The CDYL Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout population in a Burkitt’s lymphoma-derived B lymphocyte background, designed for advanced epigenetic and cancer research. This product offers a heterogeneous knockout pool targeting the CDYL gene, which encodes a chromodomain-containing transcriptional corepressor. The polyclonal format provides a robust loss-of-function model for studying CDYL-dependent gene silencing, histone modification, and chromatin dynamics, without the constraints of clonal variability. Researchers can utilize these cells to dissect CDYL’s roles in the REST corepressor complex and its broader impacts on the B cell transcriptome, making it a versatile tool for functional genomics, drug target validation, and mechanistic studies in B cell malignancies and beyond.
Derived from the Raji cell line, these B lymphocytes serve as a well-characterized model for Burkitt’s lymphoma, offering a unique platform to investigate CDYL’s function in immune-related contexts. Raji cells are Epstein-Barr virus (EBV)-positive, maintaining features of antigen presentation and antibody production, which are particularly relevant for studying epigenetic regulation in lymphomagenesis. While the REST complex is canonically associated with neuronal gene silencing, its components are expressed in many non-neuronal tissues, including B cells, where they may modulate gene expression programs. This knockout model thus enables the exploration of CDYL’s repressive activities in a physiologically malignant immune cell environment, providing insights into how aberrant chromatin regulation contributes to hematological cancers.
CDYL functions as a pivotal adaptor within the REST corepressor complex by binding trimethylated histone H3 lysine 27 (H3K27me3) via its chromodomain, then recruiting histone deacetylases HDAC1 and HDAC2 to silence target gene promoters. It acts downstream of the master transcriptional repressor REST, which recruits CoREST, CDYL, and HDACs to neuronal gene loci, such as SCG10, to maintain their repression in non-neuronal cells. Beyond REST, CDYL interacts with methyltransferases EZH2 and G9a, reinforcing H3K27me3 and H3K9me3 marks, respectively. Importantly, CDYL also possesses crotonyl-CoA hydratase activity, regulating histone crotonylation??an emerging epigenetic mark affecting chromatin structure??thereby linking metabolism to gene expression.
In the Raji host background, CDYL knockout disrupts the equilibrium of chromatin-modifying complexes, potentially derepressing neuronal genes and altering B cell-specific transcriptional networks. This unmasks the role of histone methylation and crotonylation in lymphoma biology, as CDYL’s dual activities may influence proliferation, differentiation, or immune evasion phenotypes. Given CDYL’s association with hepatocellular carcinoma and neurological disorders, this model bridges cancer epigenetics and neurobiology, enabling comparative studies of REST complex function across malignant contexts. The Raji system also facilitates examination of how viral oncoproteins (e.g., EBV) intersect with host epigenetic machinery, with CDYL serving as a critical node.
Applications for these polyclonal knockout cells encompass a spectrum of epigenetic and transcriptomic analyses. Chromatin immunoprecipitation coupled with quantitative PCR (ChIP-qPCR) can assess H3K27me3 and histone crotonylation changes at specific gene loci following CDYL loss. Co-immunoprecipitation and western blotting allow validation of REST complex integrity and HDAC recruitment, while RNA-seq and RT-qPCR reveal global and targeted gene expression shifts, including derepression of neuronal markers. Reporter assays enable dissection of CDYL’s repressive function, and histone crotonylation assays investigate its non-canonical catalytic role. This model is ideal for screening small molecules that modulate REST complex activity or histone modifications, providing a disease-relevant platform for therapeutic discovery. For additional technical details and ordering information, please contact Ascent Research.
