inbreeding depression - senecio7の日記

García-Dorado A 2007 Shortcut predictions for fitness properties at the mutation–selection–drift balance and for its buildup after size reduction under different management strategies. Genetics 176:983-997.

the fitness decline is that expected from the ancestral inbreeding depression rate
plus the decline from fixation of new deleterious mutations that accumulate as the new equilibrium is attained
minus the purging effect of selection on the transitory excess of additive variance induced by random drift of partially recessive deleterious alleles

the constraint on δ posed by selection against homozygous becomes highly relevant for h < 0.1 in large populations

our approach produces downwardly biased predictions for N = 100
suggesting that it overestimates the efficiency of natural selection when Ns = 2
this can be due to the inadequacy, in this case, of the assumption q ≪ p when accounting for natural selection
the predictions illustrate that the equilibrium inbreeding depression rate increases almost linearly with decreasing h-values for small populations
for large populations, however, δ becomes appreciable only for small h-values
then, selection against homozygous becomes a relevant limiting factor

mutations with small s- and h-values, for which our method gives downwardly biased δ-estimates, do not make a relevant contribution to the overall inbreeding depression rate
the approximation integrated over the distribution of mutational effects is highly reliable compared to the corresponding diffusion approximation

I obtained Equation 27 predictions for this case using ancestral genetic properties computed for the recurrent mutation model
δ and τ_t computed from Equations 1, 19, and 23
where q-values were computed from Equation 6.2.6. in Crow and Kimura 1970 for 5800 loci as in Wang et al. 1999

our predictions are in good agreement with simulation results in their Table 2 up to generation 50 (differences <2%)
from generation 50 to 100, however, the rate of viability decline in Wang et al. doubled, which is unexpected, particularly under the assumed multiplicative fitness model
on the contrary, our predictions indicate that, by generation 100, viability had recovered half of the previous decline
this difference can be partly ascribed to linkage in Wang et al.’s simulations, where the whole genome length is 2 M

the above difference should also be partly a consequence of the use of Equation 27
which neglects the fitness decay from deleterious fixation
instead of the analytically less tractable (26B) expression
this may become relevant in the long term