Journal article
Genome-wide CRISPR screening identifies a role for ARRDC3 in TRP53-mediated responses
JE La Marca, BJ Aubrey, B Yang, C Chang, Z Wang, A Kueh, L Tai, S Wilcox, L Milla, S Heinzel, D Vremec, L Whelan, C König, D Kaloni, AK Voss, A Strasser, ST Diepstraten, MJ Herold, GL Kelly
Cell Death and Differentiation | Published : 2024
Abstract
Whole-genome screens using CRISPR technologies are powerful tools to identify novel tumour suppressors as well as factors that impact responses of malignant cells to anti-cancer agents. Applying this methodology to lymphoma cells, we conducted a genome-wide screen to identify novel inhibitors of tumour expansion that are induced by the tumour suppressor TRP53. We discovered that the absence of Arrestin domain containing 3 (ARRDC3) increases the survival and long-term competitiveness of MYC-driven lymphoma cells when treated with anti-cancer agents that activate TRP53. Deleting Arrdc3 in mice caused perinatal lethality due to various developmental abnormalities, including cardiac defects. Not..
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Grants
Awarded by Australian Government
Funding Acknowledgements
We thank Dr Elizabeth Lieschke for advice and reagents for our work with MDFs, Dr Kerstin Brinkmann for advice and reagents for our work with MEFs, and Margaret Potts for advice and reagents for our various haematopoietic reconstitution experiments. We thank Alessia Pierotti for general laboratory assistance. We also thank all other members of the Blood Cells and Blood Cancer Division at the Walter and Eliza Hall Institute (WEHI) for their support. We thank WEHI Bioservices for looking after our mice, in particular Dan Fayle, Rebecca Meeny, Michael Watters, Jamie Leahy, Thomas Kapitelli, Lauren Wilkins, Natasha Blasch, Jaclyn Gilbert, and Giovanni Siciliano. We thank Dr Simon Monard and his team in the WEHI flow cytometry lab, the team of Dr Stephen Wilcox in the WEHI Genomics Facility, and the WEHI Lab Services staff for their contributions.