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Status |
Public on Feb 13, 2022 |
Title |
Loss of m6A methyltransferase METTL5 promotes cardiac hypertrophy through translational control of SUZ12 |
Organisms |
Mus musculus; Rattus norvegicus |
Experiment type |
Expression profiling by high throughput sequencing
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Summary |
The methyltransferase-like5 (METTL5), which catalyzes m6A in 18S rRNA at position A1832, has been shown to regulate the efficient of mRNA translation in the differentiation of ES cell and the growth of cancer cells. It remains unknown that whether and how METTL5 regulates cardiac hypertrophy. In this study, we generated a mouse model (METTL5-cKO) with cardiac-specific abolishment of METTL5 in vivo. Loss function of METTL5 promotes pressure overload-induced cardiomyocyte hypertrophy and adverse remodeling. The regulatory function of METTL5 in hypertrophic growth of cardiomyocyte were further confirmed with both gain- and loss-of-function approaches in primary isolated cardiomyocytes. Mechanically, METTL5 was identified to modulate the mRNA translation of SUZ12, a core component of PRC2 complex, and further regulate the transcriptome shift during cardiac hypertrophy. Therefore, our study uncover an important translational regulator of cardiac hypertrophy.
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Overall design |
heart mRNA profiles of 1-month old Ctrl and Mettl5-KO mice; heart mRNA profiles of 3-month old Ctrl and Mettl5-cKO mice; heart mRNA profiles of Ctrl and Mettl5-cKO mice 4 weeks post-TAC; mRNA profiles of AdGFP and AdMettl5 NRVMs under PE stimulation.
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Contributor(s) |
Han Y, Du T, Guo S, Huang Z |
Citation(s) |
35295259 |
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Submission date |
Oct 26, 2021 |
Last update date |
Mar 30, 2022 |
Contact name |
Tailai Du |
E-mail(s) |
dutlai@mail2.sysu.edu.cn
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Organization name |
Sun Yat-sen University
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Department |
The First Affiliated Hospital
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Lab |
Institute of Precision Medicine
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Street address |
No.58, Zhongshan 2nd road
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City |
Guangzhou |
State/province |
Guangdong |
ZIP/Postal code |
510080 |
Country |
China |
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Platforms (2) |
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Samples (32)
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Relations |
BioProject |
PRJNA774794 |
SRA |
SRP343256 |