However, it is also important that the replicate populations diverged somewhat in both morphology and mean fitness (Figures 3 and 7). After 10,000 generations, the standard deviation for mean cell size among the derived populations was 30% of the average difference between the derived populations and their common ancestor. For mean fitness, the standard deviation among the derived populations was 10% of the average improvement from the common ancestor. Moreover, the populations also diverged in the functional relationship between cell size and fitness (Figure 8D).

Evolutionary biologists usually regard diversification as being caused by either (i) adaptation to different environments, which often produces conspicuous phenotypic variation, or (ii) random genetic drift, which is usually seen in molecular genetic variation. Yet our experiments demonstrate diversification, in identical environments and with very large populations, of no less selected a trait than fitness itself. Someone confronted with the variability among our derived populations (and unaware of the experimental design) might attribute this diversity to environmental heterogeneity or phylogenetic constraints, but any such "just-so story" would clearly be misguided in this case. Instead, our experiment demonstrates the crucial role of chance events (historical accidents) in adaptive evolution.

In a previous analysis of the first 2000 generations of this experiment (Lenski et al., 1991), it was not possible to reject the hypothesis that the populations had diverged only transiently in mean fitness but would soon converge on the same mean fitness. It was proposed that this hypothesis could be rejected, in favor of sustained divergence, "if the level of between-population variance of mean fitness remains significant indefinitely, even in the absence of further increases in mean fitness" (Lenski et al., 1991, p. 1337). We have shown here that variation among populations in mean fitness does persist for thousands of generations, even after improvement in mean fitness has slowed to an almost imperceptible rate.

Sustained divergence in mean fitness supports a Wrightian model of evolution (Wright, 1932, 1982, 1988; Barton and Hewitt, 1989; Mani and Clarke, 1990; Wade and Goodnight, 1991), in which replicate populations found their way onto different fitness peaks. Although the experimental populations were so large that the same mutations occurred in all of them, the order in which various mutations arose would have been different (Mani and Clarke, 1990). As a consequence, some populations may have incorporated mutations that were beneficial over the short-term but led to evolutionary dead ends.

Beyond promoting the idea of fitness surfaces with adaptive peaks separated by maladapted intermediate states, Wright (1932, 1982, 1988)



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