The DYNC1LI1 Knockout Huh-7 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of Huh-7 cells with targeted disruption of the DYNC1LI1 gene. This product provides a genetically heterogeneous knockout pool that avoids the artifacts of clonal selection, suitable for population-level analyses of dynein light intermediate chain function. The editing strategy results in loss of functional protein expression, enabling robust modeling of dynein-related processes.
The Huh-7 hepatocellular carcinoma cell line, derived from a 57-year-old Japanese male, serves as a well-established model for hepatocyte biology and liver tumor biology. These cells retain hepatocyte-like features, including liver-specific gene expression and susceptibility to HCV replication, making them ideal for studying liver-specific cellular processes in a cancer context.
DYNC1LI1 encodes a light intermediate chain of cytoplasmic dynein 1, critical for retrograde transport by linking cargo adaptors to the motor complex. It interacts with dynein subunits DYNC1H1 and DYNC1I2, dynactin DCTN1, and adaptors BICD2 and HOOK1, while being regulated by LIS1, CDK5, and PLK1. Knockout impairs lysosomal positioning, endosome maturation, mitotic spindle assembly, and Golgi trafficking, primarily through disrupted motor processivity.
In Huh-7 cells, DYNC1LI1 loss has pronounced effects due to the liver’s dependence on efficient organelle trafficking. Disrupted lysosomal distribution can impair autophagy and metabolic waste clearance, processes often deregulated in hepatocellular carcinoma. Additionally, defective mitotic spindle orientation may promote chromosomal instability, contributing to tumor progression. This model thus links dynein dysfunction directly to hepatic tumor cell pathophysiology.
These polyclonal knockout cells are suited for lysosomal trafficking assays using LAMP1/2 immunofluorescence, autophagy flux measurement via LC3 turnover, live-cell imaging of organelle motility, and cell division analyses to assess spindle errors. The model also supports RNA-seq to identify transcriptional consequences of DYNC1LI1 disruption. For further information, please contact Ascent Research.
