[Enhancing effect of chuangxinmycin on synthesis of enzymes in tryptophan synthesis pathway of chuangxinmycin-resistant mutant strain of E. coli].
Chuangxinmycin (CXM) and L-trp cause repression of trp-operon in wild strain of E. coli and indolepropanic acid (IPA) causes derepression of this strain. In CXM-resistant mutant strain, CXM and IPA both cause derepression, and interaction of CXM and IPA is competitive. However, L-trp results in neither repression nor derepression in the mutant, but it can counteract the activity of CXM or IPA. These results suggest that there are repression and derepression sites on repressor of E. coli. CXM can bind to both sites, but mainly to repression site. The structure of repression site of the CXM-resistant mutant is altered, so that CXM can not bind to the repression site and binds mainly to the derepression site, thus leading to the derepression of trp-operon.
Xu
S
S
Institute of Medical Biotechnology, Beijing.
Qi
T
T
D000878:Anthranilate Synthase / Q000096:biosynthesis*; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D004794:Enzyme Repression / Q000187:drug effects; D004926:Escherichia coli / Q000187:drug effects / Q000201:enzymology*; D007211:Indoles / Q000494:pharmacology; D014367:Tryptophan Synthase / Q000096:biosynthesis*
D000900:Anti-Bacterial Agents; D007211:Indoles; C014414:chuangxinmycin; D000878:Anthranilate Synthase; D014367:Tryptophan Synthase