spinal cord development
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Homozygous Rig-1 deficient mice die within a few hours after birth because their axons are unable to cross the ventral midline in the spinal cord and hindbrain. Experiments show that Rig-1 inhibits the action of Slit, an axon growth cone repellant found at the midline. Knocking out Rig-1 and providing a Slit antagonist rescues commissural outgrowth in mice. Further evidence indicates that wildtype axons are not repelled by Slit, while Rig-1 knockout axons are strongly inhibited by Slit. Therefore, Rig-1 functions to inhibit Slit's repellent effect and guide axons across the midline during development.
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spinal cord development
- 1. What happens to Rig-1 deficient mice?
- 2. What happens to Rig-1 deficient mice? Predictions?
- 4. What’s going on here?
- 16. More in vitro evidence -- Wildtype dorsal spinal column axons cultured next to Slit2-expressing COS cells; no repelling action. -- Rig-1 knockout DSC axons strongly inhibited by Slit2-expressing COS cells.
- 17. More in vitro evidence -- Wildtype dorsal spinal column axons cultured next to Slit2-expressing COS cells; no repelling action. -- Rig-1 knockout DSC axons strongly inhibited by Slit2-expressing COS cells. There is now enough evidence to accept Model 2: Rig-1 inhibits the action of Slit, an axon growth cone repellant found at the midline.
- 18. Loss of Slit function partially rescues crossing