
The molecular chaperone HSPA2 exhibits asymmetric expression in late 2-cell and 4-cell stage mouse embryos, and its differential distribution governs the first cell-fate decision by regulating ICM-specific gene expression through interaction with CARM1.


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The first cell-fate decision is the process by which cells of an embryo take on distinct lineage identities for the first time, thus representing the beginning of developmental patterning. Here, we demonstrate that the molecular chaperone heat shock protein A2 (HSPA2), a member of the 70 kDa heat shock protein (HSP70) family, is asymmetrically expressed in the late 2-cell stage of mouse embryos. The knockdown of Hspa2 in one of the two-cell blastomeres prevented its progeny predominantly toward the inner cell mass (ICM) fate, thus indicating that the differential distribution of HSPA2 in the blastomeres of two-cell embryos can influence the selection of embryonic cell lineages. In contrast, the overexpression of Hspa2 in one of the two-cell blastomeres did not induce blastomeres to differentiate towards the ICM fate. Furthermore, we demonstrated that HSPA2 forms a complex with CARM1 and activates ICM-specific gene expression. Collectively, our results identify HSPA2 as a critical regulator of the first cell-fate decision which specifies the ICM via the execution of commitment and differentiation phases.

### Competing Interest Statement

The authors have declared no competing interest.

The asymmetric expression of HSPA2 in blastomeres governs the first embryonic cell-fate decision

the-asymmetric-expression-of-heat-shock-protein-a2-hspa2-regulates-the-first-cell-fate-decision-in-mouse-embryos


The Asymmetric Expression of Heat Shock Protein A2 (HSPA2) Regulates the First Cell-Fate Decision in Mouse Embryos
