Abstract:
:In Mycobacterium tuberculosis (MTB), rifampicin resistance is almost invariably due to mutations in the rpoB gene, whose function is critical for cell viability. Most of these mutations, at least initially, impair the fitness of the bacteria but confer a selective advantage when antibiotic pressure is exerted. Subsequent adaptation may be critical to restore fitness. The possibility was considered that MTB with mutations in the rpoB gene elicits a constitutive stress response, increasing the probability of subsequent adaptation. In order to test this hypothesis, the expression of recA and dnaE2, an inducible putative error-prone DNA polymerase, was determined in six different isogenic laboratory-generated rpoB-mutants of MTB. Expression levels were determined with real-time PCR and the data obtained were compared with those of the wild-type parent. In four of the six rpoB mutants, a two- to fivefold induction of dnaE2 was detected (P<0.05). Thus, the presence of specific mutations in rpoB is not only associated with impaired fitness but also results in a detectable, moderate yet persistent increase in the expression of dnaE2 but not recA.
journal_name
FEMS Microbiol Lettjournal_title
FEMS microbiology lettersauthors
Bergval IL,Klatser PR,Schuitema AR,Oskam L,Anthony RMdoi
10.1111/j.1574-6968.2007.00905.xsubject
Has Abstractpub_date
2007-10-01 00:00:00pages
338-43issue
2eissn
0378-1097issn
1574-6968pii
FML905journal_volume
275pub_type
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journal_title:FEMS microbiology letters
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journal_title:FEMS microbiology letters
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journal_title:FEMS microbiology letters
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journal_title:FEMS microbiology letters
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journal_title:FEMS microbiology letters
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journal_title:FEMS microbiology letters
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journal_title:FEMS microbiology letters
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journal_title:FEMS microbiology letters
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journal_title:FEMS microbiology letters
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journal_title:FEMS microbiology letters
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journal_title:FEMS microbiology letters
pub_type: 杂志文章,评审
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更新日期:2018-09-01 00:00:00