Talk abstracts
Talk on Saturday 09:42-09:54am submitted by Daniel L Kiss
Cap homeostasis is independent of poly(A) tail length
Daniel L. Kiss (Center for RNA Biology, Department of Molecular and Cellular Biochemistry, The Ohio State University, Columbus, Ohio 43210), Kenji Oman (Center for RNA Biology, Department of Physics, The Ohio State University, Columbus, Ohio 43210), Julie A. Dougherty (Center for RNA Biology, Department of Molecular and Cellular Biochemistry, The Ohio State University, Columbus, Ohio 43210), Chandrama Mukherjee (Center for RNA Biology, Department of Molecular and Cellular Biochemistry, The Ohio State University, Columbus, Ohio 43210), Ralf Bundschuh (Center for RNA Biology, Department of Physics, Department of Chemistry and Biochemistry, and Division of Hematology, The Ohio State University, C), Daniel R. Schoenberg (Center for RNA Biology, Department of Molecular and Cellular Biochemistry, The Ohio State University, Columbus, Ohio 43210)
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. We find that 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 cytoplasmic capping targets. Consistent with this observation there is little difference in poly(A) tail length of uncapped target transcripts recovered from non-translating mRNPs and capped forms of the same mRNAs on translating polysomes. Finally, an in silico analysis of cytoplasmic capping targets found significant correlations with genes encoding transcripts having uridylated or multiply modified 3’-ends, and with genes having multiple 3’-UTRs generated by alternative cleavage and polyadenylation.
Keywords: cytoplasmic capping, poly(A), cap