AI Article Synopsis
- Endogenous retroviruses (ERVs) are significant components of the human genome, with some influencing immune response and early development.
- The study identifies a specific ERV, ERVH48-1, that plays a crucial role in somatic development by affecting mesoderm and cardiomyocyte differentiation during early embryonic stages.
- ERVH48-1 operates by degrading the WNT antagonist SFRP2, which helps regulate WNT/β-catenin signaling pathways, ultimately impacting cell type commitment.
Article Abstract
Endogenous retroviruses (ERVs) occupy a significant part of the human genome, with some encoding proteins that influence the immune system or regulate cell-cell fusion in early extra-embryonic development. However, whether ERV-derived proteins regulate somatic development is unknown. Here, we report a somatic developmental function for the primate-specific ERVH48-1 (SUPYN/Suppressyn). ERVH48-1 encodes a fragment of a viral envelope that is expressed during early embryonic development. Loss of ERVH48-1 led to impaired mesoderm and cardiomyocyte commitment and diverted cells to an ectoderm-like fate. Mechanistically, ERVH48-1 is localized to sub-cellular membrane compartments through a functional N-terminal signal peptide and binds to the WNT antagonist SFRP2 to promote its polyubiquitination and degradation, thus limiting SFRP2 secretion and blocking repression of WNT/β-catenin signaling. Knockdown of SFRP2 or expression of a chimeric SFRP2 with the ERVH48-1 signal peptide rescued cardiomyocyte differentiation. This study demonstrates how ERVH48-1 modulates WNT/β-catenin signaling and cell type commitment in somatic development.
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| http://dx.doi.org/10.1016/j.stem.2024.07.006 | DOI Listing |
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