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Screening for Novel tba-1(ju89) Suppressors in C. elegans In cell biology much can be learned about how cells function properly by studying cells that function improperly. As such, to learn more about the dynamics of microtubules in neurons, we study a strain of C. elegans with a mutation in the alpha-tubulin gene tba-1. Microtubules are composed of alpha- and beta- tubulin dimers and form the sub-cellular structural unit that provides the platform for intracellular transport. Worms with the tba-1(ju89) alpha-tubulin mutation are characterized by fewer and smaller neuromuscular synapses, uncoordinated movement, and poor axon extension. By subjecting the worms with this mutation to EMS-induced mutagenesis, novel mutations can occur that suppress the effects of the original alpha-tubulin mutation. These specific suppressing mutations can be discovered by observing the progeny of the mutagenized worms and looking for offspring that exhibit improved movement. After suppressor mutants are isolated, the mutation is mapped to a specific chromosome and gene. This approach has the potential to identify proteins that interact with microtubules and mechanisms that can reverse axon and synapse loss. Approximately 25,000 F1 progeny of mutagenized hermaphrodite worms were screened, and over 20 new candidate tba-1 suppressors were identified. Support provided by: Howard Hughes Medical Institute Undergraduate Science Education Grant |
