Effects of the bovine SLICK1 mutation in PRLR on sweat gland area, FOXA1 abundance, and global gene expression in skin.

The SLICK1 mutation in the prolactin receptor (PRLR) results in a short-hair coat and increased ability to regulate body temperature during heat stress. It is unclear whether the mutation affects capacity for sweating. The objective of this observational study was to evaluate whether the SLICK1 mutation in PRLR alters characteristics of skin related to sweat gland abundance or function. Skin biopsies from 31 Holstein heifers, including 14 wild-type (SL-/-) and 17 heterozygous slick (SL+/-), were subjected to histological analysis to determine the percent of the surface area of skin sections that are occupied by sweat glands. We detected no effect of genotype on this variable. Immunohistochemical analysis of the forkhead transcription factor A1 (FOXA1), a protein essential for sweating in mice, from 6 SL-/- and 6 SL+/- heifers indicated twice as much FOXA1 in sweat glandular epithelia of SL+/- heifers as in SL-/- heifers. Results from RNA sequencing of skin biopsies from 5 SL-/- and 7 SL+/- heifers revealed few genes that were differentially expressed and none that have been associated with sweat gland development or function. In conclusion, results do not support the idea that the SLICK1 mutation changes the abundance of sweat glands in skin, but do show that functional properties of sweat glands, as indicated by increased abundance of immunoreactive FOXA1, are modified by inheritance of the mutation in PRLR.

Inheritance of the SLICK1 allele of PRLR in cattle.

The slick-hair phenotype in cattle is due to one of a series of mutations in the prolactin receptor (PRLR) that cause truncation of the C-terminal region of the protein involved in JAK2/STAT5 activation during prolactin signaling. Here we evaluated whether the inheritance of the SLICK1 allele, the first slick mutation discovered, is inherited in a fashion consistent with Hardy-Weinberg equilibrium. It was hypothesized that any deleterious effect of inheriting the allele on embryonic or fetal function would result in reduced frequency of the allele in offspring. A total of 525 Holstein and Senepol cattle produced from matings involving one or both parents with the SLICK1 allele were genotyped. The observed frequency of the SLICK1 allele (0.247) was not significantly different than the expected frequency of 0.269. These results support the idea that inheritance of the SLICK1 allele does not act in the embryo or fetus to modify its competence to complete development to term.