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Biology subjects

Medhi, D.

Publications and source records attributed to Medhi, D..

3 recordsLinked to original sources

Cell-in-drop genotyping detects megabase-scale loss of heterozygosity as a quantitative marker for CRISPR-Cas9 on-target toxicity

Targeted DNA double strand breaks catalyzed by CRISPR-Cas9 have been demonstrated to cause megabase-scale segmental deletions and whole chromosome losses in a wide variety of mouse and human cell lines. This raises safety concerns for CRISPR-Cas9 based therapeutics and highlights the need for scalable methods to assess its on-target genotoxicity in clinical contexts. In this report, we present cell-in-drop genotyping, as a high throughput approach that combines single cell encapsulation with droplet-based PCR genotyping of endogenous polymorphisms to detect loss of heterozygosity (LOH) at a targeted chromosome without any genome manipulation. With this approach, we detected megabase scale LOH induced by Cas9 DSBs, mostly frequently by segmental loss. This approach also detected LOH from loss of a critical DNA repair factor, BLM helicase, and LOH induced by other genotoxic conditions, in particular, the chemotherapeutic drugs Paclitaxel and Mitomycin C, which were demonstrated to induce LOH by different mechanisms. A modified version of the assay also captured rare local short range LOH arising from DSB-induced interhomologue recombination. Because it requires no genome manipulation, cell-in-drop genotyping offers a practical, scalable tool for evaluating genotoxic risk of CRISPR-Cas9 and other agents in research and clinical development.

bioengineering↗

Megabase-scale loss of heterozygosity provoked by CRISPR-Cas9 DNA double-strand breaks

Harnessing DNA double-strand breaks (DSBs) is a powerful approach for gene editing, but it may provoke loss of heterozygosity (LOH), which predisposes to tumorigenesis. To interrogate this risk, we developed a two- color flow cytometry-based system (Flo-LOH), detecting LOH in [~]5% of cells following a DSB. After this initial increase, cells with LOH decrease due to a competitive disadvantage with parental cells, but if isolated, they stably propagate. Segmental loss from terminal deletions with de novo telomere addition and nonreciprocal translocations is observed as well as whole chromosome loss, especially following a centromeric DSB. LOH spans megabases distal from the DSB, but also frequently tens of megabases centromere-proximal. Inhibition of microhomology-mediated end joining massively increases LOH, which is synergistically increased with concomitant inhibition of canonical nonhomologous end joining. The capacity for large-scale LOH must therefore be considered when using DSB-based gene editing, especially in conjunction with end joining inhibition.

molecular biology↗

Noncanonical contributions of MutLγ to VDE-initiated crossovers during Saccharomyces cerevisiae meiosis

In Saccharomyces cerevisiae, the meiosis-specific axis proteins Hop1 and Red1 are present nonuniformly across the genome. In a previous study, the meiosis-specific VMAl-derived endonuclease (VDE) was used to examine Spo11-independent recombination in a recombination reporter inserted in a Hop1/Red1-enriched region (HIS4) and in a Hop1/Red1-poor region (URA3). VDE-initiated crossovers at HIS4 were mostly dependent on Mlh3, a component of the MutL{gamma} meiotic recombination intermediate resolvase, while VDE-initiated crossovers at URA3 were mostly Mlh3-independent. These differences were abolished in the absence of the chromosome axis remodeler Pch2, and crossovers at both loci become partly Mlh3-dependent. To test the generality of these observations, we examined inserts at six additional loci that differed in terms of Hop1/Red1 enrichment, chromosome size, and distance from centromeres and telomeres. All six loci behaved similarly to URA3: the vast majority of VDE-initiated crossovers were Mlh3-independent. This indicates that, counter to previous suggestions, meiotic chromosome axis protein enrichment is not a primary determinant of which recombination pathway gives rise to crossovers during VDE-initiated meiotic recombination. In pch2{Delta} mutants, the fraction of VDE-induced crossovers that were Mlh3-dependent increased to levels previously observed for Spo11-initiated crossovers in pch2{Delta}, indicating that Pch2-dependent processes play an important role in controlling the distribution of factors necessary for MutL{gamma}-dependent crossovers.

genetics↗