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Research Paper|Volume 12, Issue 3|pp 2453—2470

The whole transcriptome regulation as a function of mitochondrial polymorphisms and aging in Caenorhabditis elegans

Yuanjian Song1, Yuechen Wang1, Ying Li2, Liang Wang3, WenDa Zhang4, Jing Cheng2, Yao Zhu1, Haoyu Zhang5, Qiang Zhang1, Haichen Niu1, Yingwei zheng6, Mengyu Liang7, Mengqiong Deng7, Hao Shi7, Hao Wang7, Fang Zhang8, Zuobin Zhu1
  • 1Department of Genetics, Xuzhou Medical University, Xuzhou, China
  • 2Medical Technology School of Xuzhou Medical University, Xuzhou, China
  • 3Department of Bioinformatics, School of Medical Informatics and Engineering, Xuzhou Medical University, Xuzhou, China
  • 4Department of Urology, Xuzhou Central Hospital, Xuzhou, China
  • 5School of Marine Sciences, Nanjing University of Information Science and Technology, Nanjing, China
  • 6Department of Biochemistry, Xuzhou Medical University, Xuzhou, China
  • 7Clinical College of Xuzhou Medical University, Xuzhou, China
  • 8Research Facility Center for Morphology, Xuzhou Medical University, Xuzhou, China
* Equal contribution
Received: November 2, 2019Accepted: January 7, 2020Published: February 4, 2020
https://doi.org/10.18632/aging.102754

Copyright: © 2020 Song et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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.