Mechanisms of stationary-phase mutagenesis in bacteria: mutational processes in pseudomonads

Kivisaar, Maia

doi:10.1111/j.1574-6968.2010.02027.x

Cited by 46 publications

(37 citation statements)

References 164 publications

(256 reference statements)

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“…2c, white bars), indicating that the umuDpR promoter is functional under nonstressing conditions. This result is in agreement with a previous report showing that pseudomonads have a higher baseline expression of particular SOS regulon genes, such as umuDC genes, even in the absence of DNA damage (Kivisaar, 2010). However, when cells were exposed to subinhibitory levels of MMC, higher b-galactosidase activity was observed (Fig.…”

Section: Induction Of the Umudpr Gene By MMCsupporting

confidence: 93%

“…aeruginosa PAO1 genome lacks umuDC genes (Kivisaar, 2010), and the UmuDpR protein possesses characteristics of LexA-type repressors, we tested directly whether UmuDpR is able to regulate the expression of Ps. aeruginosa SOS genes.…”

Section: Umudpr Regulates Expression Of Sos Genesmentioning

confidence: 99%

“…The two forms of the umuD gene product play different roles in the cell. UmuD is implicated in a primitive DNA-damage checkpoint (UmuD 2 C complex) and prevents DNA polymerase IV-dependent 21 frameshift mutagenesis (Kivisaar, 2010), while the cleaved UmuD9 form facilitates UmuC-dependent mutagenesis via formation of DNA polymerase V after its association with the UmuC protein (the UmuD9 2 C complex) (Patel et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

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A plasmid-encoded UmuD homologue regulates expression of Pseudomonas aeruginosa SOS genes

Díaz-Magaña¹,

Alva-Murillo

Chávez-Moctezuma

et al. 2015

Microbiology

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The Pseudomonas aeruginosa plasmid pUM505 contains the umuDC operon that encodes proteins similar to error-prone repair DNA polymerase V. The umuC gene appears to be truncated and its product is probably not functional. The umuD gene, renamed umuDpR, possesses an SOS box overlapped with a Sigma factor 70 type promoter; accordingly, transcriptional fusions revealed that the umuDpR gene promoter is activated by mitomycin C. The predicted sequence of the UmuDpR protein displays 23 % identity with the Ps. aeruginosa SOS-response LexA repressor. The umuDpR gene caused increased MMC sensitivity when transferred to the Ps. aeruginosa PAO1 strain. As expected, PAO1-derived knockout lexA 2 mutant PW6037 showed resistance to MMC; however, when the umuDpR gene was transferred to PW6037, MMC resistance level was reduced. These data suggested that UmuDpR represses the expression of SOS genes, as LexA does. To test whether UmuDpR exerts regulatory functions, expression of PAO1 SOS genes was evaluated by reverse transcription quantitative PCR assays in the lexA 2 mutant with or without the pUC_umuD recombinant plasmid. Expression of lexA, imuA and recA genes increased 3.4-5.3 times in the lexA 2 mutant, relative to transcription of the corresponding genes in the lexA + strain, but decreased significantly in the lexA 2 /umuDpR transformant. These results confirmed that the UmuDpR protein is a repressor of Ps. aeruginosa SOS genes controlled by LexA. Electrophoretic mobility shift assays, however, did not show binding of UmuDpR to 59 regions of SOS genes, suggesting an indirect mechanism of regulation.

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Section: Induction Of the Umudpr Gene By MMCsupporting

confidence: 93%

Section: Umudpr Regulates Expression Of Sos Genesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

A plasmid-encoded UmuD homologue regulates expression of Pseudomonas aeruginosa SOS genes

Díaz-Magaña¹,

Alva-Murillo

Chávez-Moctezuma

et al. 2015

Microbiology

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“…Stress-induced mutagenesis (SIM)-the increase of mutation rates in stressed or maladapted individuals-has been demonstrated in several species, including both prokaryotes and eukaryotes [15]. SIM has been observed in laboratory strains [16,17] and natural populations of Escherichia coli [18] (but see [19]), and in other species of bacteria such as pseudomonads [20], Helicobacter pylori [21], Vibrio cholera [22] and Streptococcus pneumonia [23]. SIM has also been observed in yeast [24,25], algae [26], nematodes [27], flies [28] and human cancer cells [29].…”

Section: Introductionmentioning

confidence: 99%

Stress-induced mutagenesis and complex adaptation

Ram

Hadany

2014

Proc. R. Soc. B.

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Because mutations are mostly deleterious, mutation rates should be reduced by natural selection. However, mutations also provide the raw material for adaptation. Therefore, evolutionary theory suggests that the mutation rate must balance between adaptability-the ability to adapt-and adaptedness-the ability to remain adapted. We model an asexual population crossing a fitness valley and analyse the rate of complex adaptation with and without stress-induced mutagenesis (SIM)-the increase of mutation rates in response to stress or maladaptation. We show that SIM increases the rate of complex adaptation without reducing the population mean fitness, thus breaking the evolutionary trade-off between adaptability and adaptedness. Our theoretical results support the hypothesis that SIM promotes adaptation and provide quantitative predictions of the rate of complex adaptation with different mutational strategies.

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“…Stress-induced DNA damage leads to mutation in DNA repair systems. Indeed, a high percentage of CF isolates have impaired DNA repair mechanisms (8,13,14). This initial defect then results in hypermutability and further genetic mutation (15, 16), which is particularly linked with acquired resistance to antibiotics and oxidative stress, as well as decreased production of specific virulence factors (8).…”

mentioning

confidence: 99%

Involvement of Stress-Related Genes polB and PA14_46880 in Biofilm Formation of Pseudomonas aeruginosa

Alshalchi

Anderson

2014

Infect Immun

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eradicate. However, biofilm studies have been hampered by the fact that most assays utilize nonliving surfaces as biofilm attachment substrates. In an attempt to better understand the mechanisms behind P. aeruginosa biofilm formation, we performed a genetic screen to identify novel factors involved in biofilm formation on biotic and abiotic surfaces. We found that deletion of genes polB and PA14_46880 reduced biofilm formation significantly compared to that in the wild-type strain PA14 in an abiotic biofilm system. In a biotic biofilm model, wherein biofilms form on cultured airway cells, the ⌬polB and ⌬PA14_46880 strains showed increased cytotoxic killing of the airway cells independent of the total number of bacteria bound. Notably, deletion mutant strains were more resistant to ciprofloxacin treatment. This phenotype was linked to decreased expression of algR, an alginate transcriptional regulatory gene, under ciprofloxacin pressure. Moreover, we found that pyocyanin production was increased in planktonic cells of mutant strains. These results indicate that inactivation of polB and PA14_46880 may inhibit transition of P. aeruginosa from a more acute infection lifestyle to the biofilm phenotype. Future investigation of these genes may lead to a better understanding of P. aeruginosa biofilm formation and chronic biofilm infections. Chronic Pseudomonas aeruginosa infections in the lungs of cystic fibrosis (CF) patients are characterized by development of biofilm (1, 2). This biofilm formation protects these bacteria from stressful environmental factors, including antibiotic treatment and host defense mechanisms (1, 2). In particular, the biofilm extracellular matrix enhances the survival and persistence of P. aeruginosa by shielding the bacteria from the harsh conditions of CF patient lungs (3). Decreased growth rate, development of persisters, and expression of biofilm-specific resistance factors further enhance biofilm survival in the face of antibiotic and host stress (4,5). This adaptation to the CF lung environment is controlled by a complex regulatory network (6). Additionally, longterm exposure to stresses during chronic infection results in accumulation of mutations that contribute to persistent survival (7,8), suggesting that host pressures during infections actually enhance biofilm formation (9, 10). Thus, due to biofilm formation and subsequent phenotypic and genotypic adaptation to the harsh and stressful conditions, P. aeruginosa colonization often becomes lifelong in the CF lung (11), and it is a major factor contributing to CF complications, including respiratory failure and death (12).Genetic adaptation to the CF lung environment is thought to arise by a multistep process. Stress-induced DNA damage leads to mutation in DNA repair systems. Indeed, a high percentage of CF isolates have impaired DNA repair mechanisms (8,13,14). This initial defect then results in hypermutability and further genetic mutation (15, 16), which is particularly linked with acquired resistance to antibiotics and oxidative ...

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Mechanisms of stationary-phase mutagenesis in bacteria: mutational processes in pseudomonads

Cited by 46 publications

References 164 publications

A plasmid-encoded UmuD homologue regulates expression of Pseudomonas aeruginosa SOS genes

A plasmid-encoded UmuD homologue regulates expression of Pseudomonas aeruginosa SOS genes

Stress-induced mutagenesis and complex adaptation

Involvement of Stress-Related Genes polB and PA14_46880 in Biofilm Formation of Pseudomonas aeruginosa

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