Analysis of genomic tRNA sets from Bacteria, Archaea, and Eukarya points to anticodon–codon hydrogen bonds as a major determinant of tRNA compositional variations

  1. Ilia Targanski1 and
  2. Vera Cherkasova2,3
  1. 1BioLing, Inc., Rockville, Maryland 20853, USA
  2. 2Laboratory of Gene Regulation and Development, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892, USA

Abstract

Analysis of 100 complete sets of the cytoplasmic elongator tRNA genes from Bacteria, Archaea, and Eukarya pointed to correspondences between types of anticodon and composition of the rest of the tRNA body. The number of the hydrogen bonds formed between the complementary nucleotides in the anticodon–codon duplex appeared as a major quantitative parameter determining covariations in all three domains of life. Our analysis has supported and advanced the “extended anticodon” concept that is based on the argument that the decoding performance of the anticodon is enhanced by selection of a matching anticodon stem–loop sequence, as reported by Yarus in 1982. In addition to the anticodon stem–loop, we have found covariations between the anticodon nucleotides and the composition of the distant regions of their respective tRNAs that include dihydrouridine (D) and thymidyl (T) stem–loops. The majority of the covariable tRNA positions were found at the regions with the increased dynamic potential—such as stem–loop and stem–stem junctions. The consistent occurrences of the covariations on the multigenomic level suggest that the number and pattern of the hydrogen bonds in the anticodon–codon duplex constitute a major factor in the course of translation that is reflected in the fine-tuning of the tRNA composition and structure.

Keywords

Footnotes

  • 3 Present address: Laboratory of Molecular Growth Regulation, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892, USA.

  • Reprint requests to: Vera Cherkasova, Laboratory of Molecular Growth Regulation, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892, USA; e-mail: cherkasv{at}mail.nih.gov; fax: (301) 496-7823.

  • Article published online ahead of print. Article and publication date are at http://www.rnajournal.org/cgi/doi/10.1261/rna.896108.

    • Received October 30, 2007.
    • Accepted February 23, 2008.
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