Background: In mammals, DRP1 is a key regulator of mitochondrial fission during mitochondrial dynamics, whereas ATF5 promotes the mitochondrial unfolded protein response (UPRmt). Both pathways are essential for maintaining cellular homeostasis and protecting oocytes and embryos from external stressors. However, the relationship between ATF5 expression and DRP1 under heat stress conditions during porcine oocyte maturation remains unclear. Methods: In this study, we investigated the mitochondrial dynamics and ATF5 expression in porcine oocytes exposed to heat stress during in vitro maturation (IVM). Protein and gene expression levels were assessed using immunofluorescence staining, Western blotting, and quantitative PCR. Results: During IVM, both DRP1 and ATF5 expression were increased (p < 0.01) significantly. In contrast, heat stress markedly impaired (p < 0.05) meiotic progression and cumulus cell expansion. Mitochondrial dynamics were disrupted (p < 0.05), as fission and fusion markers displayed reciprocal changes relative to those in controls. Concomitantly, the expression of ATF proteins was significantly reduced (p < 0.01) under heat stress. Heat-stressed oocytes also exhibited decreased (p < 0.05) expression of genes involved in antioxidant defense and NAD metabolism, whereas autophagy- and apoptosis-related transcripts were significantly upregulated (p < 0.05). At the blastocyst stage, embryos derived from heat-stressed oocytes exhibited nuclear localization of the UPR-associated transcription factors ATF4, CHOP, and ATF5. Conclusions: Collectively, our findings suggest that heat stress disrupts mitochondrial dynamics and ATF5 expression during porcine oocyte maturation while the UPRmt pathway remains active during early embryonic development to mitigate heat-induced cellular damage.

최근에 이루어진 세포생물학적, 유전학적 연구들을 통하여 미토콘드리아의 구조 변화가 매우 역동적이며, dynamin- related protein(DRP)와 같은 다양한 단백질에 의해 조절된다는 것이 알려지게 되었다. 미토콘드리아가 ATP 합성을 통한 세포내 신진대사에 관여하며, 소포체와 상호작용을 통하여 칼슘 이온 농도의 항상성 유지, 그리고 세포 사멸에서 중요한 역할을 한다는 사실을 고려해 볼 때, 미토콘드리아 구조 역동성 조절은 정상적인 세포의 성장