Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Nucleic Acids Res. 2010 Sep;38(16):5327-35. doi: 10.1093/nar/gkq266. Epub 2010 Apr 26.

Yeast targets for mRNA methylation.

Author information

  • 1School of Biosciences, Plant Sciences Division, University of Nottingham, Sutton Bonington, Loughborough LE12 5RD, UK.

Abstract

N(6)-Methyladenosine (m(6)A) is a modified base present in the mRNA of all higher eukaryotes and in Saccharomyces cerevisiae, where there is an increase in m(6)A levels during sporulation. The methyltransferase, Ime4, is responsible for this modification and has a role in the initiation of meiosis. However, neither the function, nor the extent of distribution of this nucleotide modification is established. We demonstrate that in S. cerevisiae, substantial levels of internal adenosine methylation are present in the GpA context in mRNA from sporulating cells, which is consistent with the preferred methylation consensus of higher eukaryotes. Based upon our quantification data, every second transcript could contain one m(6)A during meiosis. As methylation is distributed across all mRNA size ranges, it is likely that m(6)A is not limited to a small population of messages. We developed a new antibody based method for identifying m(6)A containing messages, and using this method the transcripts of three key, early regulators of meiosis, IME1, IME2 and IME4 itself, were identified as being methylated. The position of m(6)A in IME2 was narrowed down to a region in the 3'-end. Methylation of these and other targets suggests mechanisms by which IME4 could control developmental choices leading to meiosis.

PMID:
20421205
[PubMed - indexed for MEDLINE]
PMCID:
PMC2938207
Free PMC Article

Images from this publication.See all images (6)Free text

Figure 1.
Figure 2.
Figure 3.
Figure 4.
Figure 5.
Figure 6.
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire Icon for PubMed Central
    Write to the Help Desk