Amy H.Y. Tong

The paper develops a method to quantify genetic interactions from CRISPR-Cas9 screens and identifies systematic variations in screen data.

The paper constructs a genome-scale genetic interaction network from 4 million double mutants in HAP1 cells, revealing conserved genetic network principles across species and uncovering novel gene functions and cancer dependencies.

The paper shows that N-terminal acetylation by NatC protects proteins from degradation, enhancing longevity and motility, and that UBR4-KCMF1 targets unacetylated N-terminal Met followed by hydrophobic residues.

The paper identifies three types of chromatin boundaries that regulate cohesin traffic, which guides enhancer-promoter interactions and affects gene regulation.

The paper identifies ACE2 as the only common host dependency for SARS-CoV-2 across multiple cell lines, while other host factors are cell line specific.

The paper introduces FLEX, a pipeline for benchmarking CRISPR screen data, and identifies a dominant mitochondria-associated signal in genome-wide screens.

This study maps genetic interactions in FASN-deficient cells to identify genes involved in lipid uptake and metabolic adaptation.

The paper presents a high-throughput CRISPR-Cas9 screening method for identifying CD47 modulators, identifying QPCTL as a key enzyme involved in its pyroglutamyl modification.

The paper evaluates CRISPR/Cas9 knockout screens in human cell lines and designs an optimized gRNA library to improve gene knockout efficiency and accuracy.