Data from: Multi-locus homozygosity promotes actuarial senescence in a wild mammal

Genome-wide homozygosity, caused for example by inbreeding, is expected to
have deleterious effects on survival and/or reproduction. Evolutionary
theory predicts that any fitness costs are likely to be detected in late
life because natural selection will filter out negative impacts on younger
individuals with greater reproductive value. Here we infer associations
between multi-locus homozygosity, sex, disease, and age-dependent
mortality risks using Bayesian analysis of the life histories of wild
European badgers (Meles meles) in a population naturally infected with
Mycobacterium bovis (the causative agent of bovine tuberculosis). We find
important effects of multi-locus homozygosity on all parameters of the
Gompertz-Makeham mortality hazard function, but particularly in
later-life. Our findings confirm the predicted association between genomic
homozygosity and actuarial senescence. Increased homozygosity is
particularly associated with an earlier onset, and greater rates of
actuarial senescence, regardless of sex. The association between
homozygosity and actuarial senescence is further amplified among badgers
putatively infected with bovine tuberculosis. These results recommend
further investigation into the ecological and behavioural processes that
result in genome-wide homozygosity, and focused work on whether
homozygosity is harmful or beneficial during early life-stages.