The HNRNPDL Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human HAP1 near-haploid fibroblast-like cell line. This loss-of-function model features targeted disruption of the HNRNPDL gene, which encodes an RNA-binding protein involved in alternative splicing and mRNA stability. The polyclonal format provides a heterogeneous cell pool suitable for functional genomics without single-cell cloning, enabling studies of HNRNPDL??s role in circadian rhythmicity, RNA processing, and disease pathways.
The host HAP1 cell line is a human near-haploid fibroblast-like derivative of the KBM-7 chronic myeloid leukemia cell line, widely used in CRISPR-based functional genomics screens. Its near-haploid karyotype simplifies genetic manipulation and yields unambiguous knockout phenotypes. HAP1 cells maintain key characteristics and support diverse assays, including proliferation, reporter gene, and co-immunoprecipitation experiments, providing a clean genetic background devoid of compensatory gene duplications.
HNRNPDL encodes an RNA-binding protein that functions downstream of the circadian transcription factors CLOCK and BMAL1. It interacts with spliceosomal U1 and U2 snRNPs, as well as splicing factors HNRNPH1 and SRSF1, to modulate alternative splicing of key circadian genes such as PER2 and CRY1. Mechanistically, HNRNPDL binds pre-mRNA transcripts to influence splice site selection and mRNA stability, linking circadian control to cell proliferation. Knockout in HAP1 cells is expected to alter splicing patterns of clock-controlled genes, perturbing circadian rhythmicity and downstream cellular outputs.
In the HAP1 background, HNRNPDL knockout provides a robust model to dissect splicing-dependent regulation of circadian biology and RNA metabolism. Aberrant splicing of PER2 and CRY1 can be monitored by RT-qPCR or RNA-seq, while functional circadian rhythms can be assessed via luciferase reporter assays. The polyclonal population captures mutational heterogeneity relevant to physiological contexts. Moreover, HNRNPDL mutations are linked to limb-girdle muscular dystrophy 1G, myopathy, and cancer, making this model pertinent for disease-oriented research into RNA processing defects.
Key applications include functional genomics screens to identify HNRNPDL genetic interactors, transcriptome-wide splicing analyses via RNA-seq, and biochemical characterization of ribonucleoprotein complexes by co-immunoprecipitation. The model is also suited for drug screening assays targeting splicing modulation and proliferation assays for cancer studies. For further technical details or to place an order, please contact Ascent Research.
