Blanc-Potard A B, Figueroa-Bossi N, Bossi L
Centre de Génétique Moléculaire, Centre National de la Recherche Scientifique, 91198 Gif-sur-Yvette Cedex, France.
J Bacteriol. 1999 May;181(9):2938-41. doi: 10.1128/JB.181.9.2938-2941.1999.
Expression of the histidine operon of Salmonella typhimurium is increased in dnaA(Ts) mutants at 37 degrees C. This effect requires an intact his attenuator and can be suppressed by increasing the gene copy number of the hisR locus, which encodes the tRNA(His). We present data which suggest that the his deattenuation defect in dnaA(Ts) mutants results from the loss of a gene dosage gradient between the hisR locus, close to oriC, and the his operon, far from oriC. Some of the conclusions drawn here may apply to other operons as well.
鼠伤寒沙门氏菌组氨酸操纵子的表达在37℃时,于dnaA(Ts)突变体中增加。这种效应需要完整的组氨酸弱化子,并且可以通过增加编码tRNA(His)的hisR基因座的基因拷贝数来抑制。我们提供的数据表明,dnaA(Ts)突变体中的组氨酸去弱化缺陷是由于靠近oriC的hisR基因座与远离oriC的组氨酸操纵子之间基因剂量梯度的丧失所致。这里得出的一些结论可能也适用于其他操纵子。