Figure 10.

Schematic representation of the mechanism underlying transport defects in dt. (A) Under normal conditions, dystonin-a2 is present at Golgi membranes, maintaining the acetylation status of MTs in the subcellular compartments surrounding the centrosome. Stabilized MTs maintain the organization of the cis-Golgi and promote anterograde trafficking of motor proteins. (B) In dt mice, the absence of the MAP1B–dystonin-a2 interaction promotes MT instability through loss of MT acetylation. A deacetylated MT promotes Golgi fragmentation and prevents anterograde trafficking of motor proteins. Tub, tubulin.