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.

Methods
The capture, examination and sampling of live badgers was carried out under Home Office Project Licence PP3493437 and preceding versions of this licence. Data used were collected from a long-term capture-mark-recapture (CMR) study of a wild population of badgers at Woodchester Park in Gloucestershire (Delahay et al., 2013).