Dogs exhibit a wide variety of coat color types, and many genes have been identified that control pigment production, appearance, and distribution. Some breeds, such as the Nova Scotia Duck Tolling Retriever (NSDTR), exhibit variation in pheomelanin pigment intensity that is not explained by known genetic variants. A genome-wide association study comparing light red to dark red in the NSDTR identified a significantly associated region on canine chromosome 15 (CFA 15:23 Mb–38 Mb). Coverage analysis of whole genome sequence data from eight dogs identified a 6 kb copy number variant (CNV) 152 kb upstream of KITLG. Genotyping with digital droplet PCR (ddPCR) confirmed a significant association between an increased copy number with the dark-red coat color in NSDTR (p = 6.1 × 10⁻⁷). The copy number of the CNV was also significantly associated with coat color variation in both eumelanin and pheomelanin-based Poodles (p = 1.5 × 10⁻⁸, 4.0 × 10⁻⁹) and across other breeds. Moreover, the copy number correlated with pigment intensity along the hair shaft in both pheomelanin and eumelanin coats. KITLG plays an important role in melanogenesis, and variants upstream of KITLG have been associated with coat color variation in mice as well as hair color in humans consistent with its role in the domestic dog.

Horses are a precocious species that must accomplish several milestones that are critical to survival in the immediate post-birth period for their survival. One essential milestone is the successful transition from the intrauterine unconsciousness to an extrauterine state of consciousness or awareness. This transition involves a complex withdrawal of consciousness inhibitors and an increase in neuroactivating factors that support awareness. This process involves neuroactive hormones as well as inputs related to factors such as cold, visual, olfactory, and auditory stimuli. One factor not previously considered in this birth transition is a yet unreported direct neural reflex response to labor-induced physical compression of the fetus in the birth canal (squeezing). Neonatal maladjustment syndrome (NMS) is a disorder of the newborn foal characterized by altered behavior, low affinity for the mare, poor awareness of the environment, failure to bond to the mother, abnormal sucking, and other neurologically-based abnormalities. This syndrome has been associated with altered events during birth, and was believed to be caused exclusively by hypoxia and ischemia. However, recent findings revealed an association of the NMS syndrome with the persistence of high concentrations of in utero neuromodulating hormones (neurosteroids) in the postnatal period. Anecdotal evidence demonstrated that a novel physical compression (squeeze) method that applies 20 min of sustained pressure to the thorax of some neonatal foals with this syndrome might rapidly hasten recovery. This survey provides information about outcomes and time frames to recovery comparing neonatal foals that were given this squeeze treatment to foals treated with routine medical therapy alone. Results revealed that the squeeze procedure, when applied for 20 min, resulted in a faster full recovery of some foals diagnosed with NMS. The adjunctive use of a non-invasive squeeze method may improve animal welfare by hastening recovery and foal–mare interactions that minimize health problems. This would also avoid or reduce costs arising from hospitalization associated with veterinary and nursing care that sometimes leads owners to elect for euthanasia.

Background: The carrier status of lavender foal syndrome (LFS), cerebellar abiotrophy (CA), severe combined immunodeficiency (SCID), and occipitoatlantoaxial malformation (OAAM1) in foals with juvenile idiopathic epilepsy (JIE) is unknown. Hypothesis/Objectives: To determine the carrier status of LFS, CA, SCID, and OAAM1 in foals with JIE. Animals: Ten foals with JIE. Materials and Methods: Archived DNA samples were tested for known genetic mutations causing LFS, CA, SCID, and OAAM1. The inclusion criteria consisted of having been diagnosed with JIE by ruling out other causes of seizures in foals and supported by electroencephalographic examination. Results: Ten Egyptian Arabian horses (5 females and 5 males) were phenotyped as foals with JIE by electroencephalography (EEG). All foals were negative for the genetic mutations that cause LFS, CA, SCID, and OAAM1 except for 1 foal that was a carrier of CA. Conclusions and Clinical Importance: Juvenile idiopathic epilepsy of Egyptian Arabian foals and LFS appear to be phenotypically and genetically distinct disorders. There was no apparent association between JIE and LFS, CA, SCID, and OAAM1.

The authors wish to make the following corrections to this paper