Scd1 −/− blastocyst give rise to inner cell mess (ICM) impairment and embryo development arrest. (A): Immunofluorescence staining of Cdx2 (Trophectoderm cell marker) in WT and Scd1 −/− Scd1 −/− blastocyst give rise to inner cell mess (ICM) impairment and embryo development arrest. (A): Immunofluorescence staining of Cdx2 (Trophectoderm cell marker) in WT and Scd1 −/− blastocysts. Scale bars, 50 µm. (B): The total cell number of WT and Scd1 −/− blastocysts. Twotailed Student's t-test was used for statistical analysis. The Scd1 −/− group has significantly fewer cell numbers than the WT group (p = 0.0066). Each dot represents one embryo, and black bars indicate the mean cell number for each group. (C): Number of Cdx2 + cells in Scd1 −/− blastocysts compared with WT in 16-32 cells, 32-64 cells and >64 cells embryos, respectively. * p < 0.05 (t-test). (D): Immunofluorescence staining of Sox2 (inner cell mass marker) and Cdx2 in WT and Scd1 −/− blastocysts. Rescue group represent the overexpression of Scd1 in Scd1 −/− blastocysts to reflect the rescue function of Scd1 in ICM generation. Scale bars, 50 µm. (E): Numbers of Sox2 + cells in WT and Scd1 −/− blastocysts. * p < 0.05 (t-test). (F): Morphology of the embryo stem (es) cells isolated from the ICM of WT and Scd1 −/− blastocysts. Bar, 25 µm. (G): The uterus of WT and Scd1 −/− mice when E12.5 of pregnancy. The red arrow marked the embryos' location. Bar, 5 mm. (H): The embryos (E12.5) of WT and Scd1 −/− mice. Bar, 1 mm. (I): The litter size of mice in two groups. ** p < 0.01 (t-test).

Scd1 −/− blastocyst give rise to inner cell mess (ICM) impairment and embryo development arrest. (A): Immunofluorescence staining of Cdx2 (Trophectoderm cell marker) in WT and Scd1 −/− Scd1 −/− blastocyst give rise to inner cell mess (ICM) impairment and embryo development arrest. (A): Immunofluorescence staining of Cdx2 (Trophectoderm cell marker) in WT and Scd1 −/− blastocysts. Scale bars, 50 µm. (B): The total cell number of WT and Scd1 −/− blastocysts. Twotailed Student's t-test was used for statistical analysis. The Scd1 −/− group has significantly fewer cell numbers than the WT group (p = 0.0066). Each dot represents one embryo, and black bars indicate the mean cell number for each group. (C): Number of Cdx2 + cells in Scd1 −/− blastocysts compared with WT in 16-32 cells, 32-64 cells and >64 cells embryos, respectively. * p < 0.05 (t-test). (D): Immunofluorescence staining of Sox2 (inner cell mass marker) and Cdx2 in WT and Scd1 −/− blastocysts. Rescue group represent the overexpression of Scd1 in Scd1 −/− blastocysts to reflect the rescue function of Scd1 in ICM generation. Scale bars, 50 µm. (E): Numbers of Sox2 + cells in WT and Scd1 −/− blastocysts. * p < 0.05 (t-test). (F): Morphology of the embryo stem (es) cells isolated from the ICM of WT and Scd1 −/− blastocysts. Bar, 25 µm. (G): The uterus of WT and Scd1 −/− mice when E12.5 of pregnancy. The red arrow marked the embryos' location. Bar, 5 mm. (H): The embryos (E12.5) of WT and Scd1 −/− mice. Bar, 1 mm. (I): The litter size of mice in two groups. ** p < 0.01 (t-test).

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Embryos contain a large number of lipid droplets, and lipid metabolism is gradually activated during embryonic development to provide energy. However, the regulatory mechanisms remain to be investigated. Stearoyl-CoA desaturase 1 (Scd1) is a fatty acid desaturase gene that is mainly involved in intracellular monounsaturated fatty acid production, w...

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Mammalian reproductive ability is regulated by many factors, among which the fatty acid metabolism network provides energy for oocyte differentiation and primordial follicle formation during early mouse oogenesis. But the mechanism behind that is still unknown. Stearoyl-CoA desaturase 1 (Scd1) gene expression is increased during the oogenesis process, supporting the oocyte's healthy growth. Taking advantage of gene-edited mice lacking stearoyl-Coenzyme A desaturase 1 gene (Scd1-/-), we analyzed relative gene expression in perinatal ovaries from wildtype, and Scd1-/- mice. Scd1 deficiency dysregulates expression of meiosis-related genes (e.g., Sycp1, Sycp2, Sycp3, Rad51, Ddx4) and a variety of genes (e.g., Nobox, Lhx8, Bmp15, Ybx2, Dppa3, Oct4, Sohlh1, Zp3) associated with oocyte growth and differentiation, leading to a lower oocyte maturation rate. The absence of Scd1 significantly impedes meiotic progression, causes DNA damage, and results in oocyte apoptosis. Moreover, we find that Scd1 ablation dramatically disrupts the abundance of fatty acid metabolism genes (e.g., Fasn, Srebp1, Acaca) and the lipid droplet content. Thus, our findings substantiate a major role for Scd1 as a multifunctional regulator of fatty acid networks necessary for oocyte maintenance and differentiation during early follicular genesis.