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Scd1 Deficiency in Early Embryos Affects Blastocyst ICM Formation through RPs-Mdm2-p53 Pathway
Huimin Niu1, Anmin Lei2, Huibin Tian1
1Shaanxi Key Laboratory of Molecular Biology for Agriculture, College of Animal Science and Technology, Northwest A&F University, Yangling 712100, China.
International Journal of Molecular Sciences
|January 21, 2023
Summary
Stearoyl-CoA desaturase 1 (Scd1) is crucial for embryonic development, regulating lipid droplets for energy. Scd1 deficiency triggers ribosomal stress, activating the P53 pathway and causing developmental arrest.
Area of Science:
- Embryology
- Molecular Biology
- Biochemistry
Background:
- Embryos rely on lipid metabolism for energy, with lipid droplets (LDs) playing a key role.
- The precise regulatory mechanisms of lipid metabolism during early embryonic development are not fully understood.
- Stearoyl-CoA desaturase 1 (Scd1) is a key enzyme in fatty acid desaturation and intracellular monounsaturated fatty acid production.
Purpose of the Study:
- To investigate the role of Stearoyl-CoA desaturase 1 (Scd1) in early embryonic development.
- To elucidate the regulatory mechanisms by which Scd1 influences lipid metabolism and embryo viability.
- To understand the consequences of Scd1 deficiency on embryonic development and cellular pathways.
Main Methods:
- Analysis of Scd1 gene expression at critical embryonic stages (cleavage, blastocyst).
- CRISPR/Cas9 gene editing to create Scd1 knockout (KO) mouse embryos from zygotes.
- Transcriptomic analysis comparing wild-type and Scd1 KO embryos.
- Assessment of lipid droplet content and inner cell mass (ICM) formation in blastocysts.
Main Results:
- Scd1 expression significantly increased during the cleavage and blastocyst stages of embryonic development.
- Scd1 KO embryos exhibited reduced lipid droplets and impaired inner cell mass formation.
- Transcriptomic analysis revealed suppressed ribosome protein (RP) genes in Scd1 KO embryos, leading to ribosome biogenesis arrest at the 2-cell stage.
- The P53-related pathway was activated in Scd1 KO blastocysts, resulting in apoptosis and developmental arrest.
Conclusions:
- Scd1 is essential for providing energy during embryonic development by regulating intra-embryonic lipid droplet formation.
- Scd1 deficiency leads to ribosomal stress, activating the RPs-Mdm2-P53 pathway and causing embryonic developmental arrest.
- Scd1 plays a critical role in maintaining healthy embryonic development through energy support and preventing apoptosis.
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