Widney Karl A, Phillips Lauren C, Rusch Leo M, Copley Shelley D
Department of Biochemistry, University of Colorado Boulder, Boulder, CO 80309, USA.
Cooperative Institute for Research in Environmental Sciences, University of Colorado, Boulder, CO 80205, USA.
Mol Biol Evol. 2025 Jul 30;42(8). doi: 10.1093/molbev/msaf193.
Underground metabolic pathways-leaks in the metabolic network caused by promiscuous enzyme activities and nonenzymatic transformations-can provide the starting point for emergence of novel protopathways if a mutation or environmental change increases flux to a physiologically significant level. This early stage in pathway evolution, in which promiscuous enzymes are still serving their native functions and proper regulation has not yet emerged, is typically hidden from our view. We previously used laboratory evolution to evolve a novel four-step protopathway in ΔpdxB E. coli, which lacks an enzyme required for synthesis of pyridoxal 5'-phosphate (PLP). By sequencing population genomic DNA from samples archived during the evolution experiment, we have identified mutations that rose and fell in abundance in the population leading to JK1, the dominant clone after 150 population doublings. We have identified the order in which the four mutations arose in JK1 and the physiological effect of each mutation. The first mutation increases the rate of PLP synthesis. The second mutation did not impact PLP synthesis but rather created a cheater that thrived in the population by scavenging nutrients released from the fragile parental cells. Notably, the dominant lineages at the end of the experiment all derived from this cheater strain. The third mutation in JK1 destroyed a PLP phosphatase, which preserves precious PLP. Finally, the fourth mutation improved growth in glucose after the PLP synthesis problem had been solved. Together, these mutations resulted in restoration of PLP synthesis and a 32-fold increase in growth rate.
地下代谢途径——由混杂酶活性和非酶促转化导致的代谢网络泄漏——如果突变或环境变化使通量增加到生理显著水平,可为新的原始途径的出现提供起点。途径进化的这个早期阶段,即混杂酶仍在履行其天然功能且尚未出现适当调控的阶段,通常是我们看不到的。我们之前利用实验室进化在缺乏磷酸吡哆醛(PLP)合成所需酶的ΔpdxB大肠杆菌中进化出了一条新的四步原始途径。通过对进化实验期间存档样本的群体基因组DNA进行测序,我们确定了在导致JK1(经过150次群体倍增后的优势克隆)的群体中丰度上升和下降的突变。我们确定了JK1中四个突变出现的顺序以及每个突变的生理效应。第一个突变提高了PLP的合成速率。第二个突变并未影响PLP的合成,而是产生了一个作弊者,它通过 scavenging 从脆弱的亲代细胞释放的营养物质在群体中茁壮成长。值得注意的是,实验结束时的优势谱系均源自这个作弊菌株。JK1中的第三个突变破坏了一种PLP磷酸酶,该酶可保留珍贵的PLP。最后,在PLP合成问题解决后,第四个突变改善了在葡萄糖中的生长。这些突变共同作用,恢复了PLP的合成,并使生长速率提高了32倍。 (注:scavenging此处可能是“清除、掠夺”之类意思,结合语境不太好准确翻译,暂保留英文)