4.8 Article

The complete mitochondrial genome sequence of the spider Habronattus oregonensis reveals rearranged and extremely truncated tRNAs

Journal

MOLECULAR BIOLOGY AND EVOLUTION
Volume 21, Issue 5, Pages 893-902

Publisher

OXFORD UNIV PRESS
DOI: 10.1093/molbev/msh096

Keywords

mitochondrial genome; tRNA editing; aminoacyl acceptor stem; gene rearrangement; genome size; Habronattus oregonensis

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We sequenced the entire mitochondrial genome of the jumping spider Habronattus oregonensis of the arachnid order Araneae (Arthropoda: Chelicerata). A number of unusual features distinguish this genome from other chelicerate and arthropod mitochondrial genomes. Most of the transfer RNA (tRNA) gene sequences are greatly reduced in size and cannot be folded into typical cloverleaf-shaped secondary structures. At least nine of the tRNA sequences lack the potential to form TPsiC arm stem pairings and instead are inferred to have TV-replacement loops. Furthermore, sequences that Could encode the 3' aminoacyl acceptor stems in at least 10 tRNAs appear to be lacking, because fully paired acceptor stems are not possible and because the downstream sequences instead encode adjacent genes. Hence, these appear to be among the smallest known tRNA genes. We postulate that an RNA editing mechanism must exist to restore the 3' aminoacyl acceptor steins to allow the tRNAs to function. At least seven tRNAs are rearranged with respect to the chelicerate Limulus polyphemus, although the arrangement of the protein-coding genes is identical. Most mitochondrial protein-coding genes of H. oregonensis have ATN as initiation codons, as commonly found in arthropod mtDNAs, but cytochrome oxidase subunits 2 and 3 genes apparently use TTG as an initiation codon. Finally, many of the gene sequences overlap one another and are truncated. This 14,38 1 -bp genome, the first mitochondrial genome of a spider yet sequenced, is one of the smallest arthropod mitochondrial genomes known. We suggest that posttranscriptional RNA editing can likely maintain function of the tRNAs, while permitting the accumulation of mutations that Would otherwise be deleterious. Such mechanisms may have allowed for the minimization of the spider mitochondrial genome.

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