# Insulin-like growth factor 1 receptor (IGF1R)-dependent signaling regulates blastocyst formation during early embryonic development

## TL;DR

This study shows that the IGF1R receptor is not needed for early cell fate decisions in embryos but is important for proper blastocyst growth and survival.

## Contribution

The study reveals that IGF1R signaling is essential for blastocyst development and viability but not for lineage segregation in early embryos.

## Key findings

- Embryos lacking IGF1R formed blastocysts but showed delayed development and increased apoptosis.
- Exogenous IGF-1 failed to rescue IGF1R-deficient embryos and worsened apoptosis when signaling was blocked.
- IGF1R signaling is crucial for blastocyst growth dynamics and embryonic viability but not for lineage segregation.

## Abstract

Insulin-like growth factor 1 (IGF1) signaling is a conserved regulator of embryonic growth and survival. However, the specific role of IGF1 signaling mediated by its cognate receptor IGF1R during mammalian preimplantation development remains unclear and unexplored. In this study, we employed both genetic ablation using cytidine deaminase base editors and pharmacological inhibition to assess the role of IGF1R in porcine early embryonic development. Embryos lacking IGF1R advanced through early cleavage divisions and progressed to blastocyst formation; however, they displayed delayed blastocyst development and significantly increased apoptosis. Lineage segregation was largely unperturbed. Exogenous IGF-1 supplementation did not ameliorate developmental impairments in IGF1R-knockout embryos and instead exacerbated apoptotic responses when receptor signaling was compromised. Collectively, these results establish that IGF1R signaling is dispensable for cell fate specification but is crucial for regulating blastocyst growth dynamics and embryonic viability.