Hospital Universitario Ramón y Cajal, IMSALUD, Madrid, Spain.
PLoS Pathog. 2010 Jan 22;6(1):e1000735. doi: 10.1371/journal.ppat.1000735.
Extended-spectrum beta-lactamases (ESBL) constitute a key antibiotic-resistance mechanism affecting Gram-negative bacteria, and also an excellent model for studying evolution in real time. A shift in the epidemiology of ESBLs is being observed, which is characterized by the explosive diversification and increase in frequency of the CTX-M-type beta-lactamases in different settings. This provides a unique opportunity for studying a protein evolutionary radiation by the sequential acquisition of specific mutations enhancing protein efficiency and fitness concomitantly. The existence of driver antibiotic molecules favoring protein divergence has been investigated by combining evolutionary analyses and experimental site-specific mutagenesis. Phylogenetic reconstruction with all the CTX-M variants described so far provided a hypothetical evolutionary scenario showing at least three diversification events. CTX-M-3 was likely the enzyme at the origin of the diversification in the CTX-M-1 cluster, which was coincident with positive selection acting on several amino acid positions. Sixty-three CTX-M-3 derivatives containing all combinations of mutations under positively selected positions were constructed, and their phenotypic efficiency was evaluated. The CTX-M-3 diversification process can only be explained in a complex selective landscape with at least two antibiotics (cefotaxime and ceftazidime), indicating the need to invoke mixtures of selective drivers in order to understand the final evolutionary outcome. Under this hypothesis, we found congruent results between the in silico and in vitro analyses of evolutionary trajectories. Three pathways driving the diversification of CTX-M-3 towards the most complex and efficient variants were identified. Whereas the P167S pathway has limited possibilities of further diversification, the D240G route shows a robust diversification network. In the third route, drift may have played a role in the early stages of CTX-M-3 evolution. Antimicrobial agents should not be considered only as selectors for efficient mechanisms of resistance but also as diversifying agents of the evolutionary trajectories. Different trajectories were identified using a combination of phylogenetic reconstructions and directed mutagenesis analyses, indicating that such an approach might be useful to fulfill the desirable goal of predicting evolutionary trajectories in antimicrobial resistance.
超广谱β-内酰胺酶(ESBL)是影响革兰氏阴性菌的主要抗生素耐药机制,也是实时研究进化的绝佳模型。ESBL 的流行病学正在发生变化,其特征是不同环境中 CTX-M 型β-内酰胺酶的爆炸式多样化和频率增加。这为通过连续获得同时增强蛋白质效率和适应性的特定突变来研究蛋白质进化辐射提供了独特的机会。通过结合进化分析和实验定点诱变,研究了有利于蛋白质分歧的驱动抗生素分子的存在。对迄今为止描述的所有 CTX-M 变体进行系统发育重建提供了一个假设的进化情景,表明至少发生了三次多样化事件。CTX-M-3 很可能是 CTX-M-1 簇多样化的酶起源,这与对几个氨基酸位置起作用的正选择一致。构建了包含正选择位置上所有突变组合的 63 种 CTX-M-3 衍生物,并评估了它们的表型效率。CTX-M-3 的多样化过程只能在一个复杂的选择景观中解释,至少有两种抗生素(头孢噻肟和头孢他啶),这表明需要调用混合选择驱动因素才能理解最终的进化结果。在这种假设下,我们在进化轨迹的计算机和体外分析之间找到了一致的结果。确定了三种驱动 CTX-M-3 向最复杂和高效变体多样化的途径。虽然 P167S 途径的进一步多样化可能性有限,但 D240G 途径显示出强大的多样化网络。在第三条途径中,漂移可能在 CTX-M-3 进化的早期阶段发挥了作用。抗生素不应仅被视为耐药有效机制的选择剂,也应被视为进化轨迹的多样化剂。通过系统发育重建和定向诱变分析的组合确定了不同的轨迹,表明这种方法可能有助于实现预测抗生素耐药性进化轨迹的理想目标。