Antibiotic resistance comes from a variety of mechanisms, including changes in gene regulation, production of new genes with novel activities, as well as simple point mutations. All these mechanisms are representative of the kinds of mutation involved in the sorts of morphological change that Explore Evolution thinks are important. Explore Evolution misrepresents the basic biology of mutations and their significance in antibiotic resistance in claiming:
In every case where mutations lead to antibiotic resistance, resistance results from small changes to a single protein molecule.Explore Evolution, p. 104
Explore Evolution tries several times to make distinctions between different kinds of mutations. These distinctions are incorrect. In the case of antibiotic resistance, while the most intensively studied mutations are simple point mutations, such as those responsible for resistance to streptomycin, there are many other mutations that are involved. For example, resistance to some antibiotics is due to mutations that change the expression of drug transporters. Changes in gene expression are important in the evolution of many organismal traits.
Another example is gene duplication. Methicillin resistance originated with the duplication of a gene, which subsequently mutated, gaining a new function, penicillin binding. The first step was duplication of the cell wall synthesis enzyme D-Ala-D-Ala ligase. A single mutation then resulted in a novel cell wall synthesis enzyme D-Ala-D-Lac ligase, which confers vancomycin resistance.
Gene duplication, with duplicates gaining new functions though mutation, is a major source of gene gain in evolution. For example, the expansion of cell signaling systems in evolution is almost entirely through gene duplication and function gain via mutation. Most of what Explore Evolution later refers to as "molecular machines" are aggregates of duplicated genes. By failing to provide students with this background, they hinder any inquiry those students might choose to undertake into these issues.