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      Distribution of mec Regulator Genes in Methicillin - Resistant Staphylococci

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      https://www.riss.kr/link?id=E685495

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      다국어 초록 (Multilingual Abstract)

      In order to understand the role of mec regulation genes in the evolution of methicillin-resistant S. aureus (MRSA), the distribution of the mec regulator genes among the 66 clinical isolates of MRSA was analysed. And also the correlation between gene mutation and degree of phenotypic expression of resistance was studied. Fifty strains carried whole mec regulator region, while the mecI gene and nearly half of the 3'-end of the mecRI gene were deleted in fifteen strains. The mecRI MS gene was detected among all of the mecA carried strains, but the mecRI PB gene was carried by 77% of the MRSA strains. At least a portion of the 5'-end region of the mecRI gene was carried by all MRSA strains tested. Forty-seven strains were finally confirmed to have mecI gene and mecI gene of above strains was sequenced for identification of the relationship between repressor function of mecI gene on mecA transcription and MIC level of methicillin. Point mutations were detected in 11 strains of 47 strains. In 8 strains, there was one nucleotide substitution (C to T at position 202) that produced a new termination codon at position 201. In 3 strains, one nucleotide substitution from G to T at position 43 caused an amino acid substitution from Val to Phe. The MIC of methicillin of strains carrying mutated mecI genes ranged 256 μg/ml to 1024 μg/ml. Transcription level of amplified cDNA corresponding to mecA was determined by the method of RT-PCR of extracted RNA. Total RNA was extracted from two strains with mutated mecI gene and a strain with intact mecI gene. Deletional loss or the mutational inactivation of the mecI gene did not affect the level of mecA transcription. Role of mecI gene as a strong repressor function on mecA gene seemed to be skeptical.
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      In order to understand the role of mec regulation genes in the evolution of methicillin-resistant S. aureus (MRSA), the distribution of the mec regulator genes among the 66 clinical isolates of MRSA was analysed. And also the correlation between gene ...

      In order to understand the role of mec regulation genes in the evolution of methicillin-resistant S. aureus (MRSA), the distribution of the mec regulator genes among the 66 clinical isolates of MRSA was analysed. And also the correlation between gene mutation and degree of phenotypic expression of resistance was studied. Fifty strains carried whole mec regulator region, while the mecI gene and nearly half of the 3'-end of the mecRI gene were deleted in fifteen strains. The mecRI MS gene was detected among all of the mecA carried strains, but the mecRI PB gene was carried by 77% of the MRSA strains. At least a portion of the 5'-end region of the mecRI gene was carried by all MRSA strains tested. Forty-seven strains were finally confirmed to have mecI gene and mecI gene of above strains was sequenced for identification of the relationship between repressor function of mecI gene on mecA transcription and MIC level of methicillin. Point mutations were detected in 11 strains of 47 strains. In 8 strains, there was one nucleotide substitution (C to T at position 202) that produced a new termination codon at position 201. In 3 strains, one nucleotide substitution from G to T at position 43 caused an amino acid substitution from Val to Phe. The MIC of methicillin of strains carrying mutated mecI genes ranged 256 μg/ml to 1024 μg/ml. Transcription level of amplified cDNA corresponding to mecA was determined by the method of RT-PCR of extracted RNA. Total RNA was extracted from two strains with mutated mecI gene and a strain with intact mecI gene. Deletional loss or the mutational inactivation of the mecI gene did not affect the level of mecA transcription. Role of mecI gene as a strong repressor function on mecA gene seemed to be skeptical.

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      목차 (Table of Contents)

      • Introduction
      • Materials and Methods
      • Results
      • Introduction
      • Materials and Methods
      • Results
      • Discussion
      • Referecnes
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