Further evidence that ultraviolet radiation-enhanced reactivation of simian virus 40 in monkey kidney cells is not accompanied by mutagenesis

Taylor, William D.; Bockstahler, Larry E.; Montes, J. G.; Babich, Michael A.; Lytle, C. David

doi:10.1016/0165-7992(82)90095-1

Cited by 36 publications

(17 citation statements)

References 24 publications

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“…For example, the mutability of intact but not UV-irradiated parvovirus H1 is enhanced in UV pretreated human or rat cells (8), whereas only enhanced mutability of UV-treated virus is seen when simian virus 40 infects UV-treated monkey cells (7). Findings opposite to the latter have been reported (9,10).…”

contrasting

confidence: 49%

“…In E. coli, the induced response leads to enhanced mutation levels. Although some controversy exists in the literature as to whether UV irradiation of monkey cells leads to enhanced mutagenesis in infecting UV-damaged simian virus 40 (7,9,10), recent evidence suggests that the inducible repair system is mutagenic for UV-damaged virus infecting human cells (28). It remains to be seen whether the induced repair of potentially lethal damage is associated with mutator activity in the cellular DNA.…”

Section: Discussionmentioning

confidence: 98%

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Exposure of nondividing populations of primary human fibroblasts to UV (254 nm) radiation induces a transient enhancement in capacity to repair potentially lethal cellular damage.

Tyrrell¹

1984

Proc. Natl. Acad. Sci. U.S.A.

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Nondividing (arrested) populations of primary human fibroblasts from normal individuals exposed to an initial dose (1.5 or 3 J m-2) of far-UV (254 nm) radiation and then incubated in medium containing low (0.5%) serum develop enhanced resistance to inactivation of cloning efficiency by a second (challenge) dose of UV. The resistance develops within 2-4 days, after which there is a decline. Resistance develops to a higher degree and more rapidly (1-2 days) in cells derived from patients with the variant form of xeroderma pigmentosum. Excision-deficient cells from xeroderma pigmentosum complementation group A individuals also develop UV resistance after a lower (0.2 J m-2) exposure to UV. Enhanced UV resistance does not develop in UV-irradiated cell populations incubated with the protein synthesis inhibitor cycloheximide (5 IPM). These observations are consistent with the interpretation that exposure of human fibroblasts to low doses of UV induces synthesis of a protein involved in a metabolic pathway that transiently enhances the capacity of cells to repair potentially lethal damage resulting from a subsequent dose of UV.The genetic control and biochemistry of an error-prone far-UV inducible repair system in Escherichia coli has been extensively studied (see ref. 1 for overview). Recent experiments have begun to clarify the nature of the inducing signal (2) and enzymology (3) of the process. The existence of a similar phenomenon in eukaryotic cells has been largely inferred from viral reactivation studies (4). The survival of many types of UV-damaged virus is enhanced by pre-exposure of the appropriate host cells to UV radiation and incubation for an appropriate time prior to viral infection (see ref.5 for review). The nature and degree of error-proneness of the response, as deduced from enhanced mutagenesis of infecting virus (6, 7), appears to vary considerably with the particular virus and host cell system employed. For example, the mutability of intact but not UV-irradiated parvovirus H1 is enhanced in UV pretreated human or rat cells (8), whereas only enhanced mutability of UV-treated virus is seen when simian virus 40 infects UV-treated monkey cells (7). Findings opposite to the latter have been reported (9, 10).Biochemical measurements of UV-induced responses in mammalian cells have been controversial. A report of enhancement of post-replication repair by a low-dose UV-conditioning exposure (11) may also be interpreted (12) on the basis of the abnormal state of DNA replication at the time of the second exposure. Nevertheless, UV exposure of human fibroblasts has been shown to enhance levels of plasminogen activator (13) and DNA ligase (14), and agents that arrest DNA replication have been shown recently to induce synthesis of a nuclear membrane-bound protein in cell lines derived from B lymphocytes (15).Little is known about whether UV treatment actually enhances the capacity of mammalian cells to survive subsequent challenge doses of UV. Split-dose experiments are often difficult to interpret (16)...

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contrasting

confidence: 49%

Section: Discussionmentioning

confidence: 98%

Exposure of nondividing populations of primary human fibroblasts to UV (254 nm) radiation induces a transient enhancement in capacity to repair potentially lethal cellular damage.

Tyrrell¹

1984

Proc. Natl. Acad. Sci. U.S.A.

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“…(17) and mammalian (16,19) cells as a response to treatment which inhibits DNA replication. Because of the lack of defective mammalian cell mutants, however, the analysis of physiological responses analogous to E. coli SOS functions has been very difficult and has led to conflicting interpretations (16,19,23). Thus, the analysis of enhanced mutagenesis of DNA-damaged animal virus represents one way to characterize inducible repair functions in mammalian cells.…”

mentioning

confidence: 99%

Enhanced mutagenesis of UV-irradiated simian virus 40 occurs in mitomycin C-treated host cells only at a low multiplicity of infection.

Sarasin¹,

Benoit²

1986

Mol. Cell. Biol.

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Treatment of monkey kidney cells with mitomycin C (MMC) 24 h prior to infection with UV-irradiated simian virus 40 (SV40) enhanced both virus survival and virus mutagenesis. The use of SV40 as a biological probe has been taken as an easy method to analyse SOS response of mammalian cells to the stress caused by DNA damage or inhibition of DNA replication. The mutation assay we used was based on the reversion from a temperature-sensitive phenotype (tsA58 mutant) to a wild-type phenotype. The optinal conditions for producing enhanced survival and mutagenesis in the virus progeny were determined with regard to the multiplicity of infection (MOI). Results showed that the level of enhanced mutagenesis observed for UV-irradiated virus grown in MMC-treated cells was an inverse function of the MOI, while enhanced survival was observed at nearly the same level regardless of the MOI. For the unirradiated virus, almost no increase in the mutation of virus progeny issued from MMC-treated cells was observed, while a small amount of enhanced virus survival was obtained. These results show that enhanced virus mutagenesis and enhanced virus survival can be dissociated under some experimental conditions. Enhanced virus mutagenesis, analogous to the error-prone replication of phages in SOS-induced bacteria, was observed, at least for SV40, only when DNA of both virus and host cells was damaged and when infection occurred with a small number of viral particles. We therefore hypothesize that an error-prone replication mode of UV-damaged templates is observed in induced monkey kidney cells.

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“…If induced by an initial hyperthermic treatment in a clinical fractionated dose regimen, such a mechanism could conceivably reduce the efficiency of subsequent radiotherapy whose principal intracellular target is DNA. Furthermore, evidence has been presented that RER may be accompanied by enhanced mutagenesis though this may not always be the case (DasGupta & Summers, 1978;Sarasin & Benoit, 1980;Day & Ziolkowski, 1981;Lytle & Knott, 1982;Taylor et al, 1982). If HER were also mutagenic, this could represent an undesirable side effect of the irradiation of heated healthy tissue which would compromise the possible value of using thermotolerance as a means of preferentially protecting normal tissue (Hahn, 1982).…”

Section: Pre-treatment Of Cellsmentioning

confidence: 99%

Hyperthermia enhances the reactivation of irradiated adenovirus in HeLa cells

Piperakis¹,

McLennan²

1984

Br J Cancer

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Summary The reactivation of U.V.-irradiated adenovirus 2 in HeLa cells is enhanced 8-9 fold if the cells are given a brief hyperthermic shock before infection. Maximum reactivation is achieved by heating for 10min at 45.5°C and with a delay of 36h between heating and infection. The induction process requires protein synthesis only during the 3h period immediately following heating; cycloheximide does not prevent the expression of enhanced reactivation if added to the cells after this time. Heat-enhanced reactivation exhibits properties similar in some respects to radiation-enhanced reactivation and indicates an increased capacity of the heated cells to tolerate DNA damage.

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Further evidence that ultraviolet radiation-enhanced reactivation of simian virus 40 in monkey kidney cells is not accompanied by mutagenesis

Cited by 36 publications

References 24 publications

Exposure of nondividing populations of primary human fibroblasts to UV (254 nm) radiation induces a transient enhancement in capacity to repair potentially lethal cellular damage.

Exposure of nondividing populations of primary human fibroblasts to UV (254 nm) radiation induces a transient enhancement in capacity to repair potentially lethal cellular damage.

Enhanced mutagenesis of UV-irradiated simian virus 40 occurs in mitomycin C-treated host cells only at a low multiplicity of infection.

Hyperthermia enhances the reactivation of irradiated adenovirus in HeLa cells

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