The FRYL Knockout Raji Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal population derived from the Raji B lymphocyte cell line, featuring targeted disruption of the FRYL gene. FRYL encodes a mitotic regulator essential for cytokinesis and spindle orientation. As a polyclonal pool, this product provides a heterogeneous knockout model, avoiding single-clone selection biases and enabling robust functional studies of FRYL-dependent processes.
Raji cells originate from an Epstein-Barr virus (EBV)-positive Burkitt lymphoma and retain characteristics of mature B lymphocytes, including immunoglobulin production and immune responsiveness. They serve as a widely used model for B cell malignancies, cell cycle analysis, and immune signaling studies. Their rapid proliferation and defined genetic background make them particularly amenable to CRISPR/Cas9-based gene disruption aimed at dissecting mitosis regulation.
FRYL localizes to the spindle midzone and midbody, where it interacts with Aurora B kinase, PRC1, and KIF23 to orchestrate central spindle assembly and cytokinesis. Acting downstream of CDK1/Cyclin B and Aurora kinases, FRYL promotes RhoA pathway activation via ECT2, facilitating contractile ring formation through actin and myosin recruitment. Loss of FRYL disrupts these processes, leading to cytokinesis failure, polyploidy, and genomic instability??hallmarks of tumorigenesis and neurodevelopmental pathology.
In the Raji lymphoma context, FRYL knockout enables investigation of how cytokinesis defects contribute to chromosomal instability and cancer progression. The EBV-positive background may reveal interplay between viral oncoproteins and mitotic regulators. This model thus offers a platform to identify synthetic lethal interactions or therapeutic targets in cells with compromised abscission. It also extends to studies of neurodevelopmental disorders linked to FRYL mutations, facilitating cross-disciplinary research into cell cycle-related pathologies.
Applications include time-lapse microscopy for monitoring mitotic dynamics, immunofluorescence detection of midbody markers such as Aurora B or PRC1, and flow cytometry-based ploidy assessment. Western blot analysis of phospho-Aurora B serves as a biochemical correlate for upstream signaling changes. These assays support research in mitotic regulation, cancer cell biology, and drug target validation, with a particular focus on cytokinesis-blocking agents. For further information or technical support, please contact Ascent Research.
