Ifuku O, Koga N, Haze S, Kishimoto J, Arai T, Wachi Y
Shiseido Research Center, Yokohama-shi, Japan.
Biosci Biotechnol Biochem. 1995 Feb;59(2):184-9. doi: 10.1271/bbb.59.184.
Constitutive overexpression of the biotin operon (type 9 mutation) in a multicopy plasmid resulted in growth inhibition in Escherichia coli. Deletion analysis of the biotin operon indicated that overexpression of the bioB gene alone, the product of which is believed to catalyze the conversion of dethiobiotin to biotin, is sufficient for growth inhibition. This growth inhibition was still observed when the wild-type bioB gene was replaced by several mutant-type bioB genes derived from biotin auxotrophs that have base-pair substitutions creating amino acid substitutions in the bioB gene product. However, the modification of Ala 143 and Gly 99 of the bioB gene product resulted in recovery from growth inhibition. These results suggest that this phenotype of growth inhibition by overexpression of the bioB gene in E. coli is independent of the biotin-forming activity itself, but is caused by some function involving a specific conformation of the bioB gene product.
在多拷贝质粒中组成型过表达生物素操纵子（9型突变）导致大肠杆菌生长受到抑制。对生物素操纵子的缺失分析表明，仅bioB基因过表达就足以抑制生长，据信该基因产物催化脱硫生物素转化为生物素。当野生型bioB基因被几个源自生物素营养缺陷型的突变型bioB基因取代时，仍观察到这种生长抑制，这些突变型bioB基因具有碱基对替换，导致bioB基因产物中产生氨基酸替换。然而，bioB基因产物的Ala 143和Gly 99修饰导致生长抑制恢复。这些结果表明，大肠杆菌中bioB基因过表达导致的这种生长抑制表型与生物素形成活性本身无关，而是由涉及bioB基因产物特定构象的某种功能引起的。
