• Proceedings of the Zoological Society Korea Conference
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• 2001.10a
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• pp.239.3-240
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• 2001

No Abstract, See Full Text

• Toxicological Research
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• v.34 no.4
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• pp.297-302
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• 2018

Cells are constantly exposed to endogenous and exogenous chemical and physical agents that damage their genome by forming DNA lesions. These lesions interfere with the normal functions of DNA such as transcription and replication, and need to be either repaired or tolerated. DNA lesions are accurately removed via various repair pathways. In contrast, tolerance mechanisms do not remove lesions but only allow replication to proceed despite the presence of unrepaired lesions. Cells possess two major tolerance strategies, namely translesion synthesis (TLS), which is an error-prone strategy and an accurate strategy based on homologous recombination (homology-dependent gap repair [HDGR]). Thus, the mutation frequency reflects the relative extent to which the two tolerance pathways operate in vivo. In the present paper, we review the present understanding of the mechanisms of TLS and HDGR and propose a novel and comprehensive view of the way both strategies interact and are regulated in vivo.

• The Korean Journal of Food And Nutrition
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• v.10 no.3
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• pp.407-413
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• 1997

The antimutagenic mechanism of cinnamaldeyde on mutagenesis induced by 4-nitroquinoline-1-oxide(4-NQO) and N-metyl-N'-nitro-N-nitrosoguanidine (MNNG) was investigated in various DNA repair-deficient strains, E. coli B/r and K-12 series. Cinnamaldehyde did not show any effects not only on the $\beta$-galactosidase activities of GW1060 and GW1103(recA441) which synthesizes $\beta$-galactosidase consitutively at 41$^{\circ}C$ but also on that of GW1107[lexA51 (Def)] in which the SOS response always occur. These results suggest that cinnamaldehyde dose not change the function of RecA which positively controls the SOS response as well as not acting as the repressor like LexA. In addition, no inhibitory effect of cinnamaldehyde was observed on the growth of Trp+ revertant and the delay of viable cell growth was also not found by adding cinnamaldehyde. Despite the decrease in the number of revertants, a significant increase in survival of 4-NQO treated cells was observed in E. coli WP2s(uvrA), ZA159($\Delta$uvrB) and TK603(uvrA). But these effects disappeared in excision-proficient strain WP2(uvrA+) and lexA-deficient strains(CM561 and CM611). The enhancement of survival was not found in WP67(uvrA polA) deficient in polymerase I which ligates the gap between complementary DNA. From the above results, we assume that cinnamaldehyde might show antimutagenic effect by enhancing an error-free recombinational repair system.

• Journal of Microbiology and Biotechnology
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• v.21 no.4
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• pp.438-447
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• 2011

Deinococcus radiodurans is extremely resistant to various genotoxic conditions and chemicals. In this study, we characterized the effect of a sublethal concentration (100 ${\mu}M$) of cadmium (Cd) on D. radiodurans using a whole-genome DNA microarray. Time-course global gene expression profiling showed that 1,505 genes out of 3,116 total ORFs were differentially expressed more than 2-fold in response to Cd treatment for at least one timepoint. The majority of the upregulated genes are related to iron uptake, cysteine biosynthesis, protein disulfide stress, and various types of DNA repair systems. The enhanced upregulation of genes involved in cysteine biosynthesis and disulfide stress indicate that Cd has a high affinity for sulfur compounds. Provocation of iron deficiency and growth resumption of Cd-treated cells by iron supplementation also indicates that CdS forms in iron-sulfur-containing proteins such as the [Fe-S] cluster. Induction of base excision, mismatch, and recombinational repair systems indicates that various types of DNA damage, especially base excision, were enhanced by Cd. Exposure to sublethal Cd stress reduces the growth rate, and many of the downregulated genes are related to cell growth, including biosynthesis of cell membrane, translation, and transcription. The differential expression of 52 regulatory genes suggests a dynamic operation of complex regulatory networks by Cd-induced stress. These results demonstrate the effect of Cd exposure on D. radiodurans and how the related genes are expressed by this stress.

• Korean Journal of Microbiology
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• v.43 no.4
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• pp.250-255
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• 2007

The RecA protein of Deinococcus radiodurans is essential for the extreme radiation resistance of this organism. The central steps involved in recombinational DNA repair require DNA-dependent ATP hydrolysis by recA protein. Key feature of RecA protein-mediated activities is the interactions with ssDNA and dsDNA. The ssDNA is the site where RecA protein filament formation nucleates and where initiation of DNA strand exchange takes place. The effect of sequence heterogeneity of ssDNA was examined in this experiment. The rate of homopolymeric synthetic ssDNA-dependent ATP hydrolysis was constant or nearly so over a broader range of pHs. For poly(dT)-dependent ATP or dATP hydrolysis, rates were generally faster, with a broader optimum between pH 7.0 and 8.0. Activities of RecA protein were affected by the ionic environment. The ATPase activity was shown to have different sensitivity to anionic species. The presence of glutamate seemed to slimulate the hydrolytic activity. Dr RecA protein was shown to require $Mg^{2+}$ ion greater than 2 mM for binding to etheno ssDNA and the binding stoichiometry of 3 nucleotide for RecA protein monomer.