The GOLGA2 Knockout DLD-1 Polyclonal Cells are a pooled population of DLD-1 cells that have been subjected to CRISPR/Cas9-mediated gene disruption targeting the GOLGA2 locus, generating a heterogeneous loss-of-function model. As a polyclonal product, this preparation encompasses a diverse array of edited alleles within the cell population, avoiding the single-clone biases associated with monoclonal lines and enabling robust assessment of GOLGA2 function across a spectrum of knockout efficiencies. This format is particularly suited for initial phenotypic screening, pooled functional genomics, and studies requiring representation of varied mutational outcomes in a colorectal cancer background.
The host cell model, DLD-1, is an established human colorectal adenocarcinoma epithelial cell line derived from a Dukes?? type C primary tumor. Widely employed in cancer biology, DLD-1 cells retain characteristic features of colorectal cancer, including dysregulated proliferation, invasive potential, and aberrant signaling pathways. Their adherent epithelial morphology and genetic stability make them a reliable system for investigating tumor cell behavior, drug responses, and the molecular underpinnings of colorectal carcinogenesis. This background provides a clinically relevant context for interrogating the role of Golgi-associated genes in malignancy.
GOLGA2 encodes GM130, a cis-Golgi matrix protein essential for Golgi stack organization, vesicle tethering, and microtubule nucleation. GM130 functions as a structural scaffold, interacting directly with p115 (USO1), GRASP65, AKAP450, syntaxin 5, ZW10, and RINT1 to maintain Golgi ribbon integrity and facilitate vesicular trafficking. Its activity is tightly regulated by mitotic phosphorylation, predominantly by CDK1 and PLK1, which drives Golgi disassembly during cell division. Downstream, GM130 influences microtubule organization at the Golgi via AKAP450, impacting directional cell migration, and participates in vesicle tethering complexes that mediate ER-to-Golgi and intra-Golgi transport. These molecular interactions place GOLGA2 at a nexus connecting Golgi architecture with cell motility and division.
Disruption of GOLGA2 in DLD-1 cells profoundly alters Golgi morphology, leading to fragmentation and impaired vesicular trafficking. Consequently, protein secretion and post-translational modifications are perturbed, and cell migration and invasion are markedly reduced due to defective microtubule nucleation and focal adhesion dynamics. Additionally, mitotic progression is compromised, manifesting as aberrant spindle assembly and cell cycle delays, phenotypes that are directly relevant to colorectal cancer cell behavior. The polyclonal knockout population captures the functional heterogeneity inherent to GOLGA2 loss, offering a model that reflects variable penetrance of Golgi-related defects and facilitating the study of cancer cell plasticity and adaptation.
This cell model is ideally suited for a broad range of research applications, including elucidation of Golgi structural biology, analysis of secretory pathway regulation, and investigation of mitotic checkpoints. Experimental approaches such as immunofluorescence microscopy to visualize Golgi fragmentation, transwell migration and invasion assays, cell cycle analysis by flow cytometry, RNA sequencing for transcriptomic profiling, and co-immunoprecipitation of GM130 interactors are all highly compatible with this system. Proliferation assays and western blotting for GM130 expression serve as routine readouts. For further information and ordering details, please contact Ascent Research.
