The Journal of Neuroscience, November 2, 2005, ():
Molecular Control of Spinal Accessory Motor Neuron/Axon Development in the Mouse Spinal Cord
J. Neurosci. Dillon et al.
25: 10119
Supplemantal data
Files in this Data Supplement:
- supplemental material
-
Supplemental Figure 1. Retrograde labeling of SACMN via application of DiI to the SAN. To retrogradely label SACMN, small crystals of DiI were iontophoretically applied to the SAN located outside of and adjacent to the spinal cord in thick (150 mm) transverse vibratome sections of E12 mouse embryos. Each application of DiI resulted in the specific labeling of several SACMN cell bodies and their axons, which project towards the LEP.
- supplemental material
-
Supplemental Figure 2. The SAN fails to develop in Nkx2.9-null embryos as late as E13.5. Anti-L1 labeling of transverse, cervical spinal cord-containing cryosections derived from E13.5 Nkx2.9wild type and homozygous littermates. Anti-L1 reveals the presence of the SAN (arrows) in the wild type (A), but not in the homozygous (B) embryos. n= 3. Scale bar = 100 mm.
- supplemental material
-
Supplemental Figure 3. Molecular control of SACMN development in the embryonic mouse spinal cord. Schematic representation of SACMN, their axons, and the SAN, indicating the molecules required for several phases of SACMN development. Gli2 is necessary for the outgrowth of SACMN axons (shown in red), netrin-1 and Dcc are required for the dorsally directed migration of SACMN and their axons towards the LEP (shown in orange), and Nkx2.9 is required for the exit of SACMN growth cones/axons from the spinal cord (shown in blue). Despite an established role in axon guidance and fasciculation, BEN does not appear to be required for the development of SACMN and the SAN (green).
