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PLoS Genet. 2013;9(12):e1004001. doi: 10.1371/journal.pgen.1004001. Epub 2013 Dec 19.

Base pairing interaction between 5'- and 3'-UTRs controls icaR mRNA translation in Staphylococcus aureus.

Author information

1
Laboratory of Microbial Biofilms. Instituto de Agrobiotecnología (IDAB). Universidad Pública de Navarra-CSIC-Gobierno de Navarra. Campus de Arrosadía. Pamplona, Spain.
2
Genomics, Proteomics and Bioinformatics Unit. Center for Applied Medical Research. University of Navarra. Pamplona, Spain.
3
Instituto de Tecnologia Química e Biológica, Universidade Nova de Lisboa. Oeiras, Portugal.
4
Architecture et Réactivité de l'ARN, Université de Strasbourg, CNRS, IBMC. Strasbourg, France.

Abstract

The presence of regulatory sequences in the 3' untranslated region (3'-UTR) of eukaryotic mRNAs controlling RNA stability and translation efficiency is widely recognized. In contrast, the relevance of 3'-UTRs in bacterial mRNA functionality has been disregarded. Here, we report evidences showing that around one-third of the mapped mRNAs of the major human pathogen Staphylococcus aureus carry 3'-UTRs longer than 100-nt and thus, potential regulatory functions. We selected the long 3'-UTR of icaR, which codes for the repressor of the main exopolysaccharidic compound of the S. aureus biofilm matrix, to evaluate the role that 3'-UTRs may play in controlling mRNA expression. We showed that base pairing between the 3'-UTR and the Shine-Dalgarno (SD) region of icaR mRNA interferes with the translation initiation complex and generates a double-stranded substrate for RNase III. Deletion or substitution of the motif (UCCCCUG) within icaR 3'-UTR was sufficient to abolish this interaction and resulted in the accumulation of IcaR repressor and inhibition of biofilm development. Our findings provide a singular example of a new potential post-transcriptional regulatory mechanism to modulate bacterial gene expression through the interaction of a 3'-UTR with the 5'-UTR of the same mRNA.

PMID:
24367275
PMCID:
PMC3868564
DOI:
10.1371/journal.pgen.1004001
[Indexed for MEDLINE]
Free PMC Article

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