White-Ziegler C A, Angus Hill M L, Braaten B A, van der Woude M W, Low D A
Department of Pathology, University of Utah Health Sciences Center, Salt Lake City 84132, USA.
Mol Microbiol. 1998 Jun;28(6):1121-37. doi: 10.1046/j.1365-2958.1998.00872.x.
The expression of Pap pili that facilitate the attachment of Escherichia coli to uroepithelial cells is shut off outside the host at temperatures below 26 degrees C. Ribonuclease protection analysis showed that this thermoregulatory response was rapid as evidenced by the absence of papBA transcripts, coding for Pap pilin, after only one generation of growth at 23 degrees C. The histone-like nucleoid structuring protein H-NS and DNA sequences within papB were required for thermoregulation, but the PapB and PapI regulatory proteins were not. In vivo analysis of pap DNA methylation patterns indicated that H-NS or a factor regulated by H-NS bound within the pap regulatory region at 23 degrees C but not at 37 degrees C, as evidenced by H-NS-dependent inhibition of methylation of the pap GATC sites designated GATC-I and GATC-II. These GATC sites lie upstream of the papBAp promoter and have been shown previously to play a role in controlling Pap pili expression by regulating the binding of Lrp, a global regulator that is essential for activating papBAp transcription. Competitive electrophoretic mobility shift analysis showed that H-NS bound specifically to a pap DNA fragment containing the GATC-I and GATC-II sites. Moreover, H-NS blocked methylation of these pap GATC sites in vitro: H-NS blocked pap GATC methylation at 1.4 microM but was unable to do so at higher concentrations at which non-specific binding occurred. Thus, non-specific binding of H-NS to pap DNA was not sufficient to inhibit methylation of the pap GATC sites. These results suggest that the ability of H-NS to act as a methylation blocking factor is dependent upon the formation of a specific complex of H-NS with pap regulatory DNA. We hypothesize that a function of H-NS such as oligomerization was altered at 23 degrees C, which enabled H-NS to repress pap gene expression through the formation of a specific nucleoprotein complex.
有助于大肠杆菌附着于尿道上皮细胞的Pap菌毛的表达,在宿主外温度低于26摄氏度时会关闭。核糖核酸酶保护分析表明,这种温度调节反应很快,在23摄氏度仅一代生长后,编码Pap菌毛蛋白的papBA转录本就不存在,这证明了这一点。温度调节需要类组蛋白核仁结构蛋白H-NS和papB内的DNA序列,但不需要PapB和PapI调节蛋白。对pap DNA甲基化模式的体内分析表明,H-NS或受H-NS调节的因子在23摄氏度时结合在pap调节区域内,但在37摄氏度时不结合,这由H-NS依赖的对指定为GATC-I和GATC-II的pap GATC位点甲基化的抑制所证明。这些GATC位点位于papBAp启动子上游,先前已表明通过调节Lrp的结合在控制Pap菌毛表达中起作用,Lrp是一种对激活papBAp转录至关重要的全局调节因子。竞争性电泳迁移率变动分析表明,H-NS特异性结合到包含GATC-I和GATC-II位点的pap DNA片段上。此外,H-NS在体外阻断这些pap GATC位点的甲基化:H-NS在1.4 microM时阻断pap GATC甲基化,但在发生非特异性结合的较高浓度下则无法做到。因此,H-NS与pap DNA的非特异性结合不足以抑制pap GATC位点的甲基化。这些结果表明,H-NS作为甲基化阻断因子的能力取决于H-NS与pap调节DNA形成特定复合物。我们假设,H-NS的一种功能(如寡聚化)在23摄氏度时发生改变,这使得H-NS能够通过形成特定的核蛋白复合物来抑制pap基因表达。