Tasmanian devils sequenced using the MHC class I primers developed by Siddle et al [41] and screened for a deletion at the <i>Saha-UA</i> locus in this same gene region.

<p>In each individual devil the loci which can be confirmed as failing to amplify are identified (as indicated by no alleles present). No significant differences were found between healthy and diseased animals in the prevalence of the <i>Saha-UA</i> deletion or in the frequency with which alleles failed to amplify at any loci.</p

Location of eight MHC-linked microsatellites on devil chromosome four, associated with the MHC region.

<p>Six of these (Sh-I01, Sh-I02, Sh-I05, Sh-I06, Sh-I10 and Sh-I11) are located close to the four MHC class I loci (<i>Saha-UA</i>, <i>Saha-UB</i>, <i>Saha-UC</i> and <i>Saha-UD</i>) and several other genes involved in antigen presentation (TAP1, TAP2, PSMB8, PSMB9). The two remaining markers (Sh-I07, Sh-I08) are more closely linked with genes within the MHC that do not play a direct role in antigen presentation (MTCH1, FGD2).</p

MHC-linked microsatellite loci allele frequencies showing little variation between healthy and DFTD infected devils.

<p>A single locus (Sh-I07) does not conform to Hardy-Weinberg expectations for healthy devils only (p = 0.003).</p

Neutral and MHC-linked microsatellite loci summary statistics for diseased (shaded rows) and healthy devils.

<p>A single locus (Sh-I07) displays a departure from Hardy-Weinberg equilibrium for healthy devils only. Numbers of alleles and levels of heterozygosity are very similar for healthy and DFTD infected devils though with a slight trend for higher heterozygosity in infected devils.</p>*<p>denotes statically significant departure from Hardy-Weinberg equilibrium (HWE). FIS indicates homozygote (+ve) or heterozygote (−ve) excess. A is the number of alleles. Ho/He is observed and expected heterozygosities.</p

Genetic diversity, inbreeding and cancer – Supplementary material

Table S1. Examples showing the effect of loss of genetic diversity and inbreeding on organismal fitness*. N: number on samples analysed, A: average number of alleles, HE: Expected heterozygosity. Table S2. Examples of cancer cases in humans, domestic animals and wildlife, including their suggested causes (categorised as reduced genetic diversity ●, pollution ●, mitigated by parasite infection ●, and transmissible and thus mitigated by interactions with infected conspecifics or related species ●). N: number on samples analysed, A: average number of alleles, HE: Expected heterozygosity

DFTD samples 2006-2011

Tumour tissue samples used in the study were collected between 2006 and 2011 at 12 sites within the DFTD affected areas of Tasmania

Genotype calls from Stacks for Tasmanian devil RAD-seq

This VCF file contains raw genotype calls produced by Stacks as described in Epstein et al. 2016. Very briefly, the genotyping workflow was quality control -> PCR de-duplication (for paired-end samples) -> Alignment to reference -> Filter out MAPQ < 40 -> Stacks

Additional file 3: Table S7. of Development of a SNP-based assay for measuring genetic diversity in the Tasmanian devil insurance population

SNP genotypes for pedigree determination. (XLSX 279 kb