DMC1 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population designed for the targeted disruption of the DMC1 gene in the near-haploid HAP1 cell line. This gene-edited product provides a loss-of-function model for investigating the role of DMC1 in meiotic homologous recombination and related DNA repair processes. The polyclonal knockout pool preserves the genetic heterogeneity of the CRISPR-edited population, enabling robust functional studies without clonal expansion biases. This product is suitable for researchers studying genome stability, fertility, and cancer biology.
The HAP1 cell line is a near-haploid derivative of the KBM-7 chronic myeloid leukemia cell line, characterized by a single set of chromosomes except for a disomic region on chromosome 15. Originating from a male donor, HAP1 cells exhibit adherent growth and are widely employed in genetic screening and knockout generation due to their haploid genome, which simplifies phenotypic interpretation. Their malignant origin makes them a pertinent model for cancer research, particularly in studying DNA damage response pathways and therapeutic vulnerabilities.
DMC1 encodes a meiotic-specific recombinase that assembles on single-stranded DNA to mediate strand exchange between homologous chromosomes, a critical step in crossover formation and accurate chromosome segregation during gametogenesis. DMC1 functions within the homologous recombination pathway and is regulated by upstream factors including SPO11 and STRA8, as well as retinoic acid signaling and MEI1. It interacts directly with RAD51, the HOP2-MND1 complex, BRCA2, FIGNL1, MEIOB, SYCP3, and RPA to coordinate DNA repair synthesis. Disruption of DMC1 impairs meiotic progression and is linked to non-obstructive azoospermia and primary ovarian insufficiency.
In the HAP1 near-haploid background, CRISPR/Cas9-mediated disruption of the single DMC1 allele establishes a clean loss-of-function state, making these polyclonal cells a powerful tool for dissecting DMC1-dependent processes. The model is particularly valuable for studying homologous recombination deficiency in a cancer-relevant context, as HAP1 cells are derived from a leukemia line. By introducing a DMC1 knockout, researchers can investigate how loss of this recombinase influences DNA repair capacity, sensitivity to genotoxic agents, and potential synthetic lethal interactions.
These polyclonal knockout cells are ideal for a range of applications including mechanistic studies of meiotic recombination, fertility research, and DNA repair pathway analysis. They can be used in homologous recombination reporter assays to quantify repair efficiency, in DNA damage sensitivity assays with agents such as cisplatin or olaparib, and in immunofluorescence studies monitoring ??H2AX foci formation. Additional applications include RT-qPCR and Western blotting for validation of DMC1 disruption. The polyclonal format enables direct functional interrogation of the knockout phenotype without selection pressure from single-cell cloning. For further information, please contact Ascent Research.
