Differential expression of calcium-regulating genes in heat-stressed turkey breast muscle is associated with meat quality.

Aberrant postmortem Ca(2+)-regulation in the early postmortem period is associated with the occurrence of inferior meat quality in turkeys, described as pale, soft, and exudative (PSE). The objective of the current study was to quantify expression of 4 candidate genes responsible for maintaining Ca(2+) homeostasis in turkey skeletal muscle as a function of heat stress: α and β ryanodine receptors (RYR; Ca(2+)-release channels), the sarco/endoplasmic reticulum Ca(2+)-ATPase 1 (SERCA1), and the sarcoplasmic reticulum, Ca(2+)-storage protein calsequestrin (CASQ1). Two genetic lines of turkeys were used: a growth-selected commercial line and a randombred control line. Market-age birds were subjected to one of 5 heat stress treatments: no heat, 1 d, 3 d, 5 d, or 7 d of heat followed by 7 d of ambient temperature. Breast muscle samples were harvested and classified as normal or PSE using the meat quality parameters percentage of marinade uptake and percentage of cook loss. These parameters differed significantly by line, heat stress treatment, and meat quality status. Expression of candidate genes was measured using TaqMan quantitative PCR. Heat treatment was associated with significantly enhanced expression of αRYR, βRYR, and CASQ1 in normal muscle from both lines. Conversely, mRNA abundance of these genes was reduced in PSE muscle from both lines and recovered or increased by 7 d + 7 d of rest. Genetic line differences were observed at several time points. Expression of SERCA1 in both normal and PSE samples from both lines was unchanged or trended downward with heat stress. Taken together, genetic line and heat-stress treatment affected the expression of important Ca(2+)-regulating genes in association with meat quality status. The data suggest that birds whose meat leads to PSE may fail to respond to heat stress appropriately due to a delay in the upregulation of the important calcium-regulating genes: αRYR, βRYR, and CASQ1.