2025 한국동물생명공학회 학술대회 [Seul-Gi Yang] > 학회발표

Heat stress disrupts mitochondrial dynamics and ATF5 expression during porcine oocyte maturation

Seul-Gi Yang ^1,2, Hyo-Jin Park^2,3, Geun-Hwi Jo^2,3, Ye-Won Jang^1,2, Su-Hyun Han^2,3, and Deog-Bon Koo^1,2,3

¹ Department of Companion Animal Industry, College of Natural and Life Sciences, ²DU Center for Infertility, ³ Department of Biotechnology, College of Engineering, Daegu University, 201 Daegudae-ro Jillyang, Gyeongsan, Gyeongbuk 38453, Republic of Korea

In mammals, DRP1 is a key regulator of mitochondrial fission during mitochondrial dynamics, while ATF5 promotes the mitochondrial unfolded protein response (UPR^mt). Both pathways are essential for maintaining cellular homeostasis and protecting oocytes and embryos from external stress. However, the relationship between ATF5 and DRP1 expressions under heat stress conditions during porcine oocyte maturation remains poorly understood. In this study, we investigated mitochondrial dynamics and ATF5 expression in porcine oocytes exposed to heat stress during in vitro maturation (IVM). Immunohistochemical analysis revealed differential expression of phosphorylated DRP1 (pDRP1-Ser616) across follicular stages in vivo. During IVM, the expressions of pDRP1-Ser616, DRP1, and ATF5 were significantly increased under normal conditions. However, heat stress markedly impaired meiotic progression and cumulus cell expansion. Notably, DRP1 and ATF5 protein expression exhibited opposing patterns compared to the control group, indicating altered mitochondrial dynamics. Furthermore, heat-stressed oocytes showed significantly reduced expression of genes related to antioxidant enzymes and NAD metabolism, while genes associated with autophagy and apoptosis were significantly upregulated. After blastocyst formation, immunofluorescence analysis revealed nuclear localization of UPR-related proteins ATF4, CHOP, and ATF5 in embryos derived from heat-stressed oocytes. Collectively, our findings suggest that heat stress disrupts mitochondrial dynamics and ATF5 expression during porcine oocyte maturation, while the UPR^mt pathway remains active during early embryonic development to counteract heat-induced cellular damage.