The MREG Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population engineered for targeted disruption of the MREG gene in human Raji B lymphocytes. This polyclonal model provides a heterogeneous collection of cells with loss-of-function alleles in MREG, enabling robust studies of lysosomal and endosomal trafficking without clonal selection artifacts. The knockout population is designed for researchers investigating dynein-mediated organelle positioning and endocytic pathway regulation.
Raji is an EBV-positive Burkitt lymphoma-derived human B lymphoblastoid cell line, widely used as a model for B-cell biology, lymphomagenesis, and immune signaling. These cells exhibit surface immunoglobulin expression and active endocytic trafficking, making them a suitable host for studying lysosomal dynamics in the context of hematopoietic malignancies and immune cell function.
The MREG protein, transcriptionally regulated by MITF, functions as a key adaptor in the recruitment of the dynein-dynactin motor complex to lysosomes and melanosomes via direct interaction with RILP. By linking Rab7-positive late endosomes and lysosomes to dynein, MREG facilitates minus-end-directed microtubule transport, thereby controlling perinuclear lysosome clustering and organelle positioning. The signaling network includes the BLOC-1 complex, DCTN1, and dynein light chain, with Rab7 acting as a critical upstream activator. Disruption of MREG uncouples lysosomes from the dynein motor, leading to dispersal of the lysosomal compartment and potentially altering endosomal maturation, receptor recycling, and downstream signaling outputs.
In the Raji B-cell context, MREG knockout offers a physiologically relevant system to examine its role in immune cell vesicular trafficking. B lymphocytes rely on tightly regulated lysosomal positioning for antigen processing, MHC class II loading, and phagocytic degradation. The polyclonal knockout population provides a powerful tool for dissecting how dynein-mediated transport influences these processes, potentially revealing vulnerabilities in lymphoma cells that depend on lysosomal function for survival and proliferation. Moreover, the EBV-positive background adds relevance for studying viral manipulation of host trafficking pathways.
This MREG knockout model is suited for immunofluorescence microscopy to assess lysosome distribution, western blotting to confirm MREG protein loss, and live-cell imaging to track vesicle dynamics. Further applications include flow cytometry for surface marker analysis, phagocytosis assays, and lysosomal enzyme activity measurements, as well as RT-qPCR for transcriptional validation. Researchers investigating endocytic trafficking, drug delivery mechanisms, or pigmentation biology will find this polyclonal system valuable for functional studies. For additional information or technical support, please contact Ascent Research.
