TOR, Target of Rapamycin, is a highly conserved signaling pathway in eukaryotic organisms that was discovered in the 1990s through its inhibition by rapamycin. There are two complexes formed, TORC1 and TORC2, with TORC1 having either Tor1p or Tor2p and TORC2 having Tor2p. TOR pathway impacts metabolism, growth, cell cycle progression, macromolecule biosynthesis, and autophagy through nutrient sensing. Inhibition of Tor1p results in limited anabolism and halted normal cell cycle progression through the translation of defensive proteins involved in cell adaption and tolerance to environmental stress. Stress signaling through creation of reactive oxidative species (ROS) causes similar cellular response to Tor1p inhibition. This has implications in human health, as ROS damage is implicated in neurodegenerative disorders, like ALS and Huntington’s, because of reduced cellular viability through cellular damage caused by ROS. Previous research has demonstrated that reduced TOR pathway signaling extends chronological lifespan by increased mitochondrial respiration, which increases the translation of defensive proteins that help reduce cellular damage by ROS. Previous research has demonstrated a number of genes related to the TOR1 pathway that upon deletion showed improved growth in the presence of rapamycin, most notably SOD1, SOD2, CTR1, and LYS7. Double gene deletion strains of Δlys7/Δtor1, Δsod1/Δtor1, Δsod2/Δtor1, and Δctr1/Δtor1 are not well-characterized for their effects on S. cerevisiae longevity. In this work, partial inhibition of TOR by deletion of TOR1 can be studied through S. cerevisiae longevity via a chronological lifespan assay, with intention of studying the double gene deletion strains of Δlys7/Δtor1, Δsod1/Δtor1, Δsod2/Δtor1, and Δctr1/Δtor1.

Effects of Δtor1 on yeast longevity via chronological lifespan assay

253rd National Meeting (2017)

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