The corpus callosum is the largest commissural tract of the brain that connects similar regions of the cerebral hemispheres supporting cognitive functions. This topology raises an important issue: how do developing callosal axons extend along mirror-symmetrical ipsilateral (pre-crossing) and contralateral (post-crossing) trajectories?
Fanny Mann’s team discovered a molecular on/off switch that controls axonal responses to Semaphorin (Sema) 3C, an attractive guidance cue for pre-crossing axons. They showed that the surface protein Ephrin-B1 is upregulated on post-crossing axons and interacts with the Neuropilin-1 receptor to silence Sema3C signal. This activity is independent of Eph receptors and involves a N-glycosylation site (N-139) in the extracellular domain of Ephrin-B1.
These results provide an original mechanism that allows callosal axons to move across opposite gradients of Sema3C (low-to-high, high-to-low) on both sides of the midline. These results may also be relevant to other physiological and pathological situations where ephrins and semaphorins are involved.
To know more :
Mire E, Hocine M, Bazellières E, Jungas T, Davy A, Chauvet S, Mann F.
Curr Biol. 2018 Jun 4;28(11):1768-1782.e4. doi: 10.1016/j.cub.2018.04.026. Epub 2018 May 17.