The DYNC1LI1 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated through target-gene disruption of the human DYNC1LI1 locus in HeLa cells. This product provides a loss-of-function model for the cytoplasmic dynein-1 light intermediate chain 1, enabling investigation of its roles in intracellular transport, mitosis, and organelle positioning. The polyclonal population retains genetic heterogeneity typical of CRISPR-edited pools, offering a physiologically relevant context for studying dynein-dependent processes without clonal artifacts.
The HeLa host cell line is an aneuploid, HPV18-positive cervical adenocarcinoma epithelial line originally isolated from a 31-year-old African American woman. Widely used for cancer biology and cell cycle research, HeLa cells express telomerase and harbor integrated HPV18 DNA, which drives sustained proliferation. This well-characterized model provides a robust platform for studying oncogenic signaling, cytoskeletal dynamics, and cell division, making it an ideal context for interrogating dynein-mediated functions.
DYNC1LI1 encodes a light intermediate chain of the cytoplasmic dynein-1 motor complex, acting as a cargo-binding adaptor that couples dynein to dynactin and specific cargoes. It interacts directly with the dynactin complex, BICD2, RAB7A, LIS1, and NDE1 to regulate minus-end-directed transport along microtubules. The protein is regulated by upstream factors including PLK1 and NDEL1, and its activity influences the positioning of downstream targets such as late endosomes, lysosomes, the Golgi complex, and mitotic spindles. Through these interactions, DYNC1LI1 plays a central role in endosomal maturation, autophagic degradation, and mitotic spindle assembly, linking microtubule-based transport to cell cycle progression and organelle homeostasis.
In HeLa cells, knockout of DYNC1LI1 disrupts the precise spatial organization of organelles and impairs mitotic progression, leading to defects in spindle orientation and chromosome segregation. The loss-of-function model reveals the dependency of cancer cell migration and invasion on dynein-mediated trafficking, as well as the coordination between the dynein and kinesin-1 (KIF5B) motor systems. Because HeLa cells are a model of cervical adenocarcinoma, this knockout system is particularly relevant for dissecting how dynein dysfunction contributes to tumorigenic phenotypes, including aberrant cell proliferation and metastatic potential.
This polyclonal knockout product is suited for a range of advanced applications, including live-cell imaging of organelle dynamics, high-content screening for dynein modulators, and biochemical validation via western blot, immunofluorescence, and co-immunoprecipitation. Researchers can employ mitotic index assays, endosomal acidification assays, and scratch wound migration assays to quantify phenotypic changes resulting from DYNC1LI1 deficiency. The cells also provide a tool for neurodevelopmental disease modeling and studies of ciliopathies, as dynein light intermediate chains are implicated in neuronal axonal transport. For additional information or customized support, please contact Ascent Research.
