(86) Role of TRIM71 in mouse oocyte maturation and embryo development in vitro

Abstract Authors: Sook Young Yoon, Su Hee Seok, Mi Seon Park, Jung Hye Kim, Jin Hee Eum, Se Yul Han

CHA Fertility Center Gangnam, CHA University, Seoul 06125, Korea

Abstract Text:

TRIM proteins are proteins that regulate specific stages of the cell cycle and mitosis. Approximately 80 genes are known in humans, and they are composed of RING, B-box, and coiled-coil (RBCC) and N-terminal TRIM, and regulate apoptosis, cell cycle control, viral responses, cell proliferation, differentiation, cancer development, and antiviral defense mechanisms. Therefore, their abnormalities are the cause of cardiovascular, nervous system, immune, musculoskeletal, developmental disorders, and various forms of cancer. In the nematode (C. elegans), LIN41 null mutations result in premature termination of meiotic prophase and abnormal oocyte formation in the pachytene stage oocytes that enter the M phase. These oocytes inappropriately disassemble synaptonemal complexes, undergo cellularization, and activate CDK-1/cyclin B dependent kinase to enter the M phase. This ultimately causes abnormal embryonic development. Lin 41 is a molecular biological homolog of TRIM 71 in mammals and is essential for embryonic survival and neural tube formation. It is strongly expressed in the testis in humans and in the developing brain, placenta, ovaries, and testes in mice, suggesting that TRIM 71 may be involved in germ cell formation and embryonic development. In addition, RNA-seq analysis of granulosa cells that produced good quality and poor-quality embryos revealed that two TRIM molecules (TRIM 16, TRIM 29) showed significantly different expression patterns depending on the quality of the embryo. In the TRIM71 knockout mouse experiment, infertile male mice were obtained, and the testis was atrophied in hetero mice and showed sertoli cell only characteristics in homo mice. It was reported that some sertoli cell only male infertile patients had a defect in the TRIM71 gene, suggesting that TRIM71 may be a cause of infertility. In this study, we investigated the expression pattern of TRIM71 according to the in vitro maturation and oocyte maturation stages, and the effect of TRIM71 knockdown before oocyte maturation and on oocyte maturation. Immature and mature oocytes were collected from 7-week-old BDF1 mice, and TRIM71 siRNA was microinjected into immature oocytes, and embryonic development was examined after in vitro fertilization. TRIM71 was strongly expressed in the mouse testis, and its expression was relatively higher in mature oocytes than in immature oocytes. It was expressed low in two-cell embryos and blastocysts after fertilization. After TRIM 71 siRNA, embryonic development of mature oocytes was inhibited compared to the control group (p < 0.005). TRIM71 might be involved in oogenesis in mouse. TRIM71 is not an essential for the GVBD during oocyte maturation, but it might be involved in cytoplasmic maturation including polar body extrusion. Further studies are needed to understand the molecular mechanism involved in cytoplasmic maturation