Comprehensive Analysis of Stop Codon Usage in Bacteria and Its Correlation with Release Factor Abundance

Korkmaz, Gürkan; Holm, Mikael; Wiens, Tobias; Sanyal, Suparna

doi:10.1074/jbc.m114.606632

Cited by 68 publications

(111 citation statements)

References 33 publications

(26 reference statements)

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“…Finally, the efficiency of suppression depends not only on the suppressor but also on the context of the nonsense mutation (47). The premature stop codon in eccCb 1 may have been particularly sensitive to suppression because TAA is the least abundant stop codon in Mycobacterium and is likely contextually poor for termination (48). We saw no evidence of generalized readthrough of ochre codons using proteomics, further indicating that termination within the eccCb 1 gene differs from termination at the end of a gene.…”

Section: Discussionmentioning

confidence: 79%

A Nonsense Mutation in Mycobacterium marinum That Is Suppressible by a Novel Mechanism

et al. 2017

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Mycobacterial pathogens use the ESAT-6 system 1 (Esx-1) exporter to promote virulence. Previously, we used gene disruption and complementation to conclude that the MMAR_0039 gene in Mycobacterium marinum is required to promote Esx-1 export. Here we applied molecular genetics, proteomics, and wholegenome sequencing to demonstrate that the MMAR_0039 gene is not required for Esx-1 secretion or virulence. These findings suggest that we initially observed an indirect mechanism of genetic complementation. We identified a spontaneous nonsense mutation in a known Esx-1-associated gene which causes a loss of Esx-1 activity. We show that the Esx-1 function was restored by nonsense suppression. Moreover, we identified a polar mutation in the ppsC gene which reduced cellular impermeability but did not impact cytotoxicity in macrophages. Our studies reveal insight into Esx-1 export, nonsense suppression, and cell envelope lipid biogenesis.

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Section: Discussionmentioning

confidence: 79%

A Nonsense Mutation in Mycobacterium marinum That Is Suppressible by a Novel Mechanism

et al. 2017

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“…As a result, stop codons occur less frequently than most sense codons by an order of a magnitude. Furthermore, stop codon usage is often skewed 177 and, as a result, a particular stop codon can be exceptionally rare. Thus, a codon reassignment of a stop codon may affect only a few codons in the genome.…”

Section: Box 1 | Decoding Plasticity In Mitochondriamentioning

confidence: 99%

Augmented genetic decoding: global, local and temporal alterations of decoding processes and codon meaning

2015

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The non-universality of the genetic code is now widely appreciated. Codes differ between organisms, and certain genes are known to alter the decoding rules in a site-specific manner. Recently discovered examples of decoding plasticity are particularly spectacular. These examples include organisms and organelles with disruptions of triplet continuity during the translation of many genes, viruses that alter the entire genetic code of their hosts and organisms that adjust their genetic code in response to changing environments. In this Review, we outline various modes of alternative genetic decoding and expand existing terminology to accommodate recently discovered manifestations of this seemingly sophisticated phenomenon.

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“…In contrast, only subclade C1 harbours T1135C nucleotide substitution 270 in the dnaN that changes stop codon TAA into CAA coding for glutamine predicted as neutral (PROVEAN 271 score --0.005), with the next stop codon TAG found immediately downstream. Putatively, T1135C and/or 272 change of the dnaN stop codon (Korkmaz, et al 2014) may act as compensatory to the T326I substitution, 273 reducing the mutation rate to a value not significantly different from the core rate found in clade A ( Fig. 274 1, 2) via protein elongation or by affecting translation via stop codon usage bias (Korkmaz, et al 2014).…”

Section: Results and Discussion 163mentioning

confidence: 99%

“…Putatively, T1135C and/or 272 change of the dnaN stop codon (Korkmaz, et al 2014) may act as compensatory to the T326I substitution, 273 reducing the mutation rate to a value not significantly different from the core rate found in clade A ( Fig. 274 1, 2) via protein elongation or by affecting translation via stop codon usage bias (Korkmaz, et al 2014). 275…”

Section: Results and Discussion 163mentioning

confidence: 99%

Evolutionary epidemiology ofStreptococcus iniae: linking mutation rate dynamics with adaptation to novel immunological landscapes

Silayeva

Engelstädter

Barnes

2018

Preprint

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Pathogens continuously adapt to changing host environments where variation in their virulence and antigenicity is critical to their long-term evolutionary success. The emergence of novel variants is accelerated in microbial mutator strains (mutators) deficient in DNA repair genes, most often from mismatch repair and oxidised-guanine repair systems (MMR and OG respectively). Bacterial MMR/OG mutants are abundant in clinical samples and show increased adaptive potential in experimental infection models, yet the role of mutators in the epidemiology and evolution of infectious disease is not well understood. Here we investigated the role of mutation rate dynamics in the evolution of a broad host range pathogen, Streptococcus iniae, using a set of 80 strains isolated globally over 40 years. We have resolved phylogenetic relationships using non-recombinant core genome variants, measured in vivo mutation rates by fluctuation analysis, identified variation in major MMR/OG genes and their regulatory regions, and phenotyped the major traits determining virulence in streptococci. We found that both mutation rate and MMR/OG genotype are remarkably conserved within phylogenetic clades but significantly differ between major phylogenetic lineages. Further, variation in MMR/OG loci correlates with occurrence of atypical virulence-associated phenotypes, infection in atypical hosts (mammals), and atypical tissue of a vaccinated primary hosts (barramundi bone). These findings suggest that mutators are likely to facilitate adaptations preceding major diversification events, and may promote emergence of variation permitting colonisation of a novel host tissue, novel host taxa (host jumps), and immune-escape in the vaccinated host.

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Comprehensive Analysis of Stop Codon Usage in Bacteria and Its Correlation with Release Factor Abundance

Cited by 68 publications

References 33 publications

A Nonsense Mutation in Mycobacterium marinum That Is Suppressible by a Novel Mechanism

A Nonsense Mutation in Mycobacterium marinum That Is Suppressible by a Novel Mechanism

Augmented genetic decoding: global, local and temporal alterations of decoding processes and codon meaning

Evolutionary epidemiology ofStreptococcus iniae: linking mutation rate dynamics with adaptation to novel immunological landscapes

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