Research Paper Volume 12, Issue 3 pp 2453—2470
The whole transcriptome regulation as a function of mitochondrial polymorphisms and aging in Caenorhabditis elegans
- 1 Department of Genetics, Xuzhou Medical University, Xuzhou, China
- 2 Medical Technology School of Xuzhou Medical University, Xuzhou, China
- 3 Department of Bioinformatics, School of Medical Informatics and Engineering, Xuzhou Medical University, Xuzhou, China
- 4 Department of Urology, Xuzhou Central Hospital, Xuzhou, China
- 5 School of Marine Sciences, Nanjing University of Information Science and Technology, Nanjing, China
- 6 Department of Biochemistry, Xuzhou Medical University, Xuzhou, China
- 7 Clinical College of Xuzhou Medical University, Xuzhou, China
- 8 Research Facility Center for Morphology, Xuzhou Medical University, Xuzhou, China
Received: November 2, 2019 Accepted: January 7, 2020 Published: February 4, 2020
https://doi.org/10.18632/aging.102754How to Cite
Abstract
Recently, mitochondrial-nuclear interaction in aging has been widely studied. However, the nuclear genome controlled by natural mitochondrial variations that influence aging has not been comprehensively understood so far. We hypothesized that mitochondrial polymorphisms could play critical roles in the aging process, probably by regulation of the whole-transcriptome expression. Our results showed that mitochondria polymorphisms not only decreased the mitochondrial mass but also miRNA, lncRNA, mRNA, circRNA and metabolite profiles. Furthermore, most genes that are associated with mitochondria show age-related expression features (P = 3.58E-35). We also constructed a differentially expressed circRNA-lncRNA-miRNA-mRNA regulatory network and a ceRNA network affected by the mitochondrial variations. In addition, Kyoto Encyclopedia of Genes and Genomes pathway analyses showed that the genes affected by the mitochondrial variation were enriched in metabolic activity. We finally constructed a multi-level regulatory network with aging which affected by the mitochondrial variation in Caenorhabditis elegans. The interactions between these genes and metabolites have great values for further aging research. In sum, our findings provide new evidence for understanding the molecular mechanisms of how mitochondria influence aging.