Chris D. Richardson

This study shows that PEX1 deficiencies disrupt HIF1α proteostasis via autophagy, leading to increased HIF1 levels and impaired recovery under hypoxia-reoxygenation.

The paper develops RaPID-seq to study homology search during HDR and finds that DSB proximity determines template candidacy, with distant sequences not efficiently searched despite sequence identity.

POCKET-seq maps dCas9 binding genome-wide to distinguish true and false-positive interactions in CRISPR interference screens.

This study identifies SFPQ as a factor promoting homologous recombination by stabilizing RAD51 and its paralogs' mRNA, independent of DSB localization or p53 activation.

This study identifies FANCD2-FANCI's role in coordinating chromatin openness and cell cycle arrest during DNA double-strand break repair.

This study shows that the PEX1G843D mutation impairs PEX1/PEX6 assembly and leads to proteasomal degradation, but overexpression can restore peroxisome function.

The paper identifies RNF146 and tankyrase as regulators of peroxisome function and links them to Wnt signaling through their role in PARsylation and beta-catenin degradation.

The paper shows that interstrand crosslinked DNA templates (xHDRTs) significantly boost gene editing efficiency in human cells by up to five-fold, independent of template topology or cell type.

This paper introduces dead-RNAs (dRNAs) to suppress unwanted CRISPR/Cas9 off-target and HDR-corrected site cleavage, enabling precise genome editing.

The paper identifies CDC7 inhibition as a method to enhance HDR efficiency in CRISPR-Cas9 gene editing by inducing an early S-phase cell cycle arrest.

This paper introduces DISCOVER-Seq, a method to detect CRISPR off-targets in vivo with single-base resolution, applicable to multiple Cas nucleases.