Homologous Recombination between thetufGenes ofSalmonella typhimurium

Abdulkarim, Farhad; Hughes, Diarmaid

doi:10.1006/jmbi.1996.0418

Cited by 93 publications

(90 citation statements)

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“…This suggests that the direction of gene conversion is not random, and a possible explanation could relate to the chromosomal location of the individual manB isogenes. Abdulkarim & Hughes (1996) observed that for the tufA and tufB genes in S. enterica (which are evolving in concert), the rate of sequence transfer was different depending on which tuf gene was the donor. It was suggested that the distribution and frequency of chromosomal breakpoints and chi sites, in relation to the location of the individual tuf genes, contributed to the biased rates of sequence transfer in one direction (Abdulkarim & Hughes, 1996).…”

Section: Concluding Commentsmentioning

confidence: 99%

“…Abdulkarim & Hughes (1996) observed that for the tufA and tufB genes in S. enterica (which are evolving in concert), the rate of sequence transfer was different depending on which tuf gene was the donor. It was suggested that the distribution and frequency of chromosomal breakpoints and chi sites, in relation to the location of the individual tuf genes, contributed to the biased rates of sequence transfer in one direction (Abdulkarim & Hughes, 1996). At present we have no specific explanation for the unidirectional gene conversion of manB OAg genes ; however, there is a precedent in relation to the tufA and tufB genes.…”

Section: Concluding Commentsmentioning

confidence: 99%

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Molecular evolution of the GDP-mannose pathway genes (manB and manC) in Salmonella enterica The GenBank accession numbers for the sequences reported in this paper are AY012160–AY012201.

Jensen

Reeves

2001

Microbiology

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The evolutionary history of the GDP-mannose pathway in Salmonella enterica was studied via sequencing manB and manC genes from 13 representative strains for O antigens containing mannose and/or sugar derivatives of GDP-Dmannose. In addition, colanic acid (CA) manB and manC genes were sequenced from selected strains, as the basis for a detailed comparison. Interestingly, including the eight previously characterized O antigen gene clusters, 12 of the 21 S. enterica strains studied in total (each representing a different O antigen structure) possess a manB gene which displays DNA identity, ranging from 93 to 99 %, to the CA manB gene of S. enterica LT2. Furthermore, the CA-like manB genes (as well as the CA manB and manC genes) display subspecies specificity, and the CA and CA-like manB genes (for individual strains) appear to be evolving in concert via gene conversion events. In comparison, the manC genes were generally not CA-like, a situation also apparent in Escherichia coli, and therefore most strongly reflected the evolutionary history of the S. enterica O antigen GDP-mannose pathway. It appears that, in relatively recent times, gene capture from a distant source has occurred infrequently, and that groups of manB and manC genes have been maintained and are continuing to evolve within S. enterica and more closely related species.

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Section: Concluding Commentsmentioning

confidence: 99%

Section: Concluding Commentsmentioning

confidence: 99%

Molecular evolution of the GDP-mannose pathway genes (manB and manC) in Salmonella enterica The GenBank accession numbers for the sequences reported in this paper are AY012160–AY012201.

Jensen

Reeves

2001

Microbiology

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“…Studies with bacterial species (1,22,28,29,39,46,51,(57)(58)(59), Saccharomyces cerevisiae (4,7,12,13,20,24,30,32,33,35,36,40,43,44), and higher eukaryotes (14,15,52,56) have uniformly found that sequence divergence acts as a potent barrier to recombination. As first shown in conjugational crosses between Escherichia coli and Salmonella typhimurium (39), much of the recombination barrier associated with sequence divergence in prokaryotes derives from the action of the MMR machinery (1,16,22,28,29,51,57).…”

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confidence: 99%

“…As first shown in conjugational crosses between Escherichia coli and Salmonella typhimurium (39), much of the recombination barrier associated with sequence divergence in prokaryotes derives from the action of the MMR machinery (1,16,22,28,29,51,57). The MMR system of E. coli (31) is used as a paradigm for eukaryotic MMR, and homologs of the bacterial MutS protein, which binds mismatched base pairs, and of the MutL protein, which interacts with MutS, have been identified in eukaryotes (11).…”

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confidence: 99%

Mismatch Repair Proteins Regulate Heteroduplex Formation during Mitotic Recombination in Yeast

Chen

Jinks-Robertson

1998

Molecular and Cellular Biology

103

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Mismatch repair (MMR) proteins actively inhibit recombination between diverged sequences in both prokaryotes and eukaryotes. Although the molecular basis of the antirecombination activity exerted by MMR proteins is unclear, it presumably involves the recognition of mismatches present in heteroduplex recombination intermediates. This recognition could be exerted during the initial stage of strand exchange, during the extension of heteroduplex DNA, or during the resolution of recombination intermediates. We previously used an assay system based on 350-bp inverted-repeat substrates to demonstrate that MMR proteins strongly inhibit mitotic recombination between diverged sequences in Saccharomyces cerevisiae. The assay system detects only those events that reverse the orientation of the region between the recombination substrates, which can occur as a result of either intrachromatid crossover or sister chromatid conversion. In the present study we sequenced the products of mitotic recombination between 94%-identical substrates in order to map gene conversion tracts in wild-type versus MMR-defective yeast strains. The sequence data indicate that (i) most recombination occurs via sister chromatid conversion and (ii) gene conversion tracts in an MMR-defective strain are significantly longer than those in an isogenic wild-type strain. The shortening of conversion tracts observed in a wild-type strain relative to an MMR-defective strain suggests that at least part of the antirecombination activity of MMR proteins derives from the blockage of heteroduplex extension in the presence of mismatches.Homologous recombination events can be either reciprocal or nonreciprocal in nature. Reciprocal recombination (crossing over) alters the linkage relationships of loci that flank the site of an exchange, whereas nonreciprocal recombination (gene conversion) is defined as the unidirectional transfer of information from one DNA molecule to another. All present models of recombination stipulate the formation of a heteroduplex recombination intermediate, which is formed by complementary base pairing of single strands derived from different duplexes. Correction of a mismatch in heteroduplex DNA can result in a gene conversion event, and such correction is effected by the same mismatch repair (MMR) machinery that corrects errors made during DNA replication. Cocorrection of a series of contiguous mismatches generates a conversion tract, the length of which is considered to be a minimal estimate of the extent of the heteroduplex intermediate formed. The point at which the recombining molecules exchange single strands to form heteroduplex DNA is referred to as a Holliday junction, and cleavage of this junction gives rise to crossovers and noncrossovers at roughly equivalent frequencies.Homologous recombination usually involves allelic sequences on homologous chromosomes but also can occur between dispersed (ectopic) repeated sequences. Ectopic gene conversion provides a mechanism for homogenizing repeated sequences and hence is important in t...

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“…coli bacteria have a paralogous copy of the EF-Tu gene tufA, in the form of tufB, that frequently recombines with the original copy (Abdulkarim and Hughes 1996). Each of the EF-Tu genes has its own specific expression machinery, and EF-Tu produced through tufB accounts for one-third of the cellular EF-Tu as that produced by the tufA gene in bacteria (Van Delft et al 1987;van der Meide et al 1983;Zengel and Lindahl 1982).…”

Section: Electronic Supplementary Materialsmentioning

confidence: 99%

Experimental evolution of Escherichia coli harboring an ancient translation protein

Kaçar

Tran

et al. 2016

Preprint

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The ability to design synthetic genes and engineer biological systems at the genome scale opens new means by which to characterize phenotypic states and the responses of biological systems to perturbations. One emerging method involves inserting artificial genes into bacterial genomes, and examining how the genome and its new genes adapt to each other. Here we report the development and implementation of a modified approach to this method, in which phylogenetically inferred genes are inserted into a microbial genome, and laboratory evolution is then used to examine the adaptive potential of the resulting hybrid genome. Specifically, we engineered an approximately 700-million-year old inferred ancestral variant of tufB, an essential gene encoding Elongation Factor Tu, and inserted it in a modern Escherichia coli genome in place of the native tufB gene. While the ancient homolog was not lethal to the cell, it did cause a two-fold decrease in organismal fitness, mainly due to reduced protein dosage. We subsequently evolved replicate hybrid bacterial populations for 2,000 generations in the laboratory, and examined the adaptive response via fitness assays, whole-genome sequencing, proteomics and biochemical assays. We found that the hybrid lineages exhibit a general adaptive strategy in which the fitness cost of the ancient gene was ameliorated in part by up-regulation of protein production. We expect that this ancient-modern recombinant method may pave the way for the synthesis of organisms that exhibit ancient phenotypes, and that laboratory evolution of these organisms may prove useful in elucidating insights into historical adaptive processes.

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Homologous Recombination between thetufGenes ofSalmonella typhimurium

Cited by 93 publications

References 58 publications

Molecular evolution of the GDP-mannose pathway genes (manB and manC) in Salmonella enterica The GenBank accession numbers for the sequences reported in this paper are AY012160–AY012201.

Molecular evolution of the GDP-mannose pathway genes (manB and manC) in Salmonella enterica The GenBank accession numbers for the sequences reported in this paper are AY012160–AY012201.

Mismatch Repair Proteins Regulate Heteroduplex Formation during Mitotic Recombination in Yeast

Experimental evolution of Escherichia coli harboring an ancient translation protein

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