TOR1 Gene Regulates Genome Stability in Mismatch Repair Defected Cells during Chronological Aging in Saccharomyces cerevisiae

• Main Authors: Jia-Ci Chang, 張家綺
• Other Authors: 羅翊禎
• Format: Others
• Language: zh-TW
• Published: 2014
• Online Access: http://ndltd.ncl.edu.tw/handle/74447174459860328991

碩士 === 國立臺灣大學 === 食品科技研究所 === 102 === Mismatch repair (MMR) is a DNA repair system which is critical for the maintenance of genome stability. Defects in mismatch repair have been linked to colorectal and sporadic cancers. Calorie restriction (CR) has been shown to extend life span and increases stress resistance via TOR/SCH9 and RAS signaling pathways in various organisms. We have found that CR containing 0.5% glucose compared to normal treatment (2.0% glucose) can extend life span and promote HOM3 gene stability in MMR-defected cells during aging process in yeast previously. Here, we demonstrate tor1&;#8710; can mimic CR condition and extend life span of msh2&;#8710; and msh3&;#8710; mutants with low mutation frequency. We also found the levels of reactive oxygen species (ROS) were significantly increased during aging and tor1&;#8710; dramatically reduced the levels of ROS. However, tor1&;#8710; could not completely reverse mutation rates in msh2&;#8710;msh3&;#8710; mutants. According to these, we believe TOR1 gene can only partially regulates genome stability in MMR defected cells during aging. Whether RAS also affects the genome stability in MMR defected cells during aging needs to be further investigated.