Fig. 6
From: Loss of BICD2 in muscle drives motor neuron loss in a developmental form of spinal muscular atrophy
A summary of the proposed non-cell autonomous mechanism in SMALED2. In normal muscle, BICD2 ensures the correct localisation of Rab6 at the trans Golgi surface, required for the efficient trafficking of secretory vesicles (containing neurotrophins) to the plasma membrane. In SMALED2 muscle, loss of BICD2 function impairs the localisation of Rab6 to the trans Golgi surface resulting in impaired trafficking of secretory vesicles to the plasma membrane and a reduction in neurotrophin release required for motor neuron survival