Experimental study demonstrates efficient prime editing in two-cell mouse embryos via mismatch repair inhibition, indicating feasibility of same-generation founder phenotyping.
Using transient inhibition of DNA mismatch repair during a permissive stage of development, we demonstrate highly efficient prime editing of mouse embryos with few unwanted, local byproducts (average 58% precise edit frequency, 0.5% on-target error frequency across 13 substitution edits at 8 sites), enabling same-generation phenotyping of founders. Whole-genome sequencing reveals that mismatch repair inhibition increases off-target indels at low-complexity regions in the genome without any obvious phenotype in mice.
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Kim et al. (2024) studied this question.
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