BAZ1A Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function studies of the BAZ1A gene in a human colorectal adenocarcinoma model. The product provides a heterogeneous pool of HT29 cells carrying diverse CRISPR/Cas9-mediated disruptions in the BAZ1A locus, enabling researchers to interrogate the functional consequences of BAZ1A deficiency without clonal selection. This polyclonal format preserves genetic diversity and avoids clonal artifacts, making it suitable for population-level analyses of chromatin remodeling and gene regulation.
HT29 is a well-characterized human colorectal adenocarcinoma cell line derived from a primary tumor, exhibiting epithelial morphology and the capacity for enterocyte-like differentiation under appropriate culture conditions. These cells serve as a widely accepted model for colon cancer biology and intestinal epithelial differentiation, recapitulating key aspects of colorectal tumorigenesis and normal intestinal crypt physiology. The HT29 background offers a physiologically relevant context to examine how BAZ1A-dependent chromatin dynamics influence malignant phenotypes and differentiation programs.
BAZ1A encodes the ATP-utilizing chromatin assembly and remodeling factor ACF1, a non-catalytic subunit of the ISWI chromatin remodeling complex. It interacts with the ATPase SMARCA5 to harness ATP hydrolysis for sliding nucleosomes along DNA, thereby modulating chromatin accessibility. BAZ1A forms complexes with histone H3 and acetylated histones, linking nucleosome positioning to transcriptional regulation and DNA replication. Upstream, its activity is regulated by cell cycle cues, including E2F transcription factors and DNA damage signals. Downstream, BAZ1A-mediated remodeling controls access of transcription machinery to target promoters and replication origins, influencing gene expression programs critical for proliferation and cell fate decisions.
In HT29 colorectal cancer cells, disruption of BAZ1A is expected to impair ISWI complex function, leading to genome-wide alterations in nucleosome positioning and chromatin architecture. This perturbation can dysregulate transcriptional networks governing cell cycle progression, differentiation, and survival, providing a platform to dissect the role of ATP-dependent chromatin remodeling in colorectal cancer pathogenesis. As BAZ1A is implicated in bromodomain-associated cancers, this knockout model offers a valuable tool for investigating epigenetic vulnerabilities and the interplay between nucleosome sliding and oncogenic signaling in intestinal epithelial cells.
This polyclonal knockout product is applicable to a range of chromatin-focused assays. Researchers can profile histone modifications via ChIP-seq, map chromatin accessibility changes using ATAC-seq, and assess transcriptome-wide effects through RNA-seq. Western blotting confirms BAZ1A protein loss, while cell proliferation assays evaluate functional consequences. The model is also suited for epigenetic drug screening to identify compounds that exploit synthetic lethality with BAZ1A deficiency. For additional information or custom requests, please contact Ascent Research.
