This product comprises pooled CRISPR/Cas9-edited HeLa polyclonal knockout cells targeting the ATXN7L2 gene. The polyclonal population harbors a diverse array of CRISPR-induced disruptions, generating a loss-of-function model that avoids clonal artifacts and maintains robust gene inactivation. These cells enable dissection of ATXN7L2-dependent chromatin remodeling and transcriptional regulation functions governed by the SAGA histone acetyltransferase complex, without requiring single-cell subcloning.
HeLa cells, derived from a cervical adenocarcinoma, are a widely employed human epithelial line. HPV18-positivity results in E6/E7 oncoprotein-mediated inactivation of the tumor suppressors p53 and Rb, deregulating cell cycle checkpoints and apoptosis. This permissive genetic context, combined with their rapid proliferation and well-characterized karyotype, establishes HeLa cells as an optimal host for CRISPR-based functional genomic studies.
ATXN7L2 encodes an integral subunit of the SAGA complex, a large multi-protein assembly that couples histone acetylation and deubiquitination to regulate RNA polymerase II-driven transcription. Within SAGA, ATXN7L2 directly interacts with TADA2A, TADA3, KAT2A (GCN5), TRRAP, SUPT3H, and additional core components to maintain structural integrity and enzymatic function. Through this platform, ATXN7L2 facilitates acetylation of histone H3, opening chromatin at target gene promoters and enabling transcriptional activation. Consequently, loss of ATXN7L2 impairs SAGA-dependent acetylation, disrupting gene expression programs controlled by transcription factors, cell cycle regulators, and stress signals, with downstream effects on neurological and cancer-related genes.
In the HeLa context, ATXN7L2 ablation probes the interplay between epigenetic regulation and oncogenic transformation. With p53 and Rb already inactivated by HPV oncoproteins, the additional loss of a pivotal SAGA subunit uncovers dependencies on histone acetyltransferase activity for proliferation and survival. This model is particularly relevant for studying cancers with frequent SAGA alterations and for dissecting chromatin dysregulation in neurological disorders linked to the ataxin-7 family. The polyclonal pool also reflects tumor heterogeneity, offering a clinically pertinent system for drug target validation.
These ATXN7L2 knockout cells support diverse functional readouts: Western blotting and immunofluorescence for protein loss verification, ChIP-qPCR for histone acetylation changes, and RNA-seq for transcriptome-wide profiling. Co-immunoprecipitation assesses SAGA complex integrity, while proliferation assays and flow cytometry quantify growth and cell cycle effects. The model is also suited for drug sensitivity screens targeting epigenetic vulnerabilities. For further details or custom gene-editing services, contact Ascent Research.
