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Differential Response of Multiphasic Replication to UV - light
이치건,박수희,이명애,박상대 한국유전학회 1986 Genes & Genomics Vol.8 No.1
The nature of nascent DNA from both asynchronous and synchronous populations was investigated. In UV-irradiated synchronous cells, the amounts of nascent DNA, synthesized during the first 4hr in S phase, were increased to 1.5-fold. But this enhancing effect was not appeared during 5-10 hr of S phase. Asynchronous population also showed the increased level of DNA synthesis by UV-light. Effects of UV-light on the rate of DNA synthesis was somewhat different between asynchronous and synchronous populations. There's no apparent changes in synchronous population, whereas in asynchronous population the rate of DNA synthesis was greatly reduced and then gradually recovered to normal level thereafter. These results suggest that there are various classes of DNA, replicated at discrete times during S-phase and differently responding to UV-light.
자외선과 MMS 를 처리한 절제회복 결함 및 숙련 포유동물 세포의 후복제 회복
박상대,이치건,김찬길,최수영 한국유전학회 1984 Genes & Genomics Vol.6 No.2
Post-replication repair was determined in CHO-Kl, HF and XP20S cells treated with UV-light and MMS by "pulse chase" experiments. All these cell lines showed normal growing patterns of nascent DNA in spite of the presence of damaged sites on the template DNA strands, even in the excision repair defective cells. These results suggest that post-replication repair may not be affected by damages caused by UV-light and MMS.
박상대,이치건 한국유전학회 1983 Genes & Genomics Vol.5 No.3
Effects of various mutagens on replicon initiation and chain elongation of DNA replication was studied by pulse-labeling with (³H) - thymidine and sedimentation analysis of DNA. When treated with those mutagens to mammalian cells, each cell line showed the reduced rate of DNA synthesis and the interrupted DNA replication in dose dependent manner. At low doses, the inhibition of replicon initiation was primarily caused and at high fluences the inhibitory effect appeared in chain elongation and termination of DNA replication. Using the method of 'Pulse-Chase' we could also observed the postreplication repair, indicating that the nascent DNA growth normally occurred, although still damaged sites remained on parental DNA during DNA replication.
박상대,이치건,최수영,정용근,이준규 한국유전학회 1987 Genes & Genomics Vol.9 No.4
A methyl methanesulfonate (MMS) sensitive mutant of E. coli was isolated to investigate the DNA repair mechanisms involved in the damages by alkylating agents. After mutagenization with ethyl methanesulfonate (EMS), one clone showing a highly decreased survival to alkylating agents was isolated. Results of the host cell reactivation indicated that this mutant strain seemed to be defective in a gene for the repair of DNA damages induced by alkylating agents. This strain showed normal adaptive response to alkylating agents and the defect in survival was not complemented with the alkA or ada gene which encodes 3-methyladenine-DNA glycosylase II or O^6-methylguanine-DNA methyltransferase, respectively. This strain did not show any differences in the major known AP endonuclease activities. Sedimentation analysis with alkaline sucrose gradient, however, suggested that this strain might be defective in a gene involved in the incision of apurinic/apyrimidinic sites.
포유동물세포에 있어 MMS 와 자외선에 의한 복제개시 및 DNA 생장억제
김영상,박상대,성노현,이치건,윤정교 한국유전학회 1983 Genes & Genomics Vol.5 No.3
Chinese hamster ovary (CHO) cells exposed to ultraviolet (UV)-light and methyl methanesulfonate (MMS), analysed by alkaline sucrose gradient sedimentation, showed an interruption of DNA replication. In UV-irradiated cells, dose-dependent response appeared; at low fluences below 1.42J/㎡ the inhibition of replicon initiation was caused and as the fluence increased the effect on replicon initiation was masked by the inhibitory effects on strand-elongation and joining. MMS also showed the inhibitory effects in dose dependent manner at both processes of replicon initiation and chain elongation of DNA. Treatment with UV and MMS concomitantly resulted in the additive inhibition effects of DNA replication.