PCK1 Deficiency Shortens the Replicative Lifespan of Saccharomyces cerevisiae through Upregulation of PFK1
Joint Authors
Xiong, Xing-dong
Cui, Hong-jing
Yuan, Yuan
Zhao, Wei
Liu, Xin-guang
Lin, Jia-ying
Zheng, Hui-ling
Jiang, Zhi-wen
Xu, Shun
Source
Issue
Vol. 2020, Issue 2020 (31 Dec. 2020), pp.1-10, 10 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2020-02-12
Country of Publication
Egypt
No. of Pages
10
Main Subjects
Abstract EN
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 (pck1Δ) 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 pck1Δ 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 pfk1Δpck1Δ strain by deletion of PFK1 in the PCK1-deficient strain.
The results unraveled that pfk1Δpck1Δ strain significantly suppressed the ROS level and restored the RLS of pck1Δ strain.
Taken together, our data suggested that PCK1 deficiency enhanced the ROS level and shortened the RLS of S.
cerevisiae via PFK1.
American Psychological Association (APA)
Yuan, Yuan& Lin, Jia-ying& Cui, Hong-jing& Zhao, Wei& Zheng, Hui-ling& Jiang, Zhi-wen…[et al.]. 2020. PCK1 Deficiency Shortens the Replicative Lifespan of Saccharomyces cerevisiae through Upregulation of PFK1. BioMed Research International،Vol. 2020, no. 2020, pp.1-10.
https://search.emarefa.net/detail/BIM-1133485
Modern Language Association (MLA)
Yuan, Yuan…[et al.]. PCK1 Deficiency Shortens the Replicative Lifespan of Saccharomyces cerevisiae through Upregulation of PFK1. BioMed Research International No. 2020 (2020), pp.1-10.
https://search.emarefa.net/detail/BIM-1133485
American Medical Association (AMA)
Yuan, Yuan& Lin, Jia-ying& Cui, Hong-jing& Zhao, Wei& Zheng, Hui-ling& Jiang, Zhi-wen…[et al.]. PCK1 Deficiency Shortens the Replicative Lifespan of Saccharomyces cerevisiae through Upregulation of PFK1. BioMed Research International. 2020. Vol. 2020, no. 2020, pp.1-10.
https://search.emarefa.net/detail/BIM-1133485
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1133485