1B interacts with FIGN and is required for normal FIGN-associated microtubule regulation using rat radial glia, RFL-6 cells, and HEK293T. Of notable therapeutic interest, overexpression of mammalian MAP1B accelerated axonal regrowth following traumatic spinal cord injury and restored motor function. Collectively, our findings establish MAP1B as a dual regulator of glial morphogenesis and neural repair, revealing a novel therapeutic strategy for spinal cord injury that targets cytoskeletal plasticity.