Molecular basis for control of conjugation by bacterial pheromone and inhibitor peptides
Molecular basis for control of conjugation by bacterial pheromone and inhibitor peptides
复制标题
DOI：
10.1111/j.1365-2958.2006.05434.x
复制
发表时间：
2006-11-01
影响因子：
3.6
通讯作者：
Dunny, Gary M.
中科院分区：
文献类型：
--
作者：
Kozlowicz, Briana K.;Shi, Ke;Dunny, Gary M.
在许多细菌中，侧向基因转移和毒力因子的表达受细胞-细胞信号系统控制。微生物信号分子与其同源受体的分子相互作用还不清楚。对于粪肠球菌接合质粒pCF 10，PrgX蛋白充当控制由质粒编码的接合和毒力基因的表达的分子开关。携带pCF 10的供体细胞的诱导状态由两种信号肽cCF 10信息素和iCF 10抑制剂的比例决定。最近对PrgX/cCF 10相互作用的分析表明了转化为诱导状态的机制。然而，iCF 10肽拮抗cCF 10活性的方式尚不清楚，并且已经提出抑制剂肽阻断信息素肽的输入。我们现在表明，这两种肽与PrgX的相同结合口袋相互作用，但它们不同地改变蛋白质的构象及其寡聚化状态，导致相反的生物活性。
In many bacteria expression of lateral gene transfer and of virulence factors is controlled by cell-cell signalling systems. Molecular interactions of microbial signal molecules with their cognate receptors are not well understood. For the Enterococcus faecalis conjugative plasmid pCF10, the PrgX protein serves as a molecular switch controlling expression of conjugation and virulence genes encoded by the plasmid. The induction state of a pCF10-carrying donor cell is determined by the ratio of two signalling peptides, cCF10 pheromone and iCF10 inhibitor. Recent analysis of PrgX/cCF10 interactions suggests a mechanism for conversion to the induced state. However, the means by which iCF10 peptide antagonizes cCF10 activity is unclear, and it has been suggested that inhibitor peptides block import of pheromone peptides. We now show that both of these peptides interact with the same binding pocket of PrgX, but they differentially alter the conformation of the protein and its oligomerization state, resulting in opposing biological activities.