Historical Constraints and the Evolution of Development 1145
into hypotheses about sudden origins for the developmental cascades thus repressed.
(We note here a developmental version of the error so commonly committed as a
thoughtless consequence of naming the normal function of genes for the results of
their discombobulation. If the mutational silencing of a gene precludes the
development of a child's ability to read, we have not thereby identified a "reading
gene," although such taxonomies and inferences remain all too frequent in our
literature, particularly on human cognitive abilities.) For example, the fact (Swalla
and Jeffery, 1996) that a loss-of-function mutation in the Manx gene of the tunicate
Mogula can repress chordate features and lead to a tailless (anural) larva—and that
this function can be restored in interspecific hybrids with other Mogula species that
develop with a tailed (urodele) larval form—does not imply that the tunicate larval
tail and notocord (once a popular theme in theories about the origin of vertebrates, as
in the classic paper of Garstang, 1928) arose by saltational introduction of Manx
activity. (Swalla and Jeffery make no such inference, of course, and I hate to see their
fascinating discovery so misused, as in many press reports.)
As a general structural principle, applicable across a full range of natural
phenomena, from cosmology to human social organization, complex systems can
usually collapse catastrophically, whereas the construction of such functional
intricacy can only occur by sequential accumulation—a pattern that I have called "the
great asymmetry" (Gould, 1998a).
For the positive argument, more plausible continuationist scenarios can explain
the modern phenomena that most often tempt us to invoke hypothetical saltation to
resolve their origin. In an important article, for example, Akam (1998) discusses the
property of Hox action that has often led to saltational inferences: "The Hox genes
might justifiably be considered master control genes (Gehring, 1996) for segment
identity. For most segments of the insect trunk, they provide the only conduit for
channeling axial information from the early embryo to cells at the later stages of
development." Akam then exposes the same fallacy that I discussed above as negative
point 2: "It is tempting to shift this process into reverse, and to assume that segment
diversification has been achieved by a series of overt homeotic mutations generating
novel complexity."
Akam then develops a much more plausible evolutionary model for the
incremental origin of developmental patterns mediated by so-called "selector genes,"
which have generally been viewed "as stable binary switches that direct lineages of
cells to adopt alternative developmental fates" (Akam, 1998, p. 445). Akam proposes
an alternative concept "for the regulation of Hox genes within compartments" by
"enhancer modules," conceptualized as "local signals, hormone receptors or any of
the other stimuli that commonly mediate gene regulation. In this regard, it makes the
Hox genes like any other genes. It predicts that small changes, particularly in the
structure of their promotor modules, will change the phenotype of segments" (p. 448).
"By accepting a role for the regulation of Hox genes within compartments," Akam
adds (p. 448), "we demote them from their privileged status as stable binary
switches."