Hyperglutamylation impacts brood size and cilia production in Caenorhabditis elegans
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Mutations of the human ortholog of ccpp-1, CCP1, have been correlated with early onset neurodegeneration including developmental delays, muscular hypotonia, and cerebellar atrophy. A lack of a functional deglutamylase leads to hyper glutamylation of neuronal microtubules (Shashi et al. 2018). This often has deleterious effects to the person who has mutations in these enzymes. The goals of this study are 1) to look at a mutation in another deglutamylation enzyme, ccpp-6, as well as ccpp-1 to see if there was redundancy in their function; 2) to determine if the low brood size of ccpp-1 mutants can be attributed to a defect in spermatogenesis or oogenesis; 3) to carry out crosses to obtain the mutants, ccpp-1, GFP, and RFP (in order to look at germline organization defects), and ccpp-1 and ced-3 (in order to determine if the reduced brood size of the ccpp-1 mutant is caused by increased apoptosis); and 4) to determine if cilia structure is compromised by having the loss of function of both ccpp-1 and ccpp-6.
Department of Biology
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