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Tabby patterns of fur coats are defining characteristics in wild and domestic felids. Historically, three autosomal alleles at one locus (Tabby): Abyssinian (Ta ; a.k.a. ticked), mackerel (Tm ; a.k.a. striped) and blotched (tb ; a.k.a. classic, blotched) were thought to control these patterns in domestic cats and their breeds. Currently, at least three loci influence cat tabby markings, two of which are designated Tabby and Ticked. The Tabby locus is laeverin (LVRN) and affects the mackerel and blotched patterns. The unidentified gene for the Ticked locus on cat chromosome B1 was suggested to control the presence or absence of the ticked pattern (Tabby - Abyssinian (Ta ; a.k.a. ticked). The cat reference genome (Cinnamon, the Abyssinian) has the ticked phenotype and the variant dataset and coat phenotypes from the 99 Lives Cat Genome Consortium (195 cats) were used to identify candidate genes and variants associated with the Ticked locus. Two strategies were used to find the Ticked allele(s), one considered Cinnamon with the reference allele or heterozygous (Strategy A) and the other considered Cinnamon as having the variant allele or heterozygous (Strategy B). For Strategy A, two variants in Dickkopf Wnt Signaling Pathway Inhibitor 4 (DKK4), a p.Cys63Tyr (B1:41621481, c.188G>A) and a less common p.Ala18Val (B1:42620835, c.53C>T) variant are suggested as two alleles influencing the Ticked phenotype. Bioinformatic and molecular modeling analysis suggests that these changes disrupt a key disulfide bond in the Dkk4 cysteine-rich domain 1 or Dkk4 signal peptide cleavage respectively. All coding variants were excluded as Ticked alleles using Strategy B.

The development of high throughput SNP genotyping technologies has improved the genetic dissection of simple and complex traits in many species including cats. The properties of feline 62,897 SNPs Illumina Infinium iSelect DNA array are described using a dataset of over 2,000 feline samples, the most extensive to date, representing 41 cat breeds, a random bred population, and four wild felid species. Accuracy and efficiency of the array's genotypes and its utility in performing population-based analyses were evaluated. Average marker distance across the array was 37,741 Kb, and across the dataset, only 1% (625) of the markers exhibited poor genotyping and only 0.35% (221) showed Mendelian errors. Marker polymorphism varied across cat breeds and the average minor allele frequency (MAF) of all markers across domestic cats was 0.21. Population structure analysis confirmed a Western to Eastern structural continuum of cat breeds. Genome-wide linkage disequilibrium ranged from 50-1,500 Kb for domestic cats and 750 Kb for European wildcats (Felis silvestris silvestris). Array use in trait association mapping was investigated under different modes of inheritance, selection and population sizes. The efficient array design and cat genotype dataset continues to advance the understanding of cat breeds and will support monogenic health studies across feline breeds and populations.

Dogs naturally suffer the same complex diseases as humans, including mental illness. The dog is uniquely suited as a model organism to explore the genetics of neuropsychiatric disorders. Historical breed demographics have enriched purebred populations for founder effect mutations with tractable architectures, making genotypic analyses advantageous. Over a pet's lifetime, owners observe the animal's stress tolerance, arousal, and anxiety, and can inform on rich behavioral profiles for phenotypic analyses. Here we leverage these strengths in a search for inherited fac-tors that exacerbate canine compulsive disorder (CCD), the dog counterpart to human obsesssive compulsive disorder (OCD). Our rationale is that identifying pathways that predispose to disease severity will expand therapeutic options, and ultimately bring relief to those patients suffering the most. We have performed a GWAS of purebred Doberman pinschers that compares severely affected cases to moderately affected cases (24:70). This GWAS identified two statistically sig-nificant risk loci, on CFA34 and CFA11, and a third with suggestive evidence on CFA16. The locus on CFA34 includes a cluster of 5-HT3 receptor genes (HTR3C, HTR3D, and HTR3E) that implicate a serotonergic pathway that is routinely targeted by anti-OCD medications. The locus on CFA11 is syntenic with human CTXN3-SLC12A2 (5q35.1), an inherited risk factor for schiz-ophrenia. The third locus harbors teneurin-3 (TENM3), a modulator of the hypothalamic-pituitary-adrenal (HPA) axis, with effects on stress tolerance and stress-related behavior. We dis-cuss candidate genes and putative functional variants in light of pharmacological responsiveness, psychiatric comorbidity, and the potential for gene-by-environment interactions in the genetic etiology of OCD and CCD. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to the article on role of veterinary profession in promoting animal welfare, published in the previous issue.

Objective: To determine the effect of intravenous acepromazine on the electroencephalogram (EEG) of normal Beagle dogs. Sample Population: Twelve healthy beagle dogs Procedures: Dogs were sedated and the EEG recorded for 20 minutes. Acepromazine was then injected intravenously in either low or high dose with the order chosen randomly and EEG recording continued for 30 minutes. Each dog received low and high dose in the study and at least a week was allowed to elapse between doses. Five dogs for the placebo group were chosen at random from the pool of dogs and received saline instead of acepromazine, with the same EEG recordings made. Results: Multiple ANOVA and independent t-tests were used to analyze data in commercially available statistical software. EEG activity was not altered significantly by either low or high dose acepromazine administered intravenously. Conclusions and Clinical Relevance: EEG activity is not altered significantly in normal dogs by the low or high dose of acepromazine used in this study. [ABSTRACT FROM AUTHOR]