The BAZ2B Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population engineered for loss-of-function studies of the human BAZ2B gene. This heterogeneous pool of HAP1 cells with targeted disruptions enables robust functional screening and investigation of BAZ2B-dependent mechanisms without clonal selection. Validated as a versatile tool for epigenetic and cancer research, these cells facilitate high-throughput assays and pathway dissection.
The host HAP1 cell line is a near-haploid chronic myeloid leukemia (CML) line derived from KBM-7, exhibiting adherent fibroblast-like morphology and a predominantly haploid karyotype. Its simplified genome permits efficient single-allele knockout, minimizing wild-type gene copy interference. Widely used for oncogenic signaling and drug sensitivity studies, HAP1 provides a well-characterized leukemia model.
BAZ2B acts as a scaffold in the nucleolar remodeling complex (NoRC), which silences ribosomal RNA genes through chromatin modification. It recruits SMARCA5 (SNF2H) ATPase, histone deacetylases HDAC1/2, and DNA methyltransferases via interaction with BAZ2A/TIP5, establishing repressive H3K9me3 and DNA methylation marks. Transcriptional regulation by MYC and E2F factors, along with phosphorylation by ATM/ATR kinases, links BAZ2B to DNA damage signaling, nucleolar integrity, and the p53 pathway.
In the near-haploid HAP1 background, CRISPR/Cas9-mediated BAZ2B disruption yields essentially complete gene knockout at the population level, avoiding residual functional alleles. This genetic clarity enables direct examination of BAZ2B??s role in rDNA epigenetic silencing, heterochromatin maintenance, and nucleolar stress responses, free from compensatory diploid mechanisms. The model is thus ideally suited for dissecting nucleolar scaffolding functions in a leukemia milieu.
These cells support a variety of assays: ChIP-qPCR for H3K9me3 at rDNA loci, RNA-seq to profile rRNA expression changes, co-immunoprecipitation of NoRC components, immunofluorescence for nucleolar morphology, and colony formation or viability assays after DNA damage. They are a valuable resource for functional genomic screens to identify synthetic lethal interactions in acute myeloid leukemia and other cancers with BAZ2B overexpression. For additional information, please contact Ascent Research.
