Christine Strand

This paper optimizes AsCas12a for combinatorial genetic screens in human cells by improving on-target and off-target activity and enabling higher-order multiplexing.

The paper presents a method to generate isogenic cell pairs and screen them with CRISPR-Cas9 libraries to identify genetic interactions, demonstrating applications for BCL2L1, MCL1, and PARP1.

This study identifies a genetic variant in C. elegans that affects arsenic toxicity through differences in branched-chain amino acid metabolism.

The paper evaluates and introduces optimized CRISPR libraries for knockout, interference, and activation screens, showing improved performance in gene function interrogation.

The paper identifies PCR amplification as a major source of uncoupling between sgRNAs and their associated barcodes in combinatorial CRISPR screens and proposes strategies to mitigate this issue.

The paper identifies a single amino acid substitution in topoisomerase II that explains variation in drug sensitivity across C. elegans isolates and human cell lines.