The BAZ2A Knockout Jurkat Polyclonal Cells consist of a heterogeneous population of Jurkat-derived T lymphoblastoid cells with CRISPR/Cas9-mediated disruption of the BAZ2A gene. This polyclonal knockout format retains genetic diversity and is suitable for studying loss-of-function effects on rRNA transcription and chromatin remodeling without clonal bias. The model enables direct interrogation of BAZ2A function within an immune cell context.
Jurkat cells are a CD4+ T lymphoblastoid line established from acute T cell leukemia, providing a robust model for T cell receptor signaling and immune response. Their transformed phenotype and suspension growth make them ideal for investigating nucleolar biology in the context of lymphocyte proliferation and leukemogenesis.
BAZ2A is a core scaffold within the nucleolar remodeling complex (NoRC), partnering with the SNF2H ATPase to repress ribosomal RNA genes. It recruits histone deacetylase HDAC1 and DNA methyltransferase DNMT3b to rDNA promoters, catalyzing H3K9me2 deposition and de novo DNA methylation. Interaction with TTF-I anchors the NoRC complex to rDNA loci, ensuring site-specific silencing. Downstream, BAZ2A activity reduces pre-rRNA levels and ribosome biogenesis. Loss of BAZ2A disrupts this repressive axis, potentially derepressing rDNA and triggering nucleolar stress.
In Jurkat T cells, BAZ2A knockout links nucleolar function to T cell biology. Given the high proliferation of leukemic lymphocytes, impaired ribosome biogenesis may affect cell cycle progression and TCR signaling. BAZ2A is also implicated in epigenetic silencing in prostate and colon cancers, underscoring its relevance in oncogenesis. This model is thus valuable for studying acute lymphoblastic leukemia and the interplay between nucleolar stress and immune cell transformation.
The polyclonal knockout cells support diverse applications, including ChIP-qPCR for H3K9me2 at rDNA loci, RT-qPCR for pre-rRNA quantification, and western blotting for BAZ2A. Flow cytometry enables cell cycle analysis, while rDNA promoter reporter assays dissect BAZ2A-dependent repression. These cells facilitate investigation of epigenetic silencing, rRNA regulation, and cancer epigenetics, particularly in T-cell contexts. For additional information, contact Ascent Research.
