UC San Diego

Microtubules are polymeric filaments that cross the cell made up of alpha- and beta- tubulin heterodimers. These structures exist in a dynamic state in which they switch between phases of polymerization and de-polymerization; this cycling is termed dynamic instability. Dynamic instability is under tight control by microtubule-associated proteins that can either promote stabilization and growth, or destabilization and decay.

Dynamic microtubules are incredibly important for neurons to function correctly and for the normal development of the nervous system. Many neural disorders can be characterized by disruption to the microtubule network by either altering tubulin or the proteins that regulate microtubules. Here, we use an alpha-tubulin mutant in C. elegans that causes synaptic defects in a screen for microtubule associated proteins. The combination of the alpha-tubulin mutation with a loss of DLK-1 causes enhanced synaptic defects. A forward genetic screen in our lab in the double mutant background produced a mutant that ameliorates the deficits. Here, I present how I mapped this mutation to the beta-tubulin gene tbb-2. I also describe a screen I performed to look for suppressors of the tba-1 single mutant synaptic defects.