Published online 13 April 2006
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Comparison of characteristics and function of translation termination signals between and within prokaryotic and eukaryotic organisms
Department of Biochemistry, University of Otago PO Box 56, Dunedin, New Zealand 1 Department of Genetics, Microbiology and Toxicology, Stockholm University S-10691 Stockholm, Sweden
*To whom correspondence should be addressed. Tel: +64 3 479 7864; Fax: +64 3 479 7866; Email: warren.tate{at}stonebow.otago.ac.nz
Received December 9, 2005. Revised January 12, 2006. Accepted March 3, 2006.
Six diverse prokaryotic and five eukaryotic genomes were compared to deduce whether the protein synthesis termination signal has common determinants within and across both kingdoms. Four of the six prokaryotic and all of the eukaryotic genomes investigated demonstrated a similar pattern of nucleotide bias both 5' and 3' of the stop codon. A preferred core signal of 4 nt was evident, encompassing the stop codon and the following nucleotide. Codons decoded by hyper-modified tRNAs were over-represented in the region 5' to the stop codon in genes from both kingdoms. The origin of the 3' bias was more variable particularly among the prokaryotic organisms. In both kingdoms, genes with the highest expression index exhibited a strong bias but genes with the lowest expression showed none. Absence of bias in parasitic prokaryotes may reflect an absence of pressure to evolve more efficient translation. Experiments were undertaken to determine if a correlation existed between bias in signal abundance and termination efficiency. In Escherichia coli signal abundance correlated with termination efficiency for UAA and UGA stop codons, but not in mammalian cells. Termination signals that were highly inefficient could be made more efficient by increasing the concentration of the cognate decoding release factor.
Present address: Louise L. Major, Centre for Biomolecular Sciences, University of St Andrews, North Haugh, St Andrews, Fife, Scotland, KY16 9ST, UK
Alhad A. Mahagaonkar, Department of Molecular Medicine and Pathology, The University of Auckland, Private Bag 92019, Auckland 1020, New Zealand
The authors wish it to be known that, in their opinion, the first two authors should be regarded as joint First Authors
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