BCORL1 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population designed to disrupt the BCORL1 gene in the HAP1 cell line. This non-clonal knockout pool enables flexible functional studies without the constraints of monoclonal isolation, providing a heterogeneous model suitable for population-level assays and pooled genetic screens. The product is intended for researchers investigating BCORL1 function in epigenetic silencing and hematologic malignancies.
The HAP1 host cell line is a near-haploid, fibroblast-like adherent cell line derived from a chronic myeloid leukemia (CML) patient. Its haploid genome facilitates efficient single-allele disruption, allowing straightforward generation of functional knockouts. The CML origin supplies a hematologic background relevant to myeloid disease, and the cells retain key signaling features including BCR-ABL1 expression. HAP1 cells are amenable to high-throughput drug screening, colony formation assays, and population-based genetic perturbation.
BCORL1 encodes a transcriptional corepressor that functions as a core component of the non-canonical Polycomb repressive complex 1 (PRC1.1). Within this complex, BCORL1 partners with PCGF1, RING1B (or RING1A), and KDM2B to catalyze monoubiquitination of histone H2A at lysine 119 (H2AK119ub), a mark of transcriptionally repressed chromatin. The complex is recruited to target loci by transcription factors such as BCL6 or through KDM2B binding to unmethylated CpG islands, leading to silencing of developmental regulators including HOX gene clusters. BCORL1 disruption impairs H2AK119ub deposition and derepresses Polycomb target genes, altering gene expression programs critical for hematopoiesis and frequently dysregulated in leukemia.
In the haploid HAP1 system, BCORL1 knockout provides a clean loss-of-function model to study epigenetic deregulation. This is particularly relevant to acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS), where BCORL1 mutations are recurrent and linked to altered chromatin landscapes. The CML-derived background allows examination of interactions between BCR-ABL1 signaling and PRC1.1-mediated repression. Use of polyclonal knockout cells avoids clonal artifacts and captures population-level responses in proliferation, apoptosis, and drug sensitivity assays.
Typical applications include western blotting for BCORL1 and H2AK119ub levels, ChIP-seq for chromatin mark profiling, RNA-seq or RT-qPCR for target gene expression, and flow cytometry for differentiation marker analysis. Functional assays such as colony formation, drug sensitivity testing with epigenetic inhibitors, and genome-wide CRISPR screens are readily supported. The polyclonal format is especially suited for pooled screens and population-level pharmacogenomics. For technical inquiries or ordering, please contact Ascent Research.
