Deficiency Shortens the Replicative Lifespan of through Upregulation of .

The cytosolic isozyme of phosphoenolpyruvate carboxykinase () was the first rate-limiting enzyme in the gluconeogenesis pathway, which exerted a critical role in maintaining the blood glucose levels. has been established to be involved in various physiological and pathological processes, including glucose metabolism, lipid metabolism, diabetes, and tumorigenesis. Nonetheless, the association of with aging process and the detailed underlying mechanisms of on aging are still far to be elucidated. Hence, we herein constructed the -deficient (Δ) and overexpression () . The results unveiled that deficiency significantly shortened the replicative lifespan (RLS) in the , while overexpression of prolonged the RLS. Additionally, we noted that the ROS level was significantly enhanced in -deficient strain and decreased in strain. Then, a high throughput analysis by deep sequencing was performed in the Δ and wild-type strains, in an attempt to shed light on the effect of on the lifespan of aging process. The data showed that the most downregulated mRNAs were enriched in the regulatory pathways of glucose metabolism. Fascinatingly, among the differentially expressed mRNAs, was one of the most upregulated genes, which was involved in the glycolysis process and ROS generation. Thus, we further constructed the ΔΔ strain by deletion of in the -deficient strain. The results unraveled that ΔΔ strain significantly suppressed the ROS level and restored the RLS of Δ strain. Taken together, our data suggested that deficiency enhanced the ROS level and shortened the RLS of via .