or full-sib matings were conducted. The inbred and outbred
offspring of these pairings were studied both in the labo-
ratory and in a release and capture-release experiment. For
this field experiment, 778 animals were released into the
habitat where their wild ancestors had been captured a few
generations earlier. Survival was estimated indirectly (tra-
pability), and based solely on 123 mice recaptured and
followed over 10 weeks. Most of the mice were never re-
trapped, and inbreeding was not correlated with lower sur-
vivorship (trapability) among the 663 mice that were never
recaptured. Of the 123 mice recaptured at least once, in-
bred mice showed a 44% reduction in survival as estimated
from recapture data over a 10-week period. There were no
significant sex differences in estimated survival. In the lab-
oratory, relative survivorship was measured between birth
and weaning, with inbred white-footed mice showing a 6%
reduction in survival. Thus the estimated fitness declines for
inbreds were 7 times higher as measured in the field com-
pared to the laboratory. These data add further support to
the hypothesis that laboratory methods will often be rela-
tively insensitive for measuring important health and vigor
differences, with large fitness consequences in nature.
Case 3: The tComplex —What Controls
the Spread of a Selfish Gene?
Around the globe, all subspecies of the house mouse are “in-
fected” at varying frequencies with an inversion of the prox-
imal third of chromosome 17 known as the tcomplex (De-
larbre et al. 1988). When paired with a normal chromosome,
recombination across this 20 centimorgan region is essen-
tially blocked, due to four large nonoverlapping inversions,
effectively linking together hundreds of loci (Artzt et al.
1982; Herrmann et al. 1986; Hammer et al. 1989). Al-
though a heterozygote male producestandsperm in equal
proportions (Silver and Olds-Clarke 1984), up to 100% of
his offspring will inherit the thaplotype, giving this chro-
mosomal inversion its characteristic distinction as a selfish
genetic element. The extreme transmission distortion of the
tcomplex is accomplished by up to five distorter genes and
a linked responder gene. Protein products from the distorter
genes impair wild type sperm (Silver and Remis 1987),
while the responder gene protects t-bearing sperm from the
effects of the distorter gene products (Lyon 1984; Herrmann
et al. 1999). Female mice appear to transmit the tcomplex
at Mendelian frequencies. Despite its excessive meiotic drive
in males, the tcomplex cannot achieve fixation due to its
costly effects in homozygotes. Depending on the combina-
tion of thaplotypes carrying linked lethality loci, homozy-
gosity results in either complete lethality or male sterility. If
not for these dual costs balancing transmission distortion
of thetcomplex, this selfish genetic element would have
quickly gone to complete fixation within populations. Al-
though other known examples of selfish genetic elements
in rodents exist outside of Mus(Hoekstra and Hoekstra
2001), it is difficult to determine the frequency with which
selfish elements evolve, because once they go to fixation (in
the absence of allelic variation), they can no longer be eas-
ily detected.The tparadox
Four decades of research have provided a good understand-
ing oft-complex transmission distortion behavior and its
underlying genetics. What remains unclear is why thetcom-
plex is found at frequencies across wild populations that are
far lower than predicted. Despite its harmful effects in ho-
mozygotes, extreme transmission distortion through males
should result in the persistence of t-complex haplotypes
in approximately 70% of wild mice (Bruck 1957). Surveys
of wild populations indicate that actual frequencies of t-
bearing mice are far lower, ranging from 6 to 25% (Dunn
and Levene 1961; Myers 1973; Figueroa et al. 1988; Len-
ington et al. 1988; Ardlie and Silver 1998; Huang et al.
2001; Dod et al. 2003). Much theoretical work has focused
on understanding this unexpected discrepancy between ob-
served and expected t-complex frequencies. Models incor-
porating the stochastic effects of drift show that within re-
stricted parameters, drift together with limited migration
could theoretically reduce the frequency of thaplotypes
(Lewontin and Dunn 1960). However, house mouse pop-
ulations exhibit long-range gene flow over generations, in-
dicating that migration rates are high enough to invalidate
some of these earlier stochastic models (Levin et al. 1969;
Baker 1981; Berry et al. 1991). Other models have included
a component of selection against heterozygotes, and these
have resulted in predictions that are in fairly good accord
with observed frequencies (Lewontin 1968; Levin et al.
1969; Petras and Topping 1983; Durand et al. 1997). Such
heterozygote disadvantage models strongly predict the ex-
istence of a cost to heterozygotes that would counterbal-
ance the extreme transmission distortion of the tcomplex.Do theterozygotes have a disadvantage?
Attempts to unearth this heterozygote cost have been tricky,
as studies have produced greatly mixed results. The most
consistent laboratory findings are from caged breedings,
which tend to produce smaller litter sizes when either par-
ent is /t(Johnston and Brown 1969; Lenington et al.
1994). However, the decrease in litter size may be offset by64 Chapter Five