Condit Richard
Department of Zoology, University of Massachusetts, Amherst, MA, 01003.
Evolution. 1990 Mar;44(2):347-359. doi: 10.1111/j.1558-5646.1990.tb05204.x.
Previous theoretical studies have shown that bacterial transposons can become established in populations by infectious transfer, even if they reduce the fitness of their host cells. Conditions for the persistence of "parasitic" transposons are, however, restrictive: i) transposition must be replicative, rather than conservative; ii) the rate of transposition must be greater than the loss in host fitness caused by the transposon; and iii) cells must exchange plasmids at rates greater than the fitness cost of the transposon. I sought to test the validity of the model underlying this theory by performing experiments with laboratory populations of the bacterium Escherichia coli, the conjugative plasmid R100, and the transposons Tn3 and Tn5. A plasmid-borne transposon was introduced at low frequency into a population of bacteria carrying the same plasmid without the transposon in a habitat where the transposon offered no benefit to its host. The fate of the invading transposon was followed by tracking the various bacterial populations appearing in the cultures. Using independent estimates of the parameters of the model, predicted population changes were generated with numerical solutions of the model, and these were compared to experimental results. Plasmids transferred into new hosts as predicted by the model, and the resulting transconjugant populations either maintained a steady low density or rose slowly in abundance. Transposition appeared to play no role in population changes. Abundance of all cell types fit theoretical predictions of a system with no transposition, despite evidence that transposition was taking place. This is exactly what the model predicted. It thus appears unlikely that deleterious or neutral transposons have much impact on the genetics of bacterial populations. This is consistent with the hypothesis that most bacterial transposons are not parasitic DNA, but rather invade and persist in populations by providing a fitness advantage to cells carrying them.
以往的理论研究表明，细菌转座子可通过感染性转移在种群中得以确立，即便它们会降低宿主细胞的适应性。然而，“寄生性”转座子持续存在的条件较为苛刻：其一，转座必须是复制性的，而非保守性的；其二，转座速率必须大于转座子导致的宿主适应性损失；其三，细胞间交换质粒的速率必须大于转座子带来的适应性代价。我试图通过对大肠杆菌、接合质粒R100以及转座子Tn3和Tn5的实验室种群进行实验，来检验该理论背后模型的有效性。在一个转座子对其宿主无益处的生境中，将一个携带在质粒上的转座子以低频率引入一群携带相同但不含该转座子的质粒的细菌中。通过追踪培养物中出现的各种细菌种群，来观察入侵转座子的命运。利用对模型参数的独立估计，通过模型的数值解生成预测的种群变化，并将其与实验结果进行比较。质粒如模型所预测的那样转移到新宿主中，由此产生的接合子种群要么维持稳定的低密度，要么数量缓慢增加。转座似乎在种群变化中不起作用。尽管有证据表明转座正在发生，但所有细胞类型的数量都符合无转座系统的理论预测。这正是模型所预测的。因此，有害或中性转座子似乎不太可能对细菌种群的遗传学产生太大影响。这与以下假设一致，即大多数细菌转座子并非寄生性DNA，而是通过为携带它们的细胞提供适应性优势来侵入并在种群中持续存在。
