The CEP68 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population, created by targeted disruption of the CEP68 gene in the Raji human B-lymphoblast line. This product offers a genetically defined loss-of-function model for mechanistic studies in centrosome biology, mitotic regulation, and cancer research. The polyclonal format maintains a heterogeneous pool of edited alleles, capturing the collective phenotypic consequences of CEP68 loss and providing population-level robustness suitable for pooled screens, dose-response testing, and assays where clonal uniformity is not desired.
Raji cells originate from an EBV-positive Burkitt??s lymphoma and grow as a suspension lymphoblastoid line, retaining mature B-lymphocyte features such as surface immunoglobulin expression and MHC class II-mediated antigen presentation. They are a cornerstone model for B-cell lymphoma due to their rapid doubling time, sustained proliferative capacity, and karyotypic abnormalities that mirror chromosomal instability seen in aggressive disease. The endogenous EBV latency program interferes with host DNA damage checkpoints, creating a permissive environment in which centrosomal perturbations may unmask synthetic lethal interactions or amplify aneuploidy.
CEP68 is a key centrosomal scaffold that enforces centriole cohesion during interphase. It localizes to the proximal ends of centrioles, bridging mother and daughter centrioles through interactions with CEP250 (C-Nap1) and rootletin. This tethering is dynamically dismantled by mitotic kinases PLK1, Aurora A, and CDK1 to permit centrosome separation. Additional partners CEP63, CEP152, and CPAP integrate CEP68 into centriole duplication and microtubule organization. Disruption abolishes this regulation, causing premature centriole splitting, centrosome fragmentation, and mitotic spindle defects. The resulting chromosome missegregation promotes aneuploidy, a hallmark of aggressive cancers. Ciliogenesis may also be impaired in non-cycling cells.
Within the Raji lymphoma model, CEP68 knockout amplifies the cell line??s intrinsic genomic instability. Raji cells frequently harbor supernumerary centrosomes, and the additional loss of cohesion is expected to trigger multipolar mitoses, transient spindle pole clustering errors, and catastrophic chromosome segregation, accelerating aneuploidy generation. This establishes a powerful system to explore how centrosome dysfunction contributes to lymphomagenesis and to uncover cancer cell?Cspecific dependencies. The suspension culture format enables large-scale live-cell imaging of mitotic progression, flow cytometric cell cycle analysis, and immunofluorescence-based quantification of centrosome numbers, directly linking molecular lesions to cellular outcomes.
Researchers can employ this CEP68 knockout population in diverse experimental workflows. Standard assays include immunofluorescence staining for gamma-tubulin or centrin to assess centrosome integrity, western blotting for CEP68 depletion, and flow cytometry for DNA content and proliferation. Live-cell imaging with fluorescent reporters for tubulin and kinetochores captures dynamic spindle defects. The model is amenable to high-throughput phenotypic screening for compounds that restore cohesion or exploit aneuploidy. For technical support or custom product information, please contact Ascent Research.
