Format

Send to

Choose Destination
See comment in PubMed Commons below
J Biol Chem. 2008 Mar 21;283(12):7314-9. doi: 10.1074/jbc.M709595200. Epub 2008 Jan 11.

Cross-competition in editing of chloroplast RNA transcripts in vitro implicates sharing of trans-factors between different C targets.

Author information

1
Department of Molecular Biology and Genetics, Cornell University, Ithaca, New York 14853, USA.

Abstract

C-->U plant organellar RNA editing is required for the translation of evolutionarily conserved and functional proteins. 28 different C targets of RNA editing have been identified in maize chloroplasts, and hundreds of Cs are edited in mitochondria. Mutant analysis in Arabidopsis has indicated that absence of a single site-specific recognition protein can result in loss of editing of a single C target, raising the possibility that each C target requires a recognition protein. Here we show that transcripts encompassing two editing sites, ZMrpoB C467 and ZMrps14 C80, can compete editing activity from each other in vitro despite limited sequence similarity. The signal causing competition overlaps a 5'-cis element required for editing efficiency. A single five-nucleotide mutation spanning the region from -20 to -16 relative to the edited C of rpoB C467 is sufficient to eliminate its substrate editing as well as its ability to compete editing activity from rps14 C80 substrates. A corresponding mutation in an rps14 C80 competitor likewise eliminated its ability to compete editing activity from rpoB C467 substrates. Taken together, our results indicate that the RNA sequences mediating both editing efficiency and cross-competition are highly similar and that a common protein is involved in their editing. Sharing of trans-factors can facilitate editing of the large number of different C targets in plant organelles so that a different protein factor would not be required for every editing site.

PMID:
18192271
PMCID:
PMC2276328
DOI:
10.1074/jbc.M709595200
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire Icon for PubMed Central
    Loading ...
    Support Center