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Methylation of Structured RNA by the m
Mateusz Mendel1, Kuan-Ming Chen1, David Homolka1
1Department of Molecular Biology, Science III, University of Geneva, 30 Quai Ernest-Ansermet, CH-1211 Geneva 4, Switzerland.
Molecular Cell
|September 11, 2018
Summary
The methyltransferase METTL16 regulates gene expression by adding N6-methyladenosine (m6A) marks to specific RNA structures. Its absence in early mouse embryos causes developmental failure by disrupting SAM availability.
Area of Science:
- Molecular Biology
- Epigenetics
- Developmental Biology
Background:
- N6-methyladenosine (m6A) is a crucial RNA modification for gene expression control.
- While METTL3/METTL14 is a known m6A writer, the function and targets of METTL16 are largely unknown.
Purpose of the Study:
- To elucidate the structural basis and physiological roles of the m6A methyltransferase METTL16.
- To investigate METTL16's substrate specificity and its function in early embryonic development.
Main Methods:
- X-ray crystallography to determine the structure of human METTL16.
- In vitro RNA binding assays to identify substrate preferences.
- Analysis of Mettl16-deficient mouse embryos to assess developmental impact.
Main Results:
- The crystal structure of METTL16 reveals a unique RNA-binding groove essential for substrate recognition.
- METTL16 preferentially methylates structured RNAs with adenosine in a bulge.
- Mettl16 deficiency in mouse embryos leads to reduced Mat2a mRNA and widespread transcriptome dysregulation.
Conclusions:
- METTL16 plays a critical role in early embryonic development by regulating SAM synthetase (Mat2a) mRNA levels.
- METTL16-mediated m6A modification is vital for maintaining SAM availability and ensuring proper embryonic development.
- Dysregulation of METTL16 impacts transcriptome integrity, leading to developmental arrest in blastocysts.
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