Mechanisms causing rapid and parallel losses of ribose catabolism in evolving populations of Escherichia coli B
Mechanisms causing rapid and parallel losses of ribose catabolism in evolving populations of Escherichia coli B
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DOI：
10.1128/jb.183.9.2834-2841.2001
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发表时间：
2001-05-01
影响因子：
3.2
通讯作者：
Lenski, RE
中科院分区：
文献类型：
--
作者：
Cooper, VS;Schneider, D;Lenski, RE
12个大肠杆菌B群体在葡萄糖基本培养基中经过2,000代的进化，全部丧失了D-核糖分解代谢功能。分离出7个独立的Rbs（-）突变体，并测量它们相对于它们的Rbs（+）祖先的竞争适合度。这些Rbs（-）突变体比其祖先多1 - 2%的适应性。波动试验显示，从Rbs'到Rbs-的突变率异常高，每代细胞约为5 × 10 - 5，这有助于快速固定。在分子水平上，核糖分解代谢功能的丧失涉及核糖操纵子（rbs基因）的部分或全部缺失。缺失的物理范围在突变体之间变化，但每个缺失与位于rbs操纵子上游的IS 150元件相关。删除显然涉及转座到不同的位置内的rbs操纵子;重组之间的新的IS 150拷贝和上游的rbs操纵子，然后导致删除的插入序列。为了证实有益的适应性效应是由rbs操纵子的缺失引起的（而不是其他地方未检测到的突变），我们使用P1转导将功能性rbs操纵子恢复为两个Rbs（-）突变体，并且我们构建了另一个Rbs（-）菌株通过基因替换与不涉及IS 150的缺失。所有这三个新的构建体证实，在葡萄糖基本培养基中，Rbs（-）突变体相对于其Rbs（+）对应物具有竞争优势。因此，核糖分解代谢功能的快速和平行进化损失涉及（i）异常高的突变率，使得Rbs（-）突变体在所有群体中重复出现，以及（ii）葡萄糖基本培养基中的选择优势，驱使这些突变体固定。
Twelve populations of Escherichia coli B all lost D-ribose catabolic function during 2,000 generations of evolution in glucose minimal medium, We sought to identify the population genetic professes and molecular genetic events that caused these rapid and parallel losses. Seven independent Rbs(-) mutants were isolated, and their competitive fitnesses were measured relative to that of their Rbs(+) progenitor. These Rbs(-) mutants mere all about 1 to 2% more fit than the progenitor. A fluctuation test revealed an unusually high rate, about 5 x 10(-5) per cell generation, of mutation from Rbs' to Rbs-, which contributed to rapid fixation. At the molecular level, the loss of ribose catabolic function involved the deletion of part or all of the ribose operon (rbs genes). The physical extent of the deletion varied between mutants, but each deletion was associated with an IS150 element located immediately upstream of the rbs operon. The deletions apparently involved transposition into various locations within the rbs operon; recombination between the new IS150 copy and the one upstream of the rbs operon then led to the deletion of the intervening sequence. To confirm that the beneficial fitness effect was caused by deletion of the rbs operon (and not some undetected mutation elsewhere), we used P1 transduction to restore the functional rbs operon to two Rbs(-) mutants, and we constructed another Rbs(-) strain by gene replacement with a deletion not involving IS150. All three of these new constructs confirmed that Rbs(-) mutants have a competitive advantage relative to their Rbs(+) counterparts in glucose minimal medium. The rapid and parallel evolutionary losses of ribose catabolic function thus involved both (i) an unusually high mutation rater such that Rbs(-) mutants appeared repeatedly in all populations, and (ii) a selective advantage in glucose minimal medium that drove these mutants to fixation.