Differences in body temperature regulation during heat stress and seasonal depression in milk yield between Holstein, Brown Swiss, and crossbred cows.

It is not clear whether cattle that are genetically superior in regulation of body temperature during heat stress are also better able to sustain milk production during hot conditions. Objectives were to evaluate differences in body temperature regulation during heat stress between Holstein, Brown Swiss, and crossbred cows under semi-tropical conditions and test whether the seasonal depression in milk yield was greater for genetic groups less able to regulate body temperature. For the first objective, conducted during heat stress, vaginal temperature was measured at 15-min intervals for 5 d in 133 pregnant lactating cows. Vaginal temperatures were affected by time and interaction between genetic group and time. Vaginal temperatures were higher for Holsteins for most times of the day. Moreover, the maximum daily vaginal temperature was higher for Holstein (39.8 ± 0.1°C) than for Brown Swiss (39.3 ± 0.2°C) or crossbreds (39.2 ± 0.1°C). For the second objective, 6,179 lactation records from 2,976 cows were analyzed to determine effects of genetic group and season of calving (cool season = Oct to March; warm season = April to Sept) on 305-d milk yield. Milk yield was affected by genetic group and season but not by the interaction of genetic group and season. The difference in average 305-d milk yield between cows calving in cool versus hot weather was 310 kg (4% decrease) for Holstein, 480 kg (7% decrease) for Brown Swiss, and 420 kg (6% decrease) for crossbreds. In conclusion, Brown Swiss and crossbreds regulated body temperature during heat stress better than Holsteins but these breeds were not more resistant to heat stress with respect to milk yield. Thus, genetic differences in thermotolerance are likely to exist that are independent of regulation of body temperature.

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.

Effectiveness of the Australian breeding value for heat tolerance at discriminating responses of lactating Holstein cows to heat stress.

Heat stress has negative consequences for milk production and reproduction of dairy cattle. These adverse effects are likely to increase because of climate change and anticipated increases in milk yield. Some of the variation among cows in ability to resist effects of heat stress is genetic. The current objective of this observational study was to assess the effectiveness of the Australian breeding value for heat tolerance (ABVHT) based on the decline in milk yield with heat stress for predicting cow differences in effects of heat stress on regulation of body temperature, milk production, and reproductive function. Genomic breeding values for heat tolerance were calculated for 12,487 cows from a single California dairy farm. Rectal temperature in the afternoon (1100-2045 h) was measured on a subset of 626 lactating cows with ABVHT ≥102 (heat tolerant) or <102 (heat sensitive). Rectal temperature was 0.12°C lower for heat-tolerant cows than heat-sensitive cows. Vaginal temperatures were measured every 15 min for 5 d in 118 cows with ABVHT ≥108 (extreme heat tolerant) or <97 (extreme heat sensitive). Vaginal temperature was 0.07°C lower for extreme heat-tolerant cows than extreme heat-sensitive cows. Lactation records for 4,703 cows with ABVHT were used to evaluate seasonal variation in first 90-d milk yield, fat percent, and protein percent for each ABVHT quartile. Overall, cows with higher ABVHT had lower milk yield, fat percentage, and protein percentage and higher first service pregnancy rate. There was no summer depression in production or reproduction or interactions between season and ABVHT quartile. We observed that ABVHT can successfully identify heat-tolerant cows that maintain lower body temperatures during heat stress. The lack of a pronounced seasonality in milk production or reproduction precluded evaluation of whether ABVHT is related to the magnitude of effect of heat stress on those traits.

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.

Correction to: Genes associated with survival of female bovine blastocysts produced in vivo.

The first error is on page 5. A sentence lists two genes as SCNA1A and SCNA2A but they should be SCN1A and SCN2A.

Actions of putative embryokines on development of the preimplantation bovine embryo to the blastocyst stage.

Once it enters the uterus at d 4 to 5 after ovulation, the preimplantation bovine embryo is controlled in its development by regulatory signaling molecules from the mother called embryokines. Here, several cell-signaling molecules whose genes are expressed in the endometrium during d 5 to 7 after estrus were tested for the ability to affect the competence of the embryo for further development and the characteristics of the resultant blastocysts. Molecules tested were C-natriuretic peptide (CNP), IL-8, bovine morphogenetic protein 4 (BMP-4), IL-6, and leukemia inhibitory factor (LIF). None of the cell-signaling molecules tested improved the competence of the embryo to become a blastocyst; in fact, BMP-4 decreased development. All molecules modified attributes of the blastocyst formed in culture. In particular, CNP increased the number of cells in the ICM, whereas IL-8 decreased inner cell mass cell numbers and tended to increase the proportion of blastocysts that were hatching or hatched. In addition, BMP-4 decreased the proportion of blastocysts that were hatching. Interleukin-6 and, to a lesser extent, LIF activated the Janus kinase (JAK)/signal transducer and activator of transcription 3 (STAT3) signaling pathway in the inner cell mass, and LIF increased the percent of cells in the blastocyst that were positive for both NANOG and phosphorylated (activated) STAT3. In conclusion, our results indicate that CNP, IL-8, IL-6, LIF, and BMP-4 can modify embryonic development of the cow in a manner that affects characteristics of the resultant blastocyst. Further research is required to understand how these changes in characteristics of the blastocyst would affect competence of the embryo to establish and maintain pregnancy.