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bioRxivMolecular BiologyPreprint

Design and specificity of long ssDNA donors for CRISPR-based knock-in

Han LiiD, Kyle A. Beckman, Veronica PessinoiD, Bo HuangiD, Jonathan S. WeissmaniD, Manuel D. LeonettiiD

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Abstract summary

Claude Opus 5.5 · xhigh effort · 2 Nov 2026 · from the abstract · CC BY-NC-ND 4.0

Long single-stranded DNA donors enable gene-sized CRISPR knock-in in human cells, though an author update notes subsequent long-read sequencing revealed high imprecise integration rates for both donor types.

Systematic comparisons between single-stranded DNA (ssDNA) and double-stranded DNA (dsDNA) templates for CRISPR homology-directed repair (HDR) were previously lacking. While the initial study developed a synthesis and design framework for long ssDNA donors and reported higher repair specificity compared to dsDNA, an author update notes that follow-up long-read amplicon sequencing uncovered substantial imprecise integration with both donor types.

Key results

  1. SuggestedOptimized synthesis and donor design rules enable long ssDNA templates to integrate gene-sized reporters in human cell lines with lower off-target integration than equivalent PCR or plasmid dsDNA donors under initial assays.

    Demonstrated in FACS-selected human cell lines and quantified by ddPCR, though specific rates are not given in the abstract. · Abstract

  2. ClaimedA subsequent analysis by the authors using long-read amplicon sequencing found that both single-stranded and double-stranded HDR donors can produce high rates of imprecise integration in certain cell types.

    Author update note (November 12th, 2019) revising the original August 2017 conclusions based on long-read amplicon sequencing and an integrated computational pipeline. · Abstract

Methods, data and reproducibility

The study developed a synthesis protocol and design rules for long ssDNA templates to insert gene-sized reporters via CRISPR/Cas homology-directed repair in human cell lines, comparing ssDNA against PCR product and plasmid dsDNA donors using FACS selection and ddPCR.

  • Human cell lines edited with gene-sized reporters using ssDNA and dsDNA homology-directed repair donors · human
Methods & tools
CRISPR/Cas, FACS, ddPCR, PCR, long-read amplicon sequencing
Reproducibility gaps
No code or data links are provided in the abstract.
Limitations (2)
  • The authors state that the initial conclusions are outdated because analyzing only FACS-selected cells underestimates alleles where payload mis-integration disrupts selection markers. · stated by the authors
  • The authors note that quantifying integration via ddPCR provides only an indirect readout of sequence properties and misses complex imprecise integration events later detected by long-read amplicon sequencing. · stated by the authors

Read this if you design ssDNA or dsDNA templates for CRISPR homology-directed repair knock-ins and want to understand methodological pitfalls in measuring integration fidelity.

Citations
61

Abstract

CRISPR/Cas technologies have transformed our ability to manipulate genomes for research and gene-based therapy. In particular, homology-directed repair after genomic cleavage allows for precise modification of genes using exogenous donor sequences as templates. While both single-stranded DNA (ssDNA) and double-stranded DNA (dsDNA) forms of donors have been used as repair templates, a systematic comparison of the performance and specificity of repair using ssDNA versus dsDNA donors is still lacking. Here, we describe an optimized method for the synthesis of long ssDNA templates and demonstrate that ssDNA donors can drive efficient integration of gene-sized reporters in human cell lines. We next define a set of rules to maximize the efficiency of ssDNA-mediated knock-in by optimizing donor design. Finally, by comparing ssDNA donors with equivalent dsDNA sequences (PCR products or plasmids), we demonstrate that ssDNA templates have a unique advantage in terms of repair specificity while dsDNA donors can lead to a high rate of off-target integration. Our results provide a framework for designing high-fidelity CRISPR-based knock-in experiments, in both research and therapeutic settings. O_TEXTBOXUpdate: November 12th, 2019 Dear bioRxiv community, The conclusions of this pre-print (originally posted in August 2017) are outdated. While the experiments we present here are accurate, a recent and more systematic analysis revealed that the integration outcomes driven by different forms of HDR donors are more complex than our methods could originally identify. We initially analyzed donor integration only in FACS-selected cells, which under-estimates alleles where the mis-integration of payload leads to non-functional selection markers, and we quantified integration by ddPCR, which is an indirect read-out of sequence properties. These approaches could not capture the full details of donor integration events in our experiments. To address this, we have now developed a new framework based on long-read amplicon sequencing and an integrated computational pipeline to precisely analyze knock-in repair outcomes across a wide range of experimental parameters. Our new data uncover a complex repair landscape in which both single-stranded and double-stranded donors can lead to high rates of imprecise integration in some cell types. Please read our new bioRxiv pre-print entitled "Deep profiling reveals substantial heterogeneity of integration outcomes in CRISPR knock-in experiments" for further information. I hope that this example highlights one of the powers of pre-prints: the ability to update scientific discussions (and set records straight) as new results are obtained, often fueled by the availability of new technologies. Please do not hesitate to contact me directly for any questions or comments. - Manuel Leonetti (manuel.leonetti@czbiohub.org) C_TEXTBOX

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