| First Author | Pandey RR | Year | 2020 |
| Journal | Cell Rep | Volume | 32 |
| Issue | 7 | Pages | 108038 |
| PubMed ID | 32814042 | Mgi Jnum | J:293136 |
| Mgi Id | MGI:6451361 | Doi | 10.1016/j.celrep.2020.108038 |
| Citation | Pandey RR, et al. (2020) The Mammalian Cap-Specific m(6)Am RNA Methyltransferase PCIF1 Regulates Transcript Levels in Mouse Tissues. Cell Rep 32(7):108038 |
| abstractText | The 5' end of eukaryotic mRNAs is protected by the m(7)G-cap structure. The transcription start site nucleotide is ribose methylated (Nm) in many eukaryotes, whereas an adenosine at this position is further methylated at the N(6) position (m(6)A) by the mammalian Phosphorylated C-terminal domain (CTD)-interacting Factor 1 (PCIF1) to generate m(6)Am. Here, we show that although the loss of cap-specific m(6)Am in mice does not affect viability or fertility, the Pcif1 mutants display reduced body weight. Transcriptome analyses of mutant mouse tissues support a role for the cap-specific m(6)Am modification in stabilizing transcripts. In contrast, the Drosophila Pcif1 is catalytically dead, but like its mammalian counterpart, it retains the ability to associate with the Ser5-phosphorylated CTD of RNA polymerase II (RNA Pol II). Finally, we show that the Trypanosoma Pcif1 is an m(6)Am methylase that contributes to the N(6),N(6),2'-O-trimethyladenosine (m(6)2Am) in the hypermethylated cap4 structure of trypanosomatids. Thus, PCIF1 has evolved to function in catalytic and non-catalytic roles. |
