Cap homeostasis is independent of poly(A) tail length

Daniel L. Kiss, Kenji M. Oman, Julie A. Dougherty, Chandrama Mukherjee, Ralf Bundschuh, Daniel R. Schoenberg

Research output: Contribution to journalArticlepeer-review

11 Scopus citations

Abstract

Cap homeostasis is a cyclical process of decapping and recapping that maintains the cap on a subset of the cytoplasmic transcriptome. Interfering with cytoplasmic capping results in the redistribution of target transcripts from polysomes to non-translating mRNPs, where they accumulate in an uncapped but nonetheless stable form. It is generally thought that decapping is preceded by shortening of the poly(A) tail to a length that can no longer support translation. Therefore recapped target transcripts would either have to undergo cytoplasmic polyadenylation or retain a reasonably long poly(A) tail if they are to return to the translating pool. In cells that are inhibited for cytoplasmic capping there is no change in the overall distribution of poly(A) lengths or in the elution profile of oligo(dT)-bound targets. Poly(A) tail lengths were similar for target mRNAs on polysomes or in non-translating mRNPs, and the presence of polyadenylated uncapped mRNA in mRNPs was confirmed by separation into capped and uncapped pools prior to assay. Finally, in silico analysis of cytoplasmic capping targets revealed significant correlations with genes encoding transcripts with uridylated or multiply modified 3′ ends, and genes possessing multiple 3′-untranslated regions (UTRs) generated by alternative cleavage and polyadenylation.

Original languageEnglish (US)
Pages (from-to)304-314
Number of pages11
JournalNucleic Acids Research
Volume44
Issue number1
DOIs
StatePublished - Jan 8 2016

ASJC Scopus subject areas

  • Genetics

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