|Hansen, Peter - University Of Florida|
|Dikmen, Serdal - University Of Florida|
|Ortega, Martha - University Of Florida|
|Dahl, Geoff - University Of Florida|
Submitted to: Journal of Dairy Science
Publication Type: Abstract Only
Publication Acceptance Date: 4/21/2016
Publication Date: 7/9/2016
Citation: Hansen, P.J., Dikmen, S., Cole, J.B., Ortega, M.S., Dahl, G.E. 2016. Genetic solutions to infertility caused by heat stress. Journal of Dairy Science. 99(E-Suppl. 1)/Journal of Animal Science. 94(E-Suppl. 5):192(abstr. 0405).
Technical Abstract: Reproductive function in mammals is very susceptible to disruption by heat stress. In lactating dairy cows, for example, pregnancy rates per insemination can be as low as 10-15% in the summer vs. 25-40% in cool weather. Reduced fertility in females is caused by a combination of 1) the negative consequences of the physiological adjustments engaged to minimize hyperthermia during heat stress and 2) direct deleterious effects of elevated body temperature on the oocyte and embryo (i.e., heat shock). There is genetic variation body temperature regulation during heat stress as well as in cellular resistance to elevated temperature. Thus, opportunities exist for improving reproduction during heat stress by modifying livestock genetically to improve body temperature regulation and cellular resistance to heat shock. Genetic improvement can be achieved by identifying genetically-superior animals within a breed (heritability for rectal temperature during heat stress is 0.17) as well as by transferring genes from thermotolerant breeds to thermosensitive ones. A successful example of gene transfer is for a mutation in PRLR causing the slick hair phenotype. Holstein cattle inheriting this mutation have increased ability to regulate body temperature during heat stress and are less likely to experience a decrease in milk yield during summer than other Holsteins. Among the genes conferring cellular resistance to heat shock is a mutation in the promoter of HSPA1L. Selection for the beneficial allele of this gene, as well as other genes controlling cellular resistance to heat shock, might reduce the damage to the oocyte and embryo caused by elevated body temperature.