Germline variation contributes to false negatives in CRISPR-based experiments with varying burden across ancestries.


Journal

Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555

Informations de publication

Date de publication:
07 Jun 2024
Historique:
received: 05 12 2023
accepted: 20 05 2024
medline: 8 6 2024
pubmed: 8 6 2024
entrez: 7 6 2024
Statut: epublish

Résumé

Reducing disparities is vital for equitable access to precision treatments in cancer. Socioenvironmental factors are a major driver of disparities, but differences in genetic variation likely also contribute. The impact of genetic ancestry on prioritization of cancer targets in drug discovery pipelines has not been systematically explored due to the absence of pre-clinical data at the appropriate scale. Here, we analyze data from 611 genome-scale CRISPR/Cas9 viability experiments in human cell line models to identify ancestry-associated genetic dependencies essential for cell survival. Surprisingly, we find that most putative associations between ancestry and dependency arise from artifacts related to germline variants. Our analysis suggests that for 1.2-2.5% of guides, germline variants in sgRNA targeting sequences reduce cutting by the CRISPR/Cas9 nuclease, disproportionately affecting cell models derived from individuals of recent African descent. We propose three approaches to mitigate this experimental bias, enabling the scientific community to address these disparities.

Identifiants

pubmed: 38849329
doi: 10.1038/s41467-024-48957-z
pii: 10.1038/s41467-024-48957-z
doi:

Substances chimiques

RNA, Guide, CRISPR-Cas Systems 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

4892

Subventions

Organisme : U.S. Department of Defense (United States Department of Defense)
ID : WX81XWH-21-1-0934
Organisme : U.S. Department of Defense (United States Department of Defense)
ID : W81XWH-21-1-0901

Informations de copyright

© 2024. The Author(s).

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Auteurs

Sean A Misek (SA)

Broad Institute of MIT and Harvard, Cambridge, MA, 02142, USA.
Departments of Cancer Biology and Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, 02215, USA.
Koch Institute, Massachusetts Institute of Technology, Cambridge, MA, 02142, USA.

Aaron Fultineer (A)

Broad Institute of MIT and Harvard, Cambridge, MA, 02142, USA.

Jeremie Kalfon (J)

Broad Institute of MIT and Harvard, Cambridge, MA, 02142, USA.

Javad Noorbakhsh (J)

Broad Institute of MIT and Harvard, Cambridge, MA, 02142, USA.

Isabella Boyle (I)

Broad Institute of MIT and Harvard, Cambridge, MA, 02142, USA.

Priyanka Roy (P)

Broad Institute of MIT and Harvard, Cambridge, MA, 02142, USA.

Joshua Dempster (J)

Broad Institute of MIT and Harvard, Cambridge, MA, 02142, USA.

Lia Petronio (L)

Broad Institute of MIT and Harvard, Cambridge, MA, 02142, USA.

Katherine Huang (K)

Broad Institute of MIT and Harvard, Cambridge, MA, 02142, USA.

Alham Saadat (A)

Broad Institute of MIT and Harvard, Cambridge, MA, 02142, USA.

Thomas Green (T)

Broad Institute of MIT and Harvard, Cambridge, MA, 02142, USA.

Adam Brown (A)

Broad Institute of MIT and Harvard, Cambridge, MA, 02142, USA.

John G Doench (JG)

Broad Institute of MIT and Harvard, Cambridge, MA, 02142, USA.

David E Root (DE)

Broad Institute of MIT and Harvard, Cambridge, MA, 02142, USA.

James M McFarland (JM)

Broad Institute of MIT and Harvard, Cambridge, MA, 02142, USA.

Rameen Beroukhim (R)

Broad Institute of MIT and Harvard, Cambridge, MA, 02142, USA. Rameen_Beroukhim@dfci.harvard.edu.
Departments of Cancer Biology and Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, 02215, USA. Rameen_Beroukhim@dfci.harvard.edu.

Jesse S Boehm (JS)

Broad Institute of MIT and Harvard, Cambridge, MA, 02142, USA. boehm@mit.edu.
Koch Institute, Massachusetts Institute of Technology, Cambridge, MA, 02142, USA. boehm@mit.edu.

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