The EED Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human T-lymphocyte line, designed to disrupt expression of the EED gene. This polyclonal pool contains a heterogeneous mixture of edited cells with distinct loss-of-function mutations, providing a robust and unbiased model for studying EED-mediated epigenetic regulation. By avoiding clonal selection, the polyclonal format minimizes artifacts and captures a broad spectrum of genetic consequences, ensuring reliability in functional assays. The product offers a foundational tool for investigating PRC2-dependent gene silencing and its role in T-cell biology and leukemia.
The Jurkat cell line is an immortalized human T-lymphocyte line originally established from a 14-year-old male patient with T-cell acute lymphoblastic leukemia (T-ALL). Jurkat cells are widely recognized as a canonical model for T-cell signaling, apoptosis, and activation, and are extensively used in immunological and cancer research. Their leukemic origin makes them particularly relevant for studying oncogenic mechanisms and epigenetic alterations that drive malignant transformation. The EED knockout in this background offers a unique opportunity to dissect PRC2 function in a disease-relevant cellular environment that closely mirrors the pathogenesis of T-ALL.
EED is an indispensable core component of Polycomb Repressive Complex 2 (PRC2), forming a heterotrimer with EZH2 and SUZ12 that catalyzes H3K27me3, a repressive histone mark. EED directly binds pre-existing H3K27me3 via its WD40 domain, allosterically activating EZH2 and propagating the mark. EED knockout abrogates PRC2 function, depleting H3K27me3 and derepressing Polycomb targets such as HOX gene clusters, CDKN2A, and other tumor suppressors. PRC2 is regulated by upstream factors including MYC and lncRNAs HOTAIR and XIST, and interacts with cofactors AEBP2 and JARID2. The resulting loss of H3K27me3 disrupts transcriptional programs controlling proliferation, differentiation, and survival.
In the Jurkat T-ALL context, PRC2-mediated H3K27me3 is implicated in maintaining the leukemic phenotype by repressing tumor suppressor and pro-differentiation genes. Disruption of EED abrogates this silencing, potentially reactivating genes such as CDKN2A and HOX family members, which can trigger growth arrest, apoptosis, or differentiation. This knockout model enables systematic dissection of EED-dependent epigenetic dependencies in T-ALL and provides a platform for evaluating therapeutic strategies targeting PRC2, such as EED or EZH2 inhibitors. Moreover, it facilitates studies of how Polycomb silencing intersects with T-cell receptor signaling and cytokine responses, offering insights into immune cell regulation.
The EED Knockout Jurkat Polyclonal Cells are suitable for diverse applications including investigation of PRC2-mediated epigenetic regulation in leukemia, functional validation of EED as a drug target, and profiling of H3K27me3 landscapes. Researchers can confirm loss of EED and global H3K27me3 by Western blotting, assess H3K27me3 occupancy by ChIP-qPCR, and analyze transcriptomic changes via RNA-seq. Flow cytometry for T-cell activation markers (CD69, CD25), proliferation assays, and drug sensitivity screens with PRC2 inhibitors (e.g., tazemetostat) are readily performed. For further information, please contact Ascent Research.
