- 作者: Ching-Nan Lin; Wan-Jr Syu; Wei-Sheng W Sun; Jenn-Wei Chen; Tai-Hung Chen; Ming-Jaw Don; Shao-Hung Wang
- 作者服務機構: Institute of Microbiology and Immunology, National Yang-Ming University, Taipei, Taiwan, R.O.C.
- 中文摘要: --
- 英文摘要:
Plumbagin is found in many herbal plants and inhibits the growth of various bacteria.
Escherichia coli strains are relatively resistant to this drug. The mechanism of resistance is not
clear. Previous findings showed that plumbagin treatment triggered up-regulation of many genes
in E. coli including ahpC, mdaB, nfnB, nfo, sodA, yggX and ygfZ. By analyzing minimal
inhibition concentration and inhibition zones of plumbagin in various gene-disruption mutants,
ygfZ and sodA were found critical for the bacteria to resist plumbagin toxicity. We also found
that the roles of YgfZ and SodA in detoxifying plumbagin are independent of each other. This is
because of the fact that ectopically expressed SodA reduced the superoxide stress but not restore
the resistance of bacteria when encountering plumbagin at the absence of ygfZ. On the other
hand, an ectopically expressed YgfZ was unable to complement and failed to rescue the
plumbagin resistance when sodA was perturbed. Furthermore, mutagenesis analysis showed that
residue Cys228 within YgfZ fingerprint region was critical for the resistance of E. coli to
plumbagin. By solvent extraction and HPLC analysis to follow the fate of the chemical, it was
found that plumbagin vanished apparently from the culture of YgfZ-expressing E. coli. A less
toxic form, methylated plumbagin, which may represent one of the YgfZ-dependent metabolites,
was found in the culture supernatant of the wild type E. coli but not in the DygfZ mutant. Our results showed that the presence of ygfZ is not only critical for the E coli resistance to plumbagin
but also facilitates the plumbagin degradation. - 中文關鍵字: --
- 英文關鍵字: --