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.

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.