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4.5SH RNA counteracts deleterious exonization of SINE B1 in mice.
Yoshimoto, Rei; Nakayama, Yuta; Nomura, Ikuko; Yamamoto, Ikuko; Nakagawa, Yumeka; Tanaka, Shigeyuki; Kurihara, Misuzu; Suzuki, Yu; Kobayashi, Takehiko; Kozuka-Hata, Hiroko; Oyama, Masaaki; Mito, Mari; Iwasaki, Shintaro; Yamazaki, Tomohiro; Hirose, Tetsuro; Araki, Kimi; Nakagawa, Shinichi.
  • Yoshimoto R; Department of Applied Biological Sciences, Faculty of Agriculture, Setsunan University, 45-1 Nagaotoge-cho, Hirakata City, Osaka 573-0101, Japan. Electronic address: rei.yoshimoto@setsunan.ac.jp.
  • Nakayama Y; RNA Biology Laboratory, Faculty of Pharmaceutical Sciences, Hokkaido University, Kita 12-jo Nishi 6-chome, Kita-ku, Sapporo 060-0812, Japan.
  • Nomura I; RNA Biology Laboratory, Faculty of Pharmaceutical Sciences, Hokkaido University, Kita 12-jo Nishi 6-chome, Kita-ku, Sapporo 060-0812, Japan.
  • Yamamoto I; RNA Biology Laboratory, Faculty of Pharmaceutical Sciences, Hokkaido University, Kita 12-jo Nishi 6-chome, Kita-ku, Sapporo 060-0812, Japan.
  • Nakagawa Y; Department of Applied Biological Sciences, Faculty of Agriculture, Setsunan University, 45-1 Nagaotoge-cho, Hirakata City, Osaka 573-0101, Japan.
  • Tanaka S; Department of Applied Biological Sciences, Faculty of Agriculture, Setsunan University, 45-1 Nagaotoge-cho, Hirakata City, Osaka 573-0101, Japan.
  • Kurihara M; RNA Biology Laboratory, Faculty of Pharmaceutical Sciences, Hokkaido University, Kita 12-jo Nishi 6-chome, Kita-ku, Sapporo 060-0812, Japan.
  • Suzuki Y; Laboratory of Genome Regeneration, Institute for Quantitative Biosciences, University of Tokyo, 1-1-1, Yayoi, Bunkyo-ku, Tokyo 113-0032, Japan.
  • Kobayashi T; Laboratory of Genome Regeneration, Institute for Quantitative Biosciences, University of Tokyo, 1-1-1, Yayoi, Bunkyo-ku, Tokyo 113-0032, Japan.
  • Kozuka-Hata H; Medical Proteomics Laboratory, The Institute of Medical Science, University of Tokyo, 4-6-1, Shirokanedai, Minato-ku, Tokyo 108-8639, Japan.
  • Oyama M; Medical Proteomics Laboratory, The Institute of Medical Science, University of Tokyo, 4-6-1, Shirokanedai, Minato-ku, Tokyo 108-8639, Japan.
  • Mito M; RNA Systems Biochemistry Laboratory, RIKEN Cluster for Pioneering Research, 2-1 Hirosawa, Wako, Saitama 351-0198, Japan.
  • Iwasaki S; RNA Systems Biochemistry Laboratory, RIKEN Cluster for Pioneering Research, 2-1 Hirosawa, Wako, Saitama 351-0198, Japan; Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, University of Tokyo, Kashiwa, Chiba 277-8561, Japan.
  • Yamazaki T; RNA Biofunction Laboratory, Graduate School of Frontier Biosciences, Osaka University, 1-3 Yamadaoka, Suita, Osaka 565-0871, Japan.
  • Hirose T; RNA Biofunction Laboratory, Graduate School of Frontier Biosciences, Osaka University, 1-3 Yamadaoka, Suita, Osaka 565-0871, Japan; Institute for Open and Transdisciplinary Research Initiatives (OTRI), Osaka University, 1-3 Yamadaoka, Suita, Osaka 565-0871, Japan.
  • Araki K; Institute of Resource Development and Analysis, Kumamoto University, Kumamoto 860-0811, Japan; Center for Metabolic Regulation of Healthy Aging, Kumamoto University, 1-1-1, Honjo, Kumamoto 860-8556, Japan.
  • Nakagawa S; RNA Biology Laboratory, Faculty of Pharmaceutical Sciences, Hokkaido University, Kita 12-jo Nishi 6-chome, Kita-ku, Sapporo 060-0812, Japan. Electronic address: nakagawas@pharm.hokudai.ac.jp.
Mol Cell ; 83(24): 4479-4493.e6, 2023 Dec 21.
Article en En | MEDLINE | ID: mdl-38096826
ABSTRACT
4.5SH RNA is a highly abundant, small rodent-specific noncoding RNA that localizes to nuclear speckles enriched in pre-mRNA-splicing regulators. To investigate the physiological functions of 4.5SH RNA, we have created mutant mice that lack the expression of 4.5SH RNA. The mutant mice exhibited embryonic lethality, suggesting that 4.5SH RNA is an essential species-specific noncoding RNA in mice. RNA-sequencing analyses revealed that 4.5SH RNA protects the transcriptome from abnormal exonizations of the antisense insertions of the retrotransposon SINE B1 (asB1), which would otherwise introduce deleterious premature stop codons or frameshift mutations. Mechanistically, 4.5SH RNA base pairs with complementary asB1-containing exons via the target recognition region and recruits effector proteins including Hnrnpm via its 5' stem loop region. The modular organization of 4.5SH RNA allows us to engineer a programmable splicing regulator to induce the skipping of target exons of interest. Our results also suggest the general existence of splicing regulatory noncoding RNAs.
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Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Empalme del ARN / ARN Pequeño no Traducido Límite: Animals Idioma: En Año: 2023 Tipo del documento: Article
Texto completo
Imprimir
XML
PubMed Links
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Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Empalme del ARN / ARN Pequeño no Traducido Límite: Animals Idioma: En Año: 2023 Tipo del documento: Article