[논문]Transfer RNA-derived fragments in aging Caenorhabditis elegans originate from abundant homologous gene copies

Shin, GiWon; Koo, Hee Jung; Seo, Mihwa; Lee, Seung-Jae V.; Nam, Hong Gil; Jung, Gyoo Yeol

doi:10.1038/s41598-021-91724-z

[해외논문] Transfer RNA-derived fragments in aging Caenorhabditis elegans originate from abundant homologous gene copies 원문보기

Scientific reports, v.11 no.1, 2021년, pp.12304 -

Shin, GiWon (Institute of Environmental and Energy Technology, Pohang University of Science and Technology, Pohang, Gyeongbuk South Korea) , Koo, Hee Jung (School of Interdisciplinary Bioscience and Bioengineering, Pohang University of Science and Technology, Pohang, Gyeongbuk South Korea) , Seo, Mihwa (School of Interdisciplinary Bioscience and Bioengineering, Pohang University of Science and Technology, Pohang, Gyeongbuk South Korea) , Lee, Seung-Jae V. (Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon, South Korea) , Nam, Hong Gil (Center for Plant Aging Research, Institute for Basic Science, Daegu, South Korea) , Jung, Gyoo Yeol (School of Interdisciplinary Bioscience and Bioengineering, Pohang University of Science and Technology, Pohang, Gyeongbuk South Korea)

Abstract ▼ AI-Helper

Small RNAs that originate from transfer RNA (tRNA) species, tRNA-derived fragments (tRFs), play diverse biological functions but little is known for their association with aging. Moreover, biochemical aspects of tRNAs limit discovery of functional tRFs by high throughput sequencing. In particular, genes encoding tRNAs exist as multiple copies throughout genome, and mature tRNAs have various modified bases, contributing to ambiguities for RNA sequencing-based analysis of tRFs. Here, we report age-dependent changes of tRFs in Caenorhabditis elegans. We first analyzed published RNA sequencing data by using a new strategy for tRNA-associated sequencing reads. Our current method used unique mature tRNAs as a reference for the sequence alignment, and properly filtered out false positive enrichment for tRFs. Our analysis successfully distinguished de novo mutation sites from differences among homologous copies, and identified potential RNA modification sites. Overall, the majority of tRFs were upregulated during aging and originated from 5′-ends, which we validated by using Northern blot analysis. Importantly, we revealed that the major source of tRFs upregulated during aging was the tRNAs with abundant gene copy numbers. Our analysis suggests that tRFs are useful biomarkers of aging particularly when they originate from abundant homologous gene copies.

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