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METTL3 Regulates Liver Homeostasis, Hepatocyte Ploidy, and Circadian Rhythm–Controlled Gene Expression in Mice
METTL3's role in maintaining liver balance, liver cell DNA content, and daily gene activity in mice
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Abstract
Mice with liver-specific deletion of Mettl3 showed a global decrease in mA on polyadenylated RNAs and features of nonalcoholic fatty liver disease.
- Mettl3-depleted mice exhibited pathologic features such as hepatocyte ballooning, ductular reaction, and elevated serum alanine transaminase levels.
- There was increased proliferation of hepatocytes and a decrease in binucleate hepatocytes in Mettl3-deficient livers.
- Mice showed reduced levels of mA and expression of metabolic transcripts regulated by circadian rhythm.
- Nuclear protein levels of key clock transcription factors BMAL1 and CLOCK were diminished in Mettl3-deficient livers.
- Transcriptome analysis indicated a widespread loss of mA markers and changes in mRNA abundance related to metabolism.
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