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Human DUS1L catalyzes dihydrouridine modification at tRNA positions 16/17, and DUS1L overexpression perturbs translation

J. Matsuura, S. Akichika, FY. Wei, T. Suzuki, T. Yamamoto, Y. Watanabe, LS. Valášek, A. Mukasa, K. Tomizawa, T. Chujo

. 2024 ; 7 (1) : 1238. [pub] 20241002

Language English Country England, Great Britain

Document type Journal Article

Persistent link   https://www.medvik.cz/link/bmc25003958

Grant support
JPMJFR204Z MEXT | Japan Science and Technology Agency (JST)
20H03187 MEXT | Japan Society for the Promotion of Science (JSPS)
21H02731 MEXT | Japan Society for the Promotion of Science (JSPS)

Human cytoplasmic tRNAs contain dihydrouridine modifications at positions 16 and 17 (D16/D17). The enzyme responsible for D16/D17 formation and its cellular roles remain elusive. Here, we identify DUS1L as the human tRNA D16/D17 writer. DUS1L knockout in the glioblastoma cell lines LNZ308 and U87 causes loss of D16/D17. D formation is reconstituted in vitro using recombinant DUS1L in the presence of NADPH or NADH. DUS1L knockout/overexpression in LNZ308 cells shows that DUS1L supports cell growth. Moreover, higher DUS1L expression in glioma patients is associated with poorer prognosis. Upon vector-mediated DUS1L overexpression in LNZ308 cells, 5' and 3' processing of precursor tRNATyr(GUA) is inhibited, resulting in a reduced mature tRNATyr(GUA) level, reduced translation of the tyrosine codons UAC and UAU, and reduced translational readthrough of the near-cognate stop codons UAA and UAG. Moreover, DUS1L overexpression increases the amounts of several D16/D17-containing tRNAs and total cellular translation. Our study identifies a human dihydrouridine writer, providing the foundation to study its roles in health and disease.

References provided by Crossref.org

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$a Human DUS1L catalyzes dihydrouridine modification at tRNA positions 16/17, and DUS1L overexpression perturbs translation / $c J. Matsuura, S. Akichika, FY. Wei, T. Suzuki, T. Yamamoto, Y. Watanabe, LS. Valášek, A. Mukasa, K. Tomizawa, T. Chujo
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$a Human cytoplasmic tRNAs contain dihydrouridine modifications at positions 16 and 17 (D16/D17). The enzyme responsible for D16/D17 formation and its cellular roles remain elusive. Here, we identify DUS1L as the human tRNA D16/D17 writer. DUS1L knockout in the glioblastoma cell lines LNZ308 and U87 causes loss of D16/D17. D formation is reconstituted in vitro using recombinant DUS1L in the presence of NADPH or NADH. DUS1L knockout/overexpression in LNZ308 cells shows that DUS1L supports cell growth. Moreover, higher DUS1L expression in glioma patients is associated with poorer prognosis. Upon vector-mediated DUS1L overexpression in LNZ308 cells, 5' and 3' processing of precursor tRNATyr(GUA) is inhibited, resulting in a reduced mature tRNATyr(GUA) level, reduced translation of the tyrosine codons UAC and UAU, and reduced translational readthrough of the near-cognate stop codons UAA and UAG. Moreover, DUS1L overexpression increases the amounts of several D16/D17-containing tRNAs and total cellular translation. Our study identifies a human dihydrouridine writer, providing the foundation to study its roles in health and disease.
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$a Akichika, Shinichiro $u Department of Chemistry and Biotechnology, Graduate School of Engineering, University of Tokyo, Tokyo, Japan $1 https://orcid.org/0000000276602580
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$a Suzuki, Tsutomu $u Department of Chemistry and Biotechnology, Graduate School of Engineering, University of Tokyo, Tokyo, Japan $1 https://orcid.org/0000000297311731
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$a Yamamoto, Takahiro $u Department of Neurosurgery, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan
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$a Mukasa, Akitake $u Department of Neurosurgery, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan
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$a Chujo, Takeshi $u Department of Molecular Physiology, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan. tchujo@kumamoto-u.ac.jp $1 https://orcid.org/0000000323935776
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