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Elucidation of the molecular mechanism of the breakage-fusion-bridge (BFB) cycle using a CRISPR-dCas9 cellular model
Journal article   Open access   Peer reviewed

Elucidation of the molecular mechanism of the breakage-fusion-bridge (BFB) cycle using a CRISPR-dCas9 cellular model

Manrose Singh, Kaitlin Raseley, Alexis M Perez, Danny MacKenzie, Settapong T Kosiyatrakul, Sanket Desai, Noelle Batista, Navjot Guru, Katherine K Loomba, Heba Z Abid, …
Nucleic acids research, v 52(19), pp 11689-11703
28 Oct 2024
PMID: 39193906
url
https://doi.org/10.1093/nar/gkae747View
Published, Version of Record (VoR) Open

Abstract

Chromosomal Instability CRISPR-Associated Protein 9 - genetics CRISPR-Associated Protein 9 - metabolism CRISPR-Cas Systems DNA Damage DNA Replication - genetics Humans RNA, Guide, CRISPR-Cas Systems - genetics Telomere - genetics
Chromosome instability (CIN) is frequently observed in many tumors. The breakage-fusion-bridge (BFB) cycle has been proposed to be one of the main drivers of CIN during tumorigenesis and tumor evolution. However, the detailed mechanism for the individual steps of the BFB cycle warrants further investigation. Here, we demonstrate that a nuclease-dead Cas9 (dCas9) coupled with a telomere-specific single-guide RNA (sgTelo) can be used to model the BFB cycle. First, we show that targeting dCas9 to telomeres using sgTelo impedes DNA replication at telomeres and induces a pronounced increase of replication stress and DNA damage. Using Single-Molecule Telomere Assay via Optical Mapping (SMTA-OM), we investigate the genome-wide features of telomeres in the dCas9/sgTelo cells and observe a dramatic increase of chromosome end fusions, including fusion/ITS+ and fusion/ITS-. Consistently, we also observe an increase in the formation of dicentric chromosomes, anaphase bridges, and intercellular telomeric chromosome bridges (ITCBs). Utilizing the dCas9/sgTelo system, we uncover many interesting molecular and structural features of the ITCB and demonstrate that multiple DNA repair pathways are implicated in the formation of ITCBs. Our studies shed new light on the molecular mechanisms of the BFB cycle, which will advance our understanding of tumorigenesis, tumor evolution, and drug resistance.

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Collaboration types
Domestic collaboration
Web of Science research areas
Biochemistry & Molecular Biology
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