Analysis of klp-7 Gene Function in Caenorhabditis elegans Motor Neuron Function
Authors:
Pablo Romano, Dominic ShaylerMentor:
Renee Baran, Associate Professor of Biology, Occidental CollegeAnalysis of klp-7 Gene Function in Caenorhabditis elegans Motor Neuron Function Dominic Shayler and Pablo Romano Mentor: Renee Baran Abstract: Microtubules are used within a cell as part of the cytoskeleton, for transport of materials and cell motion. Dimers of alpha and beta tubulin are formed which are then incorporated into microtubules. Tubulin dimers are added and removed in a constant process of polymerization and depolymerization that is highly regulated by the cell. klp-7 is the Caenorhabditis elegans homolog of the kinesin-13 family protein MCAK/KIF2C. This protein has been shown to be involved in the regulation of tubulin depolymerization from microtubule ends. To evaluate the function of this gene in C. elegans neural development, we studied the phenotypes of a loss of function deletion allele (tm2143) and a putative gain of function allele (ju131) isolated by our lab. tm2143 mutants exhibited 68% and ju131 mutants exhibited 32% embryonic lethality when cultivated at 20oC due to loss of klp-7 functions during embryonic cell divisions. Movement defects in tm2143 mutants were recorded on video for further analysis and comparison to wild-type animals. To visualize GABAergic motor neurons by epifluorescence microscopy, genetic crosses were used to introduce a GFP transgene, juIs145, into tm2143. This marker illuminates the six dorsal (DD) GABAergic neurons. The DD neurons of tm2143 deletion mutants exhibited multiple defects in cell body morphology and position, axon extension, and commissure formation.