Testing for contemporary selection on TLR3 variation on Cousin
There were significant differences in lifetime survival probabilities
between TLR3 genotypes. Individuals (first caught as juveniles)
with the TLR3 CC genotype had a 37% increased
mortality risk compared to those with theTLR3 AC or TLR3 AAgenotypes, with a median age of death of 1, 2, and 2.5 years
respectively (COXME, P = 0.024, Fig 2, Table 1). Thus, individuals
with at least one copy of the TLR3 A allele had
increased survival than those without (P = 0.025, Table S1).
Independently – and as found previously in a smaller dataset (Brouwer
et al., 2010) – individuals with the Ase-ua4 MHC class I allele
had a 25% lower risk of mortality than those without, corresponding to
a median age of death at 3.5 years (compared to 2 years for those
individuals without) (COXME, P = 0.028, Table 1). There was no
significant effect of sex, H s, maternalH s, or MHC diversity on lifetime survival
probability (Table 1), or of the season in which an individual hatched,
although individuals hatched in the minor breeding season tended to have
increased survival (COXME, P = 0.062, Table 1).
In males, individuals with different TLR3 genotypes had
significantly different LRS. Males with TLR3 AAhad greater LRS than those with TLR3 AC(P <0.001, Table 2, Fig 3a) orTLR3 CC (P = 0.003, Table 2, Fig 3a),
with TLR3 AA males producing on average twice
the number of independent offspring (mean ± SEM: 1.40 ± 0.27) than
either TLR3 AC (mean ± SEM: 0.63 ± 0.17), orTLR3 CC males (mean ± SEM: 0.70 ± 0.21) over
their lifetime. There was no significant difference in LRS betweenTLR3 AC and TLR3 CCgenotypes (P = 0.86) in males. Thus, males with at least one copy
of the TLR3 C allele had reduced LRS than those
without (P <0.001, Table S2). In contrast in females
there was no association between TLR3 genotype and LRS (Fig 3a).
In males, LRS decreased with increasing MHC diversity (P = 0.047,
Table 2), whereas in females LRS tended to increase with increasing MHC
diversity, although this result was marginally non-significant (P= 0.064, Table 2). H s and the presence ofAse-ua4 did not predict LRS for either sex (Table 2).
As survival was strongly correlated with TLR3 genotype, we also
investigated whether TLR3 genotypes predicted reproductive rate
after controlling for parental survival – i.e. by including longevity
and controlling for breeding ability (survival to recruitment into the
adult population). In both sexes, individuals who lived longer (greater
longevity) produced significantly more offspring (GLMM, Age P<0.001, Table 2). There was also evidence for a negative
quadratic effect of longevity in both sexes (GLMM,
Age2 P <0.001, Table 2). Males ofTLR3 AA genotype tended to produce more
offspring (surviving >3 months; GLMM, P = 0.049,
Table 2, Fig 3b) than those of TLR3 AC genotype,
while TLR3 AA andTLR3 AC genotypes did not differ fromTLR3 CC genotypes (P = 0.38 and 0.54,
respectively). There was no association between the rate of reproduction
and TLR3 genotype or quadratic age in females.H s, MHC diversity, and the presence ofAse-ua4 did not predict reproductive rate for either sex (Table
2).
The difference in LRS associated with TLR3 variation equated to a
selection coefficient of 0.34 against TLR3 AC,and 0.46 against TLR3 CC genotypes of both sex,
over ca 3 overlapping generations (assuming a generation time of 4 years
(Spurgin et al., 2014)), when the selection coefficient ofTLR3 AA genotype was set as 1.