It has often been argued that gene-duplication events are most commonly fol
lowed by a mutational event that silences one member of the pair, while on
rare occasions both members of the pair are preserved as one acquires a mut
ation with a beneficial function and the other retains the original functio
n. However, empirical evidence from genome duplication events suggests that
gene duplicates are preserved in genomes far more commonly and for periods
far in excess of the expectations under this model, and whereas some gene
duplicates clearly evolve new functions, there is little evidence that this
is the most common mechanism of duplicate-gene preservation. An alternativ
e hypothesis is that gene duplicates are frequently preserved by subfunctio
nalization, whereby both members of a pair experience degenerative mutation
s that reduce their joint levels and patterns of activity to that of the si
ngle ancestral gene. We consider the ways in which thf probability of dupli
cate-gene preservation by such complementary mutations is modified by aspec
ts of gene structure, degree of linkage, mutation rates and effects, and po
pulation size. Even if most mutations cause complete loss-of-subfunction, t
he probability of duplicate-gene preservation can be appreciable if the lon
g-term effective population size is on the order of 10(5) or smaller, espec
ially if ther are more than two, independently mutable subfunctions per loc
us. Even a moderate incidence of partial loss-of-function mutations greatly
elevates the probability of preservation, nle model proposed herein leads
to quantitative predictions that are consistent with observations on die fr
equency of long-term duplicate gene preservation and with observations that
indicate tl-lat a common fate of the members of duplicate-gene pairs is th
e partitioning of tissue-specific patterns of expression of die ancestral g
ene.