PMC:6811567 / 1237-2280 JSONTXT

{"project":"2_test","denotations":[{"id":"31645615-29765029-138959912","span":{"begin":369,"end":370},"obj":"29765029"},{"id":"31645615-28615035-138959913","span":{"begin":945,"end":946},"obj":"28615035"},{"id":"31645615-28615073-138959914","span":{"begin":1011,"end":1012},"obj":"28615073"},{"id":"31645615-28280001-138959915","span":{"begin":1023,"end":1024},"obj":"28280001"},{"id":"31645615-30992277-138959916","span":{"begin":1041,"end":1042},"obj":"30992277"}],"text":"The ability to introduce targeted changes to the genome has facilitated investigation of gene function and disease modelling in increasingly diverse systems. Strategies for genome manipulation include homologous recombination and targeted nucleases such as zinc finger nuclease (ZFNs) and Clustered, Regularly Interspaced, Short Palindromic Repeat (CRISPR) technologies1. As the genetic lesion induced by nuclease-mediated editing is mostly repaired by non-homologous end joining, the size of the indel generated is unpredictable. Thus, it is essential to characterise the induced genetic lesion through genomic DNA sequencing to predict the subsequent coding region frameshift. However, recent observations in CRISPR-knockout experiments have shown that unanticipated outcomes such as alternate translation start sites or exon skipping may result in expression of unexpected protein products which retain function and obviate indel frame-shifts2. This phenomenon has been observed in cultured mammalian cells3,4, zebrafish5, and butterflies6."}