미생물학회지 (Korean Journal of Microbiology)

  • 제38권2호
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  • Pages.96-102
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  • 2002
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  • 0440-2413(pISSN)
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  • 2383-9902(eISSN)
한국미생물학회 (The Microbiological Society of Korea)
권호 표지

출아효모의 세포주기동안 DNA 상해에 의한 발현 유도에 미치는 DPB11 유전자의 영향

Effect of DPBll Gene for the Transcriptional Induction by DNA Damage During Cell Cycle in Saccharomyces cerevisiae

  • 선우양일 (동아대학교 자연과학대학 생물학과) ;
  • 임선희 (동아대학교 자연과학대학 생물학과) ;
  • 배호정 (동아대학교 자연과학대학 생물학과) ;
  • 김중현 (동아대학교 자연과학대학 생물학과) ;
  • 김은아 (동아대학교 자연과학대학 생물학과) ;
  • 김승일 (한국기초과학지원연구원) ;
  • 김수현 (한국기초과학지원연구원) ;
  • 박정은 (동아대학교 자연과학대학 생물학과) ;
  • 김재우 (동아대학교 자연과학대학 생물학과, 동아대학교병원 임상병리실)
  • 발행 : 2002.06.01
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초록

S기 checkpoint기작은 DNA복제 저해나 DNA상해 등에 반응하여, S기 세포주기 정지를 일으키거나 상해 회복에 관련된 유전자들의 전사가 유도됨으로서 진핵세포에서의 유전적인 안정성을 유지한다. 이러한 반응에 대한것ba11 변이주의 결손을 확인하기 위해서, nPB11 (DNA polymerase B possible subunit)유전자의 과다발현 효과에 대해 조사하고, HU (Hydroxyurea)와 MMS (Methyl methanesulfonate)에 대한 감수성 및 DNA상해 물질에 의한 RNR3 (Ribonulectide reductase) mRNA의 전사 유도를 조사하였다. RNR3 mRNA의 전사는 DNA합성 저해에 의해 발생한 스트레스나 화학물질에 의한 직접적 인 DNA상해 등에 의해 유도되어진다. 그 결과, dpb11-1변이주는 DNA상해 물질에 감수성을 나타내었고, RNR3 mRNA전사유도 또한 야생형 균주에 비해 약 40% 정도 감소를 나타내었다. 더욱이 dpb2-1 균주에서도 이와 동일한 결과를 얻었다. 그러므로 DPB2와 DPB11 유전자는 복제에 대한 sensor로서, 복제 정지 요인에 대한 세포주기 반응과 전사 조절에 모두 작용하는 것으로 사료된다.

The S-phase checkpoint mechanisms response to DNA damage or inhibition of DNA replication for maintenance of genetic stability in eukaryotic cells. These roles include cell cycle control arrest at S-phase and Iranscriptional induction of repair genes. To characterize the defects of dpbll mutant for both these responses, we examined the over-expression effect of DPBll gene, the sensitivity to HU, MMS, and the transcriptional pattern by DNA damage agent for RNRS mRNA. RNRS transcript is induced in response to a wide variety of agents that either damage D7A directly through chemical modification or induce stress by blocking DNA synthesis. As results, dpbll-1 cells are sensitive to DNA damage agents and the level of RNR3 mRNA is reduced approximately 40% than wild type cells. Moreover, we found the same results in dpb2-1 cells. Therefore, we propose that DPB2 and DPBll act as a sensor of replication that coordinates the transcriptional and cell cycle responses to replication blocks.

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