The formation of pyrimidine dimers in the DNA of fungi and bacteria

Unrau, P.; Wheatcroft, Roger; Cox, Brian S.; Olive, Terie

doi:10.1016/0005-2787(73)90065-8

Cited by 82 publications

(18 citation statements)

References 14 publications

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“…Since the quantum yields for these different dimers are not the same, different numbers of lesions in the two genomes are expected. On the basis of previous measurements of the yield of cyclobutane dimers (36,42,50), we estimated that R. sphaeroides should have at least 67% of the number of E. coli dimers and probably more. Interpretation of these effects must also take into account the other types of lesions derived from pyrimidine dinucleotides following UV irradiation (18).…”

Section: Discussionmentioning

confidence: 97%

DNA repair mutants of Rhodobacter sphaeroides

et al. 1995

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The genome of the photosynthetic eubacterium Rhodobacter sphaeroides 2.4.1 comprises two chromosomes and five endogenous plasmids and has a 65% G؉C base composition. Because of these characteristics of genome architecture, as well as the physiological advantages that allow this organism to live in sunlight when in an anaerobic environment, the sensitivity of R. sphaeroides to UV radiation was compared with that of the more extensively studied bacterium Escherichia coli. R. sphaeroides was found to be more resistant, being killed at about 60% of the rate of E. coli. To begin to analyze the basis for this increased resistance, a derivative of R. sphaeroides, strain 2.4.1⌬S, which lacks the 42-kb plasmid, was mutagenized with a derivative of Tn5, and the transposon insertion mutants were screened for increased UV sensitivity (UV s ). Eight UV s strains were isolated, and the insertion sites were determined by contour-clamped homogeneous electric field pulsed-field gel electrophoresis. These mapped to at least five different locations in chromosome I. Preliminary analysis suggested that these mutants were deficient in the repair of DNA damage. This was confirmed for three loci by DNA sequence analysis, which showed the insertions to be within genes homologous to uvrA, uvrB, and uvrC, the subunits of the nuclease responsible for excising UV damage.The photosynthetic bacterium Rhodobacter sphaeroides was the first prokaryote shown to have multiple chromosomes (48). Wild-type strain 2.4.1 comprises a genome of two circular chromosomes, as well as five additional plasmids with unknown functions. This genome architecture raises significant questions pertaining to DNA metabolism, an area about which virtually nothing is known in this multichromosomal prokaryote. Furthermore, the nature of DNA replication, repair, and recombination in R. sphaeroides is of interest because of other aspects of the lifestyle of this organism. Being photosynthetic, it is subjected to potentially lethal UV irradiation, making its mode of DNA repair of special interest. The high GϩC content (65%) of the R. sphaeroides genome makes this of further interest because of the expected higher content of Z DNA, the greater need for uracil repair following cytosine deamination, and the role of the latter process in UV mutagenesis when it occurs in pyrimidine dimers (49). In addition, R. sphaeroides can use a range of compounds as terminal electron acceptors, including toxic metal oxides and organic compounds with a potential for free radical formation (34). Thus, it is not only likely but probable that there are specific mechanisms that protect the genome against damage from these compounds.The current paradigm for prokaryotic DNA replication, repair, and recombination is based on DNA metabolism in Escherichia coli. Since this is an enteric organism with exposure to a limited environment and has a single chromosome with a base composition of about 50% GϩC, there is reason to expect that the E. coli model is incomplete or not entirely appropriate for free...

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Section: Discussionmentioning

confidence: 97%

DNA repair mutants of Rhodobacter sphaeroides

et al. 1995

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“…The dose decrement, ⌬D, is defined as the difference between the UV doses with and without photoreactivation that yield the same surviving fraction (17). The number of pyrimidine dimers repaired was obtained by multiplying ⌬D by the number of dimers introduced per haploid genome per joule per square meter, which has been estimated as 240 (65).…”

Section: Methodsmentioning

confidence: 99%

Role of UME6 in Transcriptional Regulation of a DNA Repair Gene in Saccharomyces cerevisiae

Sweet

Jang

Sancar

1997

Molecular and Cellular Biology

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In Saccharomyces cerevisiae UV radiation and a variety of chemical DNA-damaging agents induce the transcription of specific genes, including several involved in DNA repair. One of the best characterized of these genes is PHR1, which encodes the apoenzyme for DNA photolyase. Basal-level and damage-induced expression of PHR1 require an upstream activation sequence, UAS PHR1 , which has homology with DRC elements found upstream of at least 19 other DNA repair and DNA metabolism genes in yeast. Here we report the identification of the UME6 gene of S. cerevisiae as a regulator of UAS PHR1 activity. Multiple copies of UME6 stimulate expression from UAS PHR1 and the intact PHR1 gene. Surprisingly, the effect of deletion of UME6 is growth phase dependent. In wild-type cells PHR1 is induced in late exponential phase, concomitant with the initiation of glycogen accumulation that precedes the diauxic shift. Deletion of UME6 abolishes this induction, decreases the steady-state concentration of photolyase molecules and PHR1 mRNA, and increases the UV sensitivity of a rad2 mutant. Despite the fact that UAS PHR1 does not contain the URS1 sequence, which has been previously implicated in UME6-mediated transcriptional regulation, we find that Ume6p binds to UAS PHR1 with an affinity and a specificity similar to those seen for a URS1 site. Similar binding is also seen for DRC elements from RAD2, RAD7, and RAD53, suggesting that UME6 contributes to the regulated expression of a subset of damage-responsive genes in yeast.

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“…In the wild-type strain, the relevant UV dose was 50 J/m 2 , whereas only 1.2 J/m 2 was sufficient to reduce viability of the NER-deficient rad1D and rad14D mutants to a comparable level. According to published data, these doses generate %14,000 cyclobutane pyrimidine dimers (CPDs) per haploid genome in the wild-type strain and 460 CPDs per genome in NER-deficient mutants (Unrau et al 1973;Reynolds 1987). Following irradiation with an approximately equitoxic UV dose, we screened for white ade2 adeX double-mutant colonies among the parental background of red ade2 single-mutant colonies.…”

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confidence: 99%

The Mechanism of Nucleotide Excision Repair-Mediated UV-Induced Mutagenesis in Nonproliferating Cells

Kozmin

Jinks-Robertson

2013

Genetics

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Following the irradiation of nondividing yeast cells with ultraviolet (UV) light, most induced mutations are inherited by both daughter cells, indicating that complementary changes are introduced into both strands of duplex DNA prior to replication. Early analyses demonstrated that such two-strand mutations depend on functional nucleotide excision repair (NER), but the molecular mechanism of this unique type of mutagenesis has not been further explored. In the experiments reported here, an ade2 adeX colonycolor system was used to examine the genetic control of UV-induced mutagenesis in nondividing cultures of Saccharomyces cerevisiae. We confirmed a strong suppression of two-strand mutagenesis in NER-deficient backgrounds and demonstrated that neither mismatch repair nor interstrand crosslink repair affects the production of these mutations. By contrast, proteins involved in the error-prone bypass of DNA damage (Rev3, Rev1, PCNA, Rad18, Pol32, and Rad5) and in the early steps of the DNA-damage checkpoint response (Rad17, Mec3, Ddc1, Mec1, and Rad9) were required for the production of two-strand mutations. There was no involvement, however, for the Pol h translesion synthesis DNA polymerase, the Mms2-Ubc13 postreplication repair complex, downstream DNA-damage checkpoint factors (Rad53, Chk1, and Dun1), or the Exo1 exonuclease. Our data support models in which UV-induced mutagenesis in nondividing cells occurs during the Pol z-dependent filling of lesion-containing, NER-generated gaps. The requirement for specific DNA-damage checkpoint proteins suggests roles in recruiting and/or activating factors required to fill such gaps. MUTAGENESIS associated with induced DNA damage is generally considered to occur during S phase, when polymerase-blocking lesions are bypassed in an error-prone manner by a translesion synthesis (TLS) DNA polymerase. In the yeast Saccharomyces cerevisiae, ultraviolet (UV)-induced mutagenesis is dependent on Pol z (Rev3-Rev7) and Rev1, with rev1, rev3, or rev7 mutants exhibiting a "reversionless" phenotype in response to UV irradiation (Lawrence 2002). Just as induced mutagenesis is considered to be a consequence of error-prone TLS, nucleotide excision repair (NER) is thought to counteract such mutagenesis by removing UV-induced lesions before they can be encountered during DNA replication.Although NER is generally considered to be an error-free, mutation-avoidance mechanism, data obtained .30 years ago demonstrated a pro-mutation role of NER in the UVinduced mutagenesis that occurs in nondividing yeast cells (Eckardt and Haynes 1977;James and Kilbey 1977;James et al. 1978;Eckardt et al. 1980). Either the induction of recessive lethal mutations in diploid strains (James and Kilbey 1977;James et al. 1978) or the induction of forward mutations in the de novo adenine biosynthetic pathway in haploid strains was monitored (Eckardt and Haynes 1977;Eckardt et al. 1980). Despite the differences in assay systems used, the authors reached the same conclusions. First, UVinduced mutations in nondi...

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The formation of pyrimidine dimers in the DNA of fungi and bacteria

Cited by 82 publications

References 14 publications

DNA repair mutants of Rhodobacter sphaeroides

DNA repair mutants of Rhodobacter sphaeroides

Role of UME6 in Transcriptional Regulation of a DNA Repair Gene in Saccharomyces cerevisiae

The Mechanism of Nucleotide Excision Repair-Mediated UV-Induced Mutagenesis in Nonproliferating Cells

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