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Four-membrane protein M6a is concentrated in the growing tips of axons. An antibody to this protein strongly inhibits axon outgrowth of various central neurons in culture. We are analyzing physiological function of this molecule.
Top left: a wild-type mouse brain. Top right: a brain from the double mutant for M6a and its homolog M6b genes. The bundle of callosal axons (green) connecting brain hemispheres (arrow) is significantly thinner in the double mutant. Bottom: individual callosal axon trajectories traced in the brains. In the double mutant brain (right), the axons are not simply shorter but also disorganized, and some are even misdirected subcortically (arrows).
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Sato, Y., Mita, S., Fukushima, N., Fujisawa, H., Saga, Y. and Hirata, T. (2011) Induction of axon growth arrest without growth cone collapse through the N-terminal region of four-transmembrane glycoprotein M6a. Dev. Neurobiol. 71 733-746. doi: 10.1002/dneu.20941
Sato, Y., Watanabe, N., Fukushima, N., Mita, S. and Hirata, T. (2011) Actin-independent behavior and membrane deformation exhibited by the four-transmembrane protein M6a. PLoS One 6 e26702. 1-13. doi:10.1371/journal.pone.0026702.
Mita, S., Monasterio-Schrader, P., Fünfschilling, U., Kawasaki, T., Mizuno, H., Iwasato, T., Nave, K.-A., Werner, H.B., and Hirata, T. (2015) Transcallosal projections require glycoprotein M6-dependent neurite growth and guidance. Cerebral Cortex 25, 4111-4125. doi: 10.1093/cercor/bhu129
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