BLM helicase deficiency impairs porcine oocyte maturation via induction of organelle dysfunction

BLM helicase plays a well-established role in safeguarding genomic integrity and cellular homeostasis by regulating DNA replication, transcription, and repair. However, its function during meiotic maturation in porcine oocytes remains largely unexplored. Here, we first delineated the subcellular localization of BLM helicase at key stages of porcine oocyte meiotic progression. Functional inhibition of BLM helicase during in vitro maturation severely compromised oocyte development, as evidenced by a significant reduction in the proportion of oocytes achieving first polar body extrusion. This maturational failure was accompanied by pronounced organellar defects, characterized by increased mitochondrial mass but reduced mitochondrial membrane potential, elevated reactive oxygen species accumulation, endoplasmic reticulum abnormalities alongside the upregulation of ER stress-related genes, a sharp decline in lysosomal signal intensity, disrupted Golgi apparatus distribution, and a marked reduction in GM130 protein levels. Collectively, these findings establish BLM helicase as an indispensable regulator of porcine oocyte maturation and lay essential groundwork for further mechanistic studies into its role during oocyte development.