MTFR2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the Raji B lymphocyte cell line, engineered to disrupt the MTFR2 gene. This polyclonal population contains a heterogeneous mix of cells carrying diverse loss-of-function mutations at the MTFR2 locus, thereby avoiding clonal artifacts and capturing a broader range of functional responses. The knockout model provides a robust loss-of-function system for investigating mitochondrial fission regulation within a lymphomagenic background.
The Raji host cell line is a suspension cell line originally established from a Burkitt??s lymphoma patient. It exhibits a lymphoblast-like morphology, expresses B cell surface markers, and retains Epstein-Barr virus-immortalized characteristics. These features make Raji cells an extensively used model in B cell biology, lymphoma research, and drug response studies. Their suspension growth format facilitates scalable culture, high-throughput flow cytometry, and metabolic flux analyses.
MTFR2 (Mitochondrial Fission Regulator 2) encodes a key activator of DRP1 (encoded by DNM1L)-mediated mitochondrial division. It operates downstream of AMPK signaling and cellular energy stress to promote DRP1 recruitment to the mitochondrial outer membrane, where DRP1 assembles into constricting oligomers. MTFR2 cooperates with mitochondrial fission factors such as DNM1L, MFF, and FIS1 to drive membrane scission. Knockout of MTFR2 disrupts this process, causing mitochondrial elongation due to unopposed fusion mediated by the mitofusins MFN1 and MFN2 and the inner membrane GTPase OPA1. This imbalance in mitochondrial dynamics secondarily alters apoptosis signaling, oxidative phosphorylation efficiency, and mitochondrial quality control pathways.
In the Raji lymphoma context, MTFR2 knockout induces a shift toward hyperfused mitochondrial networks, which can modulate metabolic reprogramming, reactive oxygen species production, and apoptotic sensitivity. Such mitochondrial remodeling is increasingly recognized as a determinant of cancer cell survival, chemotherapy resistance, and adaptation to bioenergetic stress. Hence, this polyclonal knockout model offers a valuable platform to mechanistically dissect how mitochondrial fission perturbations influence B cell lymphoma behavior, and to evaluate the functional consequences on cell proliferation, viability, and drug susceptibility.
Typical applications include probing mitochondrial dynamics in lymphoma, screening for small-molecule modulators of the DRP1 fission pathway, and assessing metabolic vulnerabilities using Seahorse extracellular flux analysis. Apoptosis and cell death responses can be quantified by flow cytometry (Annexin V/propidium iodide), while mitochondrial morphology is directly visualized by immunofluorescence against the outer membrane marker Tom20. Western blot and RT-qPCR confirm MTFR2 knockout efficiency, and proliferation assays track growth phenotypes. These polyclonal cells are also suitable for co-culture experiments or CRISPR-based synthetic lethality screens. For further information or technical support, please contact Ascent Research.
