| First Author | Montenegro-Venegas C | Year | 2010 |
| Journal | Mol Biol Cell | Volume | 21 |
| Issue | 20 | Pages | 3518-28 |
| PubMed ID | 20719958 | Mgi Jnum | J:182832 |
| Mgi Id | MGI:5316943 | Doi | 10.1091/mbc.E09-08-0709 |
| Citation | Montenegro-Venegas C, et al. (2010) MAP1B regulates axonal development by modulating Rho-GTPase Rac1 activity. Mol Biol Cell 21(20):3518-28 |
| abstractText | Cultured neurons obtained from MAP1B-deficient mice have a delay in axon outgrowth and a reduced rate of axonal elongation compared with neurons from wild-type mice. Here we show that MAP1B deficiency results in a significant decrease in Rac1 and cdc42 activity and a significant increase in Rho activity. We found that MAP1B interacted with Tiam1, a guanosine nucleotide exchange factor for Rac1. The decrease in Rac1/cdc42 activity was paralleled by decreases in the phosphorylation of the downstream effectors of these proteins, such as LIMK-1 and cofilin. The expression of a constitutively active form of Rac1, cdc42, or Tiam1 rescued the axon growth defect of MAP1B-deficient neurons. Taken together, these observations define a new and crucial function of MAP1B that we show to be required for efficient cross-talk between microtubules and the actin cytoskeleton during neuronal polarization. |
