Differentiating the lifespan and development of C. elegans with distinctive mtDNA deletions

Mitochondrial DNA damage is a large driver of mitochondrial dysfunction, which is linked to chronic, aging-related diseases. mtDNA’s proximity to ROS, generated as a byproduct of ATP synthesis in the mitochondria, makes it highly susceptible to damage, especially deletions. Yet there is insufficient characterization of the developmental damage caused by specific and diverse mtDNA deletions. C. elegans are a model organism with short lifespans and high mtDNA similarity to humans. This project examines the differences in lifespan and development across three groups of C. elegans; N2, with undamaged mtDNA, strains with various mtDNA deletions, and a strain with an unidentified nuclear mutation that causes loss of the common uadf5 deletion. The mtDNA deletions examined are stably maintained and cause distinctive damage to tRNAs and/or proteins. It is hypothesized strains with mtDNA deletions will exhibit slower development and stunted lifespans in proportion to deletion-related damage.