Generation of bi-paternal offspring by direct modification of imprinted genes in mammals (PRJCA032124)
we targeted these defects at their source embryos from same-sex parents aiming to establish a stable, maintainable imprinting pattern de novo in mammalian cells. Using bi-paternal mouse embryos, which exhibit severe imprinting defects and are typically non-viable, we introduced frameshift mutations, gene deletions, and regulatory edits at 20 key imprinted loci, ultimately achieving the successful development of fully adult animals. The findings provide strong evidence that imprinting abnormalities are a primary barrier to unisexual reproduction in mammals.