The MTR4/hnRNPK complex surveils aberrant polyadenylated RNAs with multiple exons

Kenzui Taniue (), Anzu Sugawara, Chao Zeng, Han Han, Xinyue Gao, Yuki Shimoura, Atsuko Nakanishi Ozeki, Rena Onoguchi-Mizutani, Masahide Seki, Yutaka Suzuki, Michiaki Hamada and Nobuyoshi Akimitsu ()
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Kenzui Taniue: The University of Tokyo
Anzu Sugawara: The University of Tokyo
Chao Zeng: Waseda University
Han Han: The University of Tokyo
Xinyue Gao: The University of Tokyo
Yuki Shimoura: The University of Tokyo
Atsuko Nakanishi Ozeki: The University of Tokyo
Rena Onoguchi-Mizutani: The University of Tokyo
Masahide Seki: The University of Tokyo
Yutaka Suzuki: The University of Tokyo
Michiaki Hamada: Waseda University
Nobuyoshi Akimitsu: The University of Tokyo

Nature Communications, 2024, vol. 15, issue 1, 1-13

Abstract: Abstract RNA surveillance systems degrade aberrant RNAs that result from defective transcriptional termination, splicing, and polyadenylation. Defective RNAs in the nucleus are recognized by RNA-binding proteins and MTR4, and are degraded by the RNA exosome complex. Here, we detect aberrant RNAs in MTR4-depleted cells using long-read direct RNA sequencing and 3′ sequencing. MTR4 destabilizes intronic polyadenylated transcripts generated by transcriptional read-through over one or more exons, termed 3′ eXtended Transcripts (3XTs). MTR4 also associates with hnRNPK, which recognizes 3XTs with multiple exons. Moreover, the aberrant protein translated from KCTD13 3XT is a target of the hnRNPK-MTR4-RNA exosome pathway and forms aberrant condensates, which we name KCTD13 3eXtended Transcript-derived protein (KeXT) bodies. Our results suggest that RNA surveillance in human cells inhibits the formation of condensates of a defective polyadenylated transcript-derived protein.

Date: 2024
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DOI: 10.1038/s41467-024-51981-8

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