The DYNC2LI1 Knockout HAP1 Polyclonal Cells represent a CRISPR/Cas9-mediated gene-disrupted polyclonal population targeting the human DYNC2LI1 gene in the HAP1 cell line. This product provides a loss-of-function model to study the role of DYNC2LI1 in cellular processes. The polyclonal nature offers a heterogeneous knockout pool, suitable for studying pooled genetic effects without clonal isolation.
The host HAP1 cell line is a near-haploid human cell line derived from the chronic myeloid leukemia cell line KBM-7 (male origin). Its near-haploid karyotype simplifies genetic studies by reducing the complexity of gene redundancy, making it an optimal system for knockout-based investigations. HAP1 cells have been widely adopted as a robust platform for gene function analysis, drug screening, and pathway dissection.
DYNC2LI1 encodes a dynein light intermediate chain essential for retrograde intraflagellar transport (IFT) within cilia. Mechanistically, the protein links the dynein-2 motor (interacting with DYNC2H1) to the IFT-A complex, including IFT122, IFT140, and IFT144, facilitating transport of cargo from the ciliary tip to the cell body. This function is critical for ciliogenesis and Hedgehog signal transduction. DYNC2LI1 acts downstream of ciliary trafficking signals and the IFT-B complex. Hedgehog signaling, initiated by Sonic Hedgehog (SHH) binding to Patched1 (PTCH1), relieves repression of Smoothened (SMO), leading to activation of GLI transcription factors (GLI1, GLI2, GLI3). DYNC2LI1-mediated retrograde transport is required for proper GLI processing and SUFU-mediated repression, thus controlling target gene expression. DYNC2LI1 also interacts with TCTEX1D2 to regulate dynein-2 activity.
In the HAP1 near-haploid background, DYNC2LI1 disruption is expected to cause defective ciliogenesis and aberrant Hedgehog signaling, providing a clear phenotype for functional interrogation. The haploid state amplifies the loss-of-function effects, enabling unambiguous dissection of DYNC2LI1’s role in retrograde transport and ciliary-dependent pathway regulation.
This polyclonal knockout model is suitable for ciliopathy disease modeling (e.g., short-rib polydactyly syndrome, asphyxiating thoracic dystrophy), Hedgehog signaling studies, genetic interaction screens, and drug sensitivity assays. Typical experiments include immunofluorescence for ciliary markers, RT-qPCR of Hedgehog targets (GLI1, PTCH1), Western blotting for GLI processing, ciliogenesis assays, and flow cytometry for cell cycle effects. These cells facilitate exploration of DYNC2LI1 as a therapeutic target. For further details, please contact Ascent Research.
