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The cytosolic isozyme of phosphoenolpyruvate carboxykinase ( PCK1 ) was the first rate-limiting enzyme in the gluconeogenesis pathway, which exerted a critical role in maintaining the blood glucose levels.  PCK1  has been established to be involved in various physiological and pathological processes, including glucose metabolism, lipid metabolism, diabetes, and tumorigenesis. Nonetheless, the association of  PCK1  with aging process and the detailed underlying mechanisms of  PCK1  on aging are still far to be elucidated. Hence, we herein constructed the  PCK1 -deficient ( pck1 Δ) and  PCK1  overexpression ( PCK1 OE )  Saccharomyces cerevisiae . The results unveiled that  PCK1  deficiency significantly shortened the replicative lifespan (RLS) in the  S. cerevisiae , while overexpression of  PCK1  prolonged the RLS. Additionally, we noted that the ROS level was significantly enhanced in  PCK1 -deficient strain and decreased in  PCK1 OE  strain. Then, a high throughput analysis by deep sequencing was performed in the  pck1 Δ and wild-type strains, in an attempt to shed light on the effect of  PCK1  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,  PFK1  was one of the most upregulated genes, which was involved in the glycolysis process and ROS generation. Thus, we further constructed the  pfk1 Δ pck1 Δ strain by deletion of  PFK1  in the  PCK1 -deficient strain. The results unraveled that  pfk1 Δ pck1 Δ strain significantly suppressed the ROS level and restored the RLS of  pck1 Δ strain. Taken together, our data suggested that  PCK1  deficiency enhanced the ROS level and shortened the RLS of  S. cerevisiae  via  PFK1 .

PCK1Deficiency Shortens the Replicative Lifespan ofSaccharomyces cerevisiaethrough Upregulation ofPFK1