1268 THE STRUCTURE OF EVOLUTIONARY THEORY
almost mantra-like, statement about the deleterious nature of most mutations achieves
such an evident explanation that the resulting "aha" seems almost humorous in its
suddenly obvious character. Each mutation arises for a perfectly good reason (usually
chemical rather than adaptational in this case) at the gene level. But the effects then
imposed upon organismal phenotypes must be designated as spandrels—that is, as
nonadaptive side consequences expressed at another level. These effects will usually
be deleterious, because the organism, as a highly complex, well integrated, and
biochemically efficient object, will more often be hindered than helped by a change
that arises as an "injection" from elsewhere, established by causes directly operating
only in this elsewhere, and not subject to initial scrutiny at the level of injection. For
the same reason, and in another mantra, we designate mutations as "random"—not in
the mathematical sense of equally likely in all directions, but in the special
evolutionary sense (see Eble, 1999) that such mutations originate without reference to
the adaptive needs of the organism. When we recognize the phenotypic expression of
mutations as cross-level spandrels, this property of "randomness" becomes entirely
sensible, and no longer puzzling as a supposed sign of organic inefficiency.
Gene duplication, and other modes of origin for the repeated elements that
constitute such a high percentage of the genomes of complex organisms (and that
have been so puzzling under Darwinian assumptions about organisms as "lean and
mean" machines honed to optimality by the relentless power of natural selection),
represent the most important "playing field" yet identified for the evolutionary
importance of cross-level spandrels. (I thank my colleague Jurgen Brosius for helping
me to understand and work through the implications of this concept—see Brosius and
Gould, 1992; Brosius, 1999; and Brosius and Tiedge, 1996.)
In some cases, of course, gene amplication originates as an immediate
adaptation at the organismal level, especially when the availability of more gene
product provides a selective advantage to the organism. But, more commonly,
amplification occurs for causal reasons at the genie level itself, often by the
conventional Darwinian mechanism of increased reproductive success, in this case by
generating more copies of oneself, and inserting them into various places in one's
surrounding totality—that is, in the genome itself. (Such an argument about direct
Darwinian selection at the gene level provides the rationale, as previously discussed
(p. 693), for the important hypothesis of "selfish DNA"—see Orgel and Crick, 1980;
and Doolittle and Sapienza, 1980 for the original publications.) Yet evolutionists
have also recognized (see Ohno, 1970 for the classic statement) that these extra
copies may strongly impact the evolutionary future of organisms by supplying
flexibility for change through their redundancy. But this otherwise sensible argument
also seems to raise a central dilemma in causality itself—since flexibility for future
change cannot cause the current origin or maintenance of any feature! We can resolve
this problem by recognizing augmented copies as nonadaptive (and cross-level)
spandrels at the time of their initial expression at the organismic level. Later
recruitment and utilization of spandrels represents a perfectly