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Cytoplasmic capping returns a cap to specific mRNAs, thus protecting uncapped RNAs from decay. Prior to the identification of cytoplasmic capping, uncapped mRNAs were thought to be degraded. Here, we test whether long noncoding RNAs (lncRNAs) are substrates of the cytoplasmic capping enzyme (cCE). The subcellular localisation of 14 lncRNAs associated with sarcomas were examined in U2OS osteosarcoma cells. We used 5′ rapid amplification of cDNA ends (RACE) to assay uncapped forms of these lncRNAs. Inhibiting cytoplasmic capping elevated uncapped forms of selected lncRNAs indicating a plausible role of cCE in targeting them. Analysis of published cap analysis of gene expression (CAGE) data shows increased prevalence of certain 5'‐RACE cloned sequences, suggesting that these uncapped lncRNAs are targets of cytoplasmic capping. [ABSTRACT FROM AUTHOR]

In mammalian transcriptomes approximately 25% of 5′ ends determined by Capped Analysis of Gene Expression (CAGE) map to locations within spliced exons. The current study sought to determine if the cytoplasmic capping complex participates in generating these downstream CAGE tags. 5′-RACE was used to amplify the uncapped ends of target transcripts that accumulate when cytoplasmic capping is blocked. Sequencing of these RACE products mapped the positions of uncapped ends either exactly to or just downstream of archived CAGE tags. These findings support a role for cytoplasmic capping in generating the downstream capped ends identified by CAGE. [ABSTRACT FROM AUTHOR]