Strong asymmetric mutation bias in endosymbiont genomes coincide with loss of genes for replication restart pathways
2006 (English)In: Molecular biology and evolution, ISSN 0737-4038, E-ISSN 1537-1719, Vol. 23, no 5, 1031-1039 p.Article in journal (Refereed) Published
A large majority of bacterial genomes show strand asymmetry, such that G and T preferentially accumulate on the leading strand. The mechanisms are unknown, but cytosine deaminations are thought to play an important role. Here, we have examined DNA strand asymmetry in three strains of the aphid endosymbiont Buchnera aphidicola. These are phylogenetically related, have similar genomic GC contents, and conserved gene order structures, yet B. aphidicola (Bp) shows a fourfold higher replication-induced strand bias than B. aphidicola (Sg) and (Ap). We rule out an increase in the overall substitution frequency as the major cause of the stronger strand bias in B. aphidicola (Bp). Instead, the results suggest that the higher GC skew in this species is caused by a different spectrum of mutations, including a relatively higher frequency of C to T mutations on the leading strand and/or of G to A mutations on the lagging strand. A comparative analysis of 20 γ-proteobacterial genomes revealed that endosymbiont genomes lacking recA and other genes involved in replication restart processes, such as priA, which codes for primosomal helicase PriA, displayed the strongest strand bias. We hypothesize that cytosine deaminations accumulate during single-strand exposure at arrested replication forks and that inefficient restart mechanisms may lead to high DNA strand asymmetry in bacterial genomes.
Place, publisher, year, edition, pages
2006. Vol. 23, no 5, 1031-1039 p.
Buchnera/genetics, Codon, DNA/*genetics, DNA Replication, Evolution; Molecular, Gammaproteobacteria/genetics, Genes; Bacterial, Genetics, Genome, Models; Genetic, Models; Statistical, Mutation, Sequence Analysis; DNA, Variation (Genetics)
IdentifiersURN: urn:nbn:se:uu:diva-23084DOI: 10.1093/molbev/msj107PubMedID: 16476690OAI: oai:DiVA.org:uu-23084DiVA: diva2:50857