The 18S rRNA m6 A methyltransferase METTL5 promotes mouse embryonic stem cell differentiation

EMBO Rep. 2020 Oct 5;21(10):e49863. doi: 10.15252/embr.201949863. Epub 2020 Aug 11.

Abstract

RNA modifications represent a novel layer of regulation of gene expression. Functional experiments revealed that N6 -methyladenosine (m6 A) on messenger RNA (mRNA) plays critical roles in cell fate determination and development. m6 A mark also resides in the decoding center of 18S ribosomal RNA (rRNA); however, the biological function of m6 A on 18S rRNA is still poorly understood. Here, we report that methyltransferase-like 5 (METTL5) methylates 18S rRNA both in vivo and in vitro, which is consistent with previous reports. Deletion of Mettl5 causes a dramatic differentiation defect in mouse embryonic stem cells (mESCs). Mechanistically, the m6 A deposited by METTL5 is involved in regulating the efficient translation of F-box and WD repeat domain-containing 7 (FBXW7), a key regulator of cell differentiation. Deficiency of METTL5 reduces FBXW7 levels and leads to the accumulation of its substrate c-MYC, thereby delaying the onset of mESC differentiation. Our study uncovers an important role of METTL5-mediated 18S m6 A in mESC differentiation through translation regulation and provides new insight into the functional significance of rRNA m6 A.

Keywords: rRNA; FBXW7; m6A; mESC differentiation; mRNA translation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Differentiation / genetics
  • Methyltransferases* / genetics
  • Mice
  • Mouse Embryonic Stem Cells*
  • RNA, Messenger
  • RNA, Ribosomal, 18S / genetics

Substances

  • RNA, Messenger
  • RNA, Ribosomal, 18S
  • Methyltransferases

Associated data

  • GEO/GSE138341