Interaction Between Sympk and Oct4 Promotes Mouse Embryonic Stem Cell Proliferation

Area of Science:

• Stem cell biology
• Molecular and cell biology

Background:

• Symplekin (Sympk) is a scaffold protein with known roles in RNA processing and epithelial cell regulation.
• Its function in embryonic stem cells (ESCs), where it is highly expressed, is currently unknown.

Purpose of the Study:

• To investigate the role of Symplekin (Sympk) in mouse embryonic stem cells (ESCs).
• To determine Sympk's contribution to ESC self-renewal, pluripotency, and genomic stability.

Main Methods:

• CRISPR/Cas9 gene editing to delete Sympk in mouse ESCs.
• Assessing colony formation, teratoma formation, and chimeric mouse development to evaluate pluripotency.
• Analyzing gene expression related to proliferation and differentiation.
• Investigating the interaction between Sympk and Oct4 using the DUF3453 domain.

Main Results:

• Sympk overexpression enhanced ESC colony formation and pluripotency, while Sympk deletion reduced these.
• Sympk sustained ESC pluripotency and genomic stability during long-term culture.
• The DUF3453 domain of Sympk is crucial for Oct4 interaction and colony formation.
• Sympk modulated gene expression, activating proliferation genes and suppressing differentiation genes.

Conclusions:

• Symplekin (Sympk) interacts with Oct4 to promote ESC self-renewal and pluripotency.
• Sympk is essential for maintaining genomic integrity in ESCs.
• Sympk holds potential for applications in stem cell therapies.