BCL7A Knockout Jurkat Polyclonal Cells are a heterogeneous pool of Jurkat T lymphocytes with CRISPR/Cas9-mediated disruption of the BCL7A gene, providing a polyclonal loss-of-function model. This cell population contains diverse BCL7A mutations, enabling studies without clonal artifacts. BCL7A encodes a subunit of the SWI/SNF chromatin remodeling BAF complex implicated in transcriptional regulation and tumor suppression.
The host Jurkat cell line is an immortalized human T lymphocyte line originally derived from the peripheral blood of a 14-year-old male with acute T-cell leukemia. Widely utilized as a model for T-cell signaling, activation, and leukemia biology, Jurkat cells retain many features of T lymphocytes, including surface markers and signaling cascades. This well-characterized background provides a relevant context for investigating the role of chromatin remodeling complexes in T-cell function and malignant transformation.
BCL7A functions as a core component of the BAF (BRG1/BRM-associated factor) complex, a mammalian SWI/SNF ATP-dependent chromatin remodeling assembly that modulates DNA accessibility to regulate gene expression. Within this complex, BCL7A interacts with key subunits including BRG1, BAF155, and BAF170, and forms heterodimers with related proteins BCL7B and BCL7C. The BAF complex is recruited to specific genomic loci to facilitate chromatin reorganization, thereby influencing transcription of genes critical for cell proliferation and differentiation. Downstream targets of BCL7A-containing BAF complexes may include MYC and CCND1, linking BCL7A to cell cycle control. Loss of BCL7A is associated with impaired chromatin remodeling and altered transcriptional profiles, consistent with its proposed role as a tumor suppressor in various cancers.
In the Jurkat T-cell context, BCL7A knockout disrupts BAF complex stoichiometry and function, potentially leading to dysregulated expression of genes involved in T-cell activation, proliferation, and apoptosis. This model enables dissection of SWI/SNF-mediated chromatin regulation in a lymphoid lineage, recapitulating aspects of T-cell leukemia pathogenesis where BAF complex mutations are recurrent. The polyclonal nature of the knockout population reflects the heterogeneity of gene editing outcomes, providing a robust system for evaluating overall pathway dependencies rather than relying on a single clonal isolate.
These cells support biochemical characterization of BAF complex assembly, ChIP-qPCR for promoter occupancy, and RNA-seq transcriptome profiling. Proliferation, apoptosis, and cell cycle assays enable functional investigation of BCL7A??s tumor-suppressive role. This polyclonal knockout model advances understanding of chromatin remodeling in T-cell malignancies and BAF complex vulnerabilities. For additional technical support and ordering information, please contact Ascent Research.
