Some abstracts do not have video files because ASAS was denied recording rights.
405
Genetic solutions to infertility caused by heat stress
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 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 gamete 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 identified in cattle. 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.
Keywords: heat stress, infertility, reproduction, body temperature