Authors
Eileen Clemens, Sarah Brivio, Mohammed Al-Khafaji, Peter Eijlers, Maheshika Kurukulasuriya, Irmgard U Haussmann, David MacLeod, Marius Wenzel, Berndt Müller, Matthias Soller, Jonathan Pettitt
Published in
Nucleic acids research. Volume 54. Issue 8. Apr 23, 2026.
Abstract
Cap-adjacent 2'-O-ribose methylation (cOMe) of the first two transcribed nucleotides of RNA polymerase II transcripts is a conserved feature in many eukaryotes. In mammals, these modifications are key to a transcript surveillance system that regulates the interferon response, but the broader functions of cOMe remain poorly understood. To understand the role of cOMe in Caenorhabditis elegans, we functionally characterized the methyltransferases (CMTR-1 and CMTR-2) responsible for installing these modifications. These enzymes have distinct expression patterns, protein interaction partners, and loss-of-function phenotypes. Loss of CMTR-1 causes dramatic reductions in cOMe, impaired growth, and sterility. In contrast, animals lacking CMTR-2 are superficially wild-type, though CMTR-2 loss enhances the severity of the cmtr-1 mutant phenotype. Depletion of CMTR-1 causes downregulation of transcripts associated with germline sex determination and upregulation of those involved in the intracellular pathogen response (IPR). We show that the absence of the decapping exonuclease, EOL-1, an IPR component, completely suppresses the sterility and growth defects caused by CMTR-1 loss, and reverses the associated steady-state transcript changes. Our work shows the physiological relevance of cOMe in protecting transcripts from decapping exonucleases, raising the possibility that cOMe plays a role in RNA-mediated immune surveillance beyond the vertebrates.
PMID:
42059201
Bibliographic data and abstract were imported from PubMed on 14 Sep 2026.
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