BAZ1A Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the Jurkat T-lymphoblast line, featuring targeted disruption of the BAZ1A gene. This loss-of-function model is designed for studies of chromatin remodeling, DNA replication, and DNA damage response. The polyclonal format reduces clonal selection artifacts and maintains genetic heterogeneity for population-level analyses.
Jurkat cells are a well-established model for T-cell receptor signaling, cytokine production, and immune regulation. Originating from an acute T-cell leukemia, these lymphoblasts are integral to T-ALL research and exhibit rapid proliferation, making them amenable to high-throughput functional genomics and drug sensitivity assays.
BAZ1A is a core subunit of the ACF/WSTF-ISWI ATP-dependent chromatin remodeling complex that partners with SMARCA5 to regulate nucleosome spacing and assembly. This activity is essential for DNA replication fork progression, transcriptional regulation, and DNA repair. BAZ1A is recruited to chromatin via interactions with PCNA at replication forks and Ku70/Ku80/DNA-PKcs at damage sites. Upstream DNA damage and replication stress signals, including ATM/ATR-mediated phosphorylation and E2F transcription, control BAZ1A function. Its disruption impairs replication fork stability, alters nucleosome occupancy, and sensitizes cells to replication stress, culminating in genomic instability.
In Jurkat cells, loss of BAZ1A compromises the coordination between chromatin dynamics and T-cell functions. The acute proliferation of these lymphoblasts demands efficient replication and repair; thus, BAZ1A knockout renders them vulnerable to DNA damage and cell cycle arrest. This is particularly relevant to T-ALL, where genomic instability is a hallmark. Disrupted heterochromatin maintenance may further impact gene expression programs governing cytokine secretion and TCR signaling. Consequently, this model offers a unique platform to dissect how chromatin remodeling complexes influence leukemogenesis and T-cell biology.
This cell population is applicable to a range of functional assays. DNA fiber assays can measure replication fork speed, while RT-qPCR quantifies origin firing changes. ChIP-qPCR enables mapping of nucleosome occupancy and histone modifications. Co-immunoprecipitation and Western blotting permit analysis of BAZ1A interaction with SMARCA5 and PCNA, and of damage signaling through ATM/ATR/??H2AX. Flow cytometry facilitates cell cycle profiling, and viability assays under replication stress (e.g., hydroxyurea) support synthetic lethal screening. For further information, please contact Ascent Research.
