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Context-dependent functional compensation between Ythdf m6A reader proteins.

Lior Lasman1, Vladislav Krupalnik1, Sergey Viukov1

  • 1Department of Molecular Genetics, Weizmann Institute of Science, Rehovot 7610001, Israel.

Genes & Development
|September 18, 2020
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Summary
This summary is machine-generated.

The study reveals dosage-dependent redundancy among N6-methyladenosine (m6A) reader proteins Ythdf1, Ythdf2, and Yththdf3. Their functions overlap, particularly in early development and mouse embryonic stem cells, challenging previous assumptions of distinct roles.

Keywords:
RNA methylationm6Astem cells

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Area of Science:

  • Molecular Biology
  • Epigenetics
  • RNA Biology

Background:

  • N6-methyladenosine (m6A) is a prevalent mRNA modification crucial for development and disease.
  • m6A modification is regulated by writer, eraser, and reader proteins.
  • The YTH domain family (Ythdf1, Ythdf2, Ythdf3) are m6A readers with potentially overlapping functions.

Purpose of the Study:

  • To investigate the in vivo and in vitro roles of Ythdf1, Ythdf2, and Ythdf3 reader proteins.
  • To determine the functional redundancy and compensation mechanisms among Ythdf readers.
  • To elucidate the impact of m6A writer (Mettl3) and reader knockouts on mouse development and stem cells.

Main Methods:

  • Systematic knockout (KO) of Mettl3 writer and individual/combined Ythdf reader genes in mice.
  • Assessment of gametogenesis, postnatal viability, and early development in KO models.
  • In vitro studies using mouse embryonic stem cells (mESCs) to evaluate differentiation and mRNA decay.

Main Results:

  • Mettl3-KO severity correlates with earlier deletion timing; Ythdf2 plays a dominant role in gametogenesis.
  • Ythdf reader redundancy is gene dosage-dependent during early development.
  • Compensation among Ythdf readers in mESCs leads to resistance to differentiation and altered mRNA decay only in triple-KO.

Conclusions:

  • A model of profound, dosage-dependent redundancy for Ythdf readers is proposed.
  • Ythdf readers exhibit overlapping functions, particularly when coexpressed in the same cell types.
  • The study highlights the complex regulatory network of m6A modification in mammalian development.