Figure 2.

The fragmentation of the Golgi apparatus in pmn motor neurons. (A) An electron micrograph showing vesiculation of the Golgi stack in a lumbar spinal cord motor neuron from a pmn mouse aged 35 days. (B) Schematic representation of the molecular defects leading to Golgi fragmentation. Loss of TBCE function impedes polymerization of microtubules at the cis-Golgi [box 1] and potentially also their GCC185/CLASP-dependent nucleation at the trans-Golgi [box 2]. Levels of β-COP and ε-COP are reduced [box 1], vesicles containing high amounts of Golgi SNAREs GS15 and GS28 accumulate [box3] and tethers p115 and GM130 disperse away from membranes [box 4].