1096 THE STRUCTURE OF EVOLUTIONARY THEORY
But the discovery that homological pathways also persist among animal phyla that
have evolved independently since the Cambrian explosion has reversed previous
certainties and brought Geoffroy's despised archetypal theories into renewed
respectability.
The roots of this great discovery extend back (at least terminologically) to
another key figure of this book, the English geneticist William Bateson (see Chapter
5, pp. 396-415). Bateson became fascinated by a class of mutations with the peculiar,
and often large, effect of causing the characteristic form of one member in a serial
array to develop in a different location usually occupied by another member of the
same array. Bateson called such mutations "homeotic," and their peculiar forms,
almost humorous in some cases, gave them a special salience among geneticists.
Unsurprisingly—for arthropods are serial organisms par excellence, while this
particular insect became the lynchpin of genetics—the homeotic mutations of
Drosophila became classics of the genre, famous for their oddness as well as their
utility (for geneticists, not for the afflicted flies!).
We all remember our undergraduate textbook pictures—and the attendant,
inevitable thoughts of Hollywood monster movies—of flies with such mutations as
antennapedia (legs where antennae "ought" to be), bithorax (with another pair of
wings rather than halteres on the third thoracic segment, thus seeming to "revert" the
fly—a false interpretation as we shall see—to the ancestral four winged condition),
and bithoraxoid (with a supernumerary pair of legs on the first abdominal segment,
thus giving eight legs in toto and seeming to mock the very definition of the class
Hexapoda). In my favorite example, a homeotic mutation in mosquitoes actually
replaces the biting stylets with a pair of legs, thus rendering the creature "ouchless." I
entertained various fantasies about breeding these lovely mutants, introducing them
into natural populations, and destroying this scourge of humanity from within. But,
alas and unsurprisingly, the scheme would never work, and I couldn't interest a single
venture capitalist—for the mutation is effectively lethal; a mosquito that cannot bite
to draw blood cannot feed at all.
E. B. Lewis used such homeotic mutations to develop his model for the
evolution and operation of the bithorax complex in Drosophila, the breakthrough that
effectively began the modern study of evo-devo and that won a most deserved Nobel
Prize for its pioneer. (The Nobel awards include no category for evolutionary studies.
Only twice has a prize been given for work in evolutionary biology, each time by
nuancing the definition of medicine to include work with legitimate consequences for
health, but scarcely in the mainstream of medical research—first to Lorenz,
Tinbergen, and von Frisch, for foundational studies in ethology, and second to my
dear colleagues Ed Lewis, Christiane Nusslein-Volhard, and Eric Wieschaus for
unlocking the genetic basis of fundamental architectures in animal development.)
In a simple and brilliant model, Lewis (1978) inferred that the bithorax complex
evolved by gene duplication, with all members (up to eight) remaining aligned in a
tandem array on the third chromosome. Since these BX-C genes regulated
developmental positions in the posterior part of the thorax