DYNC2LI1 Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population providing a powerful loss-of-function model for the DYNC2LI1 gene. Comprising a heterogeneous pool of MES-OV cells with targeted disruptions at the DYNC2LI1 locus, this product enables functional studies without clonal isolation. The polyclonal format offers a broad representation of knockout variants, reducing clonal artifacts and facilitating robust population-level analyses.
The host MES-OV cell line is a human ovarian adenocarcinoma model derived from a patient with serous cystadenocarcinoma. It is widely employed to study epithelial ovarian cancer biology, including tumor progression, metastasis, and therapeutic responses. This clinically relevant background allows examination of DYNC2LI1 function within an oncogenic context.
DYNC2LI1 encodes a light intermediate chain of the dynein-2 motor complex essential for retrograde intraflagellar transport (IFT) in primary cilia. It interacts with dynein-2 subunits including DYNC2H1, DYNLRB1, and WDR34 to return ciliary proteins to the cell body. Transcriptional regulation by RFX2, RFX3, and FOXJ1 controls DYNC2LI1 expression, and its function influences downstream effectors of Hedgehog signaling such as GLI1, GLI2, PTCH1, and CCND1. Disruption of DYNC2LI1 impairs IFT retrograde flow, leading to defective Hedgehog signal transduction and ciliopathy phenotypes.
In MES-OV ovarian cancer cells, DYNC2LI1 knockout provides a unique model for dissecting ciliary and Hedgehog signaling roles in tumor biology. Primary cilia and Hedgehog pathway activity are implicated in cancer, yet their functions in ovarian cancer remain underexplored. This knockout system enables investigation of how disrupted ciliary trafficking alters Hedgehog output and cell cycle regulation in an oncogenic background.
Applications include mechanistic studies of ciliogenesis and IFT, modeling of short-rib thoracic dysplasia, and Hedgehog pathway investigation in cancer. Key assays comprise immunofluorescence for ciliary markers ARL13B and acetylated tubulin, Shh stimulation reporter assays, RT-qPCR for GLI1 and PTCH1, co-immunoprecipitation of dynein-2 components, and RNA-seq profiling. The polyclonal knockout cells also support drug screening for ciliopathy and Hedgehog pathway modulators. For further details, contact Ascent Research.
