Research Paper|Volume 11, Issue 22|pp 10485—10498

Identification of functional tRNA-derived fragments in senescence-accelerated mouse prone 8 brain

Shuai Zhang^1,^2,³, Hejian Li^1,^2,³, Ling Zheng^1,^2,³, Hong Li^1,^2,³, Chengqiang Feng^1,^2,³, Wensheng Zhang^1,^2,^3,⁴

¹Zhuhai Branch of State Key Laboratory of Earth Surface Processes and Resource Ecology, Beijing Normal University, Zhuhai, Guangdong 519087, China
²Engineering Research Center of Natural Medicine, Ministry of Education, Faculty of Geographical Science, Beijing Normal University, Beijing 100875, China
³Beijing Key Laboratory of Traditional Chinese Medicine Protection and Utilization, Faculty of Geographical Science, Beijing Normal University, Beijing 100875, China
⁴National and Local United Engineering Research Center for Panax Notoginseng Resources Protection and Utilization Technology, Kunming, Yunnan 650000, China

Received: July 27, 2019Accepted: November 8, 2019Published: November 20, 2019

https://doi.org/10.18632/aging.102471

Copyright © 2019 Zhang 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

Transfer RNA-derived fragments (tRFs) are known to contribute to multiple illnesses, including cancers, viral infections, and age-related neurodegeneration. In this study, we used senescence-accelerated mouse prone 8 (SAMP8) as a model of neurodegenerative disorders such as Alzheimer’s disease and Parkinson’s disease, and a control, the senescence-accelerated mouse resistant 1 (SAMR1) model, to comprehensively explore differences in tRF expression between them. We discovered 570 tRF transcripts among which eight were differentially expressed. We then obtained 110 potential target genes in a miRNA-like pattern. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) annotation suggest that these target genes participate in a variety of brain functions; e.g., synapse formation (GO: 0045202) and the synaptic vesicle cycle pathway. We further assessed in detail those tRFs whose miRNA-like pattern was most likely to promote the progression of either Alzheimer’s or Parkinson’s disease, such as AS-tDR-011775 acting on Mobp and Park2. Our findings suggest the eight dysregulated tRFs we uncovered here may be beneficially exploited as potential diagnostic biomarkers and/or therapeutic targets to treat age-related brain diseases.