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Mutation rates in plastid genomes: they are lower than you might think.

ABSTRACT: Within plastid-bearing species, the mutation rate of the plastid genome is often assumed to be greater than that of the mitochondrial genome. This assumption is based on early, pioneering studies of land plant molecular evolution, which uncovered higher rates of synonymous substitution in plastid versus mitochondrial DNAs. However, much of the plastid-containing eukaryotic diversity falls outside of land plants, and the patterns of plastid DNA evolution for embryophytes do not necessarily reflect those of other groups. Recent analyses of plastid and mitochondrial substitution rates in diverse lineages have uncovered very different trends than those recorded for land plants. Here, I explore these new data and argue that for many protists the plastid mutation rate is lower than that of the mitochondrion, including groups with primary or secondary plastids as well as nonphotosynthetic algae. These findings have far-reaching implications for how we view plastid genomes and how their sequences are used for evolutionary analyses, and might ultimately reflect a general tendency toward more efficient DNA repair mechanisms in plastids than in mitochondria.

SUBMITTER: Smith DR

PROVIDER: S-EPMC4453064 | biostudies-literature | 2015 Apr

REPOSITORIES: biostudies-literature

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Mutation rates in plastid genomes: they are lower than you might think.

Smith David Roy DR

Genome biology and evolution 20150413 5

Within plastid-bearing species, the mutation rate of the plastid genome is often assumed to be greater than that of the mitochondrial genome. This assumption is based on early, pioneering studies of land plant molecular evolution, which uncovered higher rates of synonymous substitution in plastid versus mitochondrial DNAs. However, much of the plastid-containing eukaryotic diversity falls outside of land plants, and the patterns of plastid DNA evolution for embryophytes do not necessarily reflec ...[more]

PMID: 25869380

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Project description:The causes and consequences of spatiotemporal variation in mutation rates remain to be explored in nearly all organisms. Here we examine relationships between local mutation rates and replication timing in three bacterial species whose genomes have multiple chromosomes: Vibrio fischeri, Vibrio cholerae, and Burkholderia cenocepacia Following five mutation accumulation experiments with these bacteria conducted in the near absence of natural selection, the genomes of clones from each lineage were sequenced and analyzed to identify variation in mutation rates and spectra. In lineages lacking mismatch repair, base substitution mutation rates vary in a mirrored wave-like pattern on opposing replichores of the large chromosomes of V. fischeri and V. cholerae, where concurrently replicated regions experience similar base substitution mutation rates. The base substitution mutation rates on the small chromosome are less variable in both species but occur at similar rates to those in the concurrently replicated regions of the large chromosome. Neither nucleotide composition nor frequency of nucleotide motifs differed among regions experiencing high and low base substitution rates, which along with the inferred ~800-kb wave period suggests that the source of the periodicity is not sequence specific but rather a systematic process related to the cell cycle. These results support the notion that base substitution mutation rates are likely to vary systematically across many bacterial genomes, which exposes certain genes to elevated deleterious mutational load.IMPORTANCE That mutation rates vary within bacterial genomes is well known, but the detailed study of these biases has been made possible only recently with contemporary sequencing methods. We applied these methods to understand how bacterial genomes with multiple chromosomes, like those of Vibrio and Burkholderia, might experience heterogeneous mutation rates because of their unusual replication and the greater genetic diversity found on smaller chromosomes. This study captured thousands of mutations and revealed wave-like rate variation that is synchronized with replication timing and not explained by sequence context. The scale of this rate variation over hundreds of kilobases of DNA strongly suggests that a temporally regulated cellular process may generate wave-like variation in mutation risk. These findings add to our understanding of how mutation risk is distributed across bacterial and likely also eukaryotic genomes, owing to their highly conserved replication and repair machinery.

Project description:Resistance to the frontline antibiotic rifampicin constitutes a challenge to the treatment and control of tuberculosis. Here, we analyzed the mutational landscape of Mycobacterium smegmatis during long-term evolution with increasing concentrations of rifampicin, using a mutation accumulation assay combined with whole-genome sequencing. Antibiotic treatment enhanced the acquisition of mutations, doubling the genome-wide mutation rate of the wild-type cells. While antibiotic exposure led to extinction of almost all wild-type lines, the hypermutable phenotype of the ΔnucS mutant strain (noncanonical mismatch repair deficient) provided an efficient response to the antibiotic, leading to high rates of survival. This adaptative advantage resulted in the emergence of higher levels of rifampicin resistance, an accelerated acquisition of drug resistance mutations in rpoB (β RNA polymerase), and a wider diversity of evolutionary pathways that led to drug resistance. Finally, this approach revealed a subset of adaptive genes under positive selection with rifampicin that could be associated with the development of antibiotic resistance. IMPORTANCE Rifampicin is the most important first-line antibiotic against mycobacterial infections, including tuberculosis, one of the top causes of death worldwide. Acquisition of rifampicin resistance constitutes a major global public health problem that makes the control of the disease challenging. Here, we performed an experimental evolution assay under antibiotic selection to analyze the response and adaptation of mycobacteria, leading to the acquisition of rifampicin resistance. This approach explored the total number of mutations that arose in the mycobacterial genomes under long-term rifampicin exposure, using whole-genome sequencing. Our results revealed the effect of rifampicin at a genomic level, identifying different mechanisms and multiple pathways leading to rifampicin resistance in mycobacteria. Moreover, this study detected that an increase in the rate of mutations led to enhanced levels of drug resistance and survival. In summary, all of these results could be useful to understand and prevent the emergence of drug-resistant isolates in mycobacterial infections.

Dataset Information

Mutation rates in plastid genomes: they are lower than you might think.

Publications

Mutation rates in plastid genomes: they are lower than you might think.

Similar Datasets

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