Reductionism in Biology 351string(s) of nucleic acid bases, could not provide the systematic link between the
functional ‘gene’ and the macromolecular ‘genes’ required by a reduction. There is
of course no trouble identifying ‘tokens’ — particular bits of matter we can point
to–of the population biologist’s genes with ‘tokens’ of the molecular biologist’s
genes. But token-identities won’t suffice for reduction, even if they are enough for
physicalism to be true. The second problem facing reductionism in biology is the
absence of laws, either at the level of the reducing theory or the reduced theory,
or between them. If there aren’t any laws in either theory, there is no scope for
reduction at all.
Whereas the antireductionists were at most able to show that the criterion of
connectability with respect to the Mendelian and the molecular gene was not ful-
filled as the two theories were in fact stated, we can go much further in vindicating
their conclusion. We can demonstrate that the criterion required by “layer-cake”
reductionism cannot be satisfied as a fundamental matter of biological process.
Individuation of types in biology is almost always via function: to call something
a wing, or a fin, or a gene is to identify it in terms of its function. But biological
functions are naturally-selected effects. And natural selection for adaptations —
i.e. environmentally appropriate effects — is blind to differences in physical struc-
ture that have the same or roughly similar effects. Natural selection “chooses”
variants bysome of their effects, those which fortuitously enhance survival and
reproduction. When natural selection encourages variants to become packaged
together into larger units, the adaptations become functions. Selection for adap-
tation and function kicks in at a relatively low level in the organization of matter.
Accordingly, the structural diversity of the tokens of a given Mendelian or classical
or population biological or generally ‘functional’ gene will mean that there is no
single molecular structure or manageably finite number of sets of structures that
can be identified with a single functional gene.
Philosophers will recognize the relationship between the functional gene and the
DNA sequence as one of “multiple realization” common to the relation functional-
ism in the philosophy of psychology alleges to obtain between psychological states
and neural ones. The blindness of selection for effects to differences in structure
provides the explanation for why multiple realization obtains between genes and
polynucleotide molecules. Indeed almost every functional kind in biology will be
multiply realized, owing to the fact that the kind has an evolutionary etiology.
Functional biology tells us that there is a hemoglobin gene, and yet there is
no unique sequence of nucleic acids that is identical to this hemoglobin gene —
nothing that could provide a macromolecular definition of the hemoglobin gene of
functional biology. Of course there is some ungainly disjunction of all the actual
ways nucleic acid sequences nowadays do realize or in the past have realized the
hemoglobin gene — i.e. all the sequences that can be translated, and transcribed
into RNA which in a local ribosome will code for one or another of the different
types — fetal, adult, or the varying defective hemoglobin protein sequences. But
this ungainly disjunction, even if we knew it, and we don’t, won’t serve to define
the functional hemoglobin gene. The reason is obvious to the molecular biologist.