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Cited by 28RNA Research and SplicingLiver physiology and pathologyDevelopmental Biology and Gene Regulation

Postnatal liver functional maturation requires Cnot complex-mediated decay of mRNAs encoding cell cycle and immature liver genes

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Suzuki, Toru, Kikuguchi, Chisato, Nishijima, Saori, Nagashima, Takeshi, Takahashi, Akinori, Okada, Mariko, Yamamoto, Tadashi·2019·Development
DOI 10.1242/dev.168146PMC PMC6398447
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Abstract

Liver development involves dramatic gene expression changes mediated by transcriptional and post-transcriptional control. Here, we show that the Cnot deadenylase complex plays a crucial role in liver functional maturation. The Cnot3 gene encodes an essential subunit of the Cnot complex. Mice lacking Cnot3 in liver have reduced body and liver masses, and they display anemia and severe liver damage. Histological analyses indicate that Cnot3-deficient (Cnot3−/−) hepatocytes are irregular in size and morphology, resulting in formation of abnormal sinusoids. We observe hepatocyte death, increased abundance of mitotic and mononucleate hepatocytes, and inflammation. Cnot3−/− livers show increased expression of immune response-related, cell cycle-regulating and immature liver genes, while many genes relevant to liver functions, such as oxidation-reduction, lipid metabolism and mitochondrial function, decrease, indicating impaired liver functional maturation. Highly expressed mRNAs possess elongated poly(A) tails and are stabilized in Cnot3−/− livers, concomitant with an increase of the proteins they encode. In contrast, transcription of liver function-related mRNAs was lower in Cnot3−/− livers. We detect efficient suppression of Cnot3 protein postnatally, demonstrating the crucial contribution of mRNA decay to postnatal liver functional maturation.

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  • Whether liver cells exhibit fetal or adult phenotypes is controlled by families of factors that regulate the synthesis, splicing, stability, and translation of mRNAs.

    “Whether liver cells exhibit fetal or adult phenotypes is controlled by families of factors that regulate the synthesis, splicing, stability, and translation of mRNAs (Panduro et al. 1987; Bhate et al. 2015; Suzuki et al. 2019; Gong et al. 2020).”

    From ESRP2–microRNA-122 axis promotes the postnatal onset of liver polyploidization and maturation (2025) · cites this paper as Suzuki et al. 2019

    The Introduction describes transcription factors regulating liver development, and the Results and Discussion link Cnot-mediated mRNA stability to postnatal liver maturation. Our copy does not establish that mRNA splicing or translation controls the fetal-versus-adult phenotype, so those parts of the attributed claim are unsupported. The supplied passages have section labels but no page numbers. (LLM, conf=0.86)

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Cited by

Sorted by citations

Authors
Suzuki, T., Kikuguchi, C., Nishijima, S., Nagashima, T., Takahashi, A., Okada, M., & Yamamoto, T.
Affiliations
  • RIKEN Center for Integrative Medical Sciences (JP)
  • Okinawa Institute of Science and Technology Graduate University (JP)
  • Tohoku University (JP)
Corresponding author
Yamamoto, Tadashi
ORCID
Venue
Development
Publisher
The Company of Biologists
Published
2019-02-15
Volume
146
Issue
4
Pages
dev168146
ISSN
  • 0950-1991 (ISSN-L)
  • 1477-9129
DOI
10.1242/dev.168146
PMC
PMC6398447
OpenAlex
W2911359974
Cited by
28
References
3
Citations by year
2026: 3 · 2025: 3 · 2024: 4 · 2023: 1 · 2022: 3 · 2021: 6 · 2020: 5 · 2019: 3
FWCI
1.41
Type
journal article
Language
en
Open access
Licence
Locations
  • Development (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, other-oa)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Institutional Repositories DataBase (IRDB) (submittedVersion, cc-by-nc-nd)
  • Okinawa Institute of Science and Technology Graduate University (Okinawa Institute of Science and Technology Graduate University) (submittedVersion, cc-by-nc-nd)
  • HighWire Press Open Archive (submittedVersion)
Funders
  • Japan Society for the Promotion of Science (21229006)
  • Japan Ministry of Education, Culture, Sports, Science and Technology (18K07079)
  • Okinawa Institute of Science and Technology
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA Research and Splicing
  • Health Sciences › Medicine › Hepatology › Liver physiology and pathology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
Keywords
CNOT3, mRNA degradation, postnatal liver development, hepatocyte death, poly(A) tail length, cell cycle genes, liver inflammation, hepatocyte morphology, liver sinusoids, post-transcriptional regulation
MeSH terms
Albumins, Anemia, Animals, Animals, Newborn, Bile Ducts, Cell Cycle, Female, Inflammation, Lipids, Liver, Male, Promoter Regions, Genetic, RNA, Messenger, Time Factors, Transcription Factors, Apoptosis, Mice, Knockout, Gene Expression Regulation, Developmental, Gene Expression Profiling, Hepatocytes, Mice

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

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