The KATNAL1 Knockout HT29 Polyclonal Cells are a genetically modified population of HT29 colorectal adenocarcinoma epithelial cells, generated by CRISPR/Cas9-mediated disruption of the human KATNAL1 gene. This polyclonal knockout product provides a loss-of-function model to study the biological roles of the KATNAL1-encoded protein, the catalytic subunit of the katanin microtubule-severing complex. The mixed-cell population enables robust and reproducible investigation of KATNAL1-dependent processes without the need for single-cell clone isolation, making it suitable for a wide range of cell biological and cancer research applications.
HT29 cells originate from a colorectal adenocarcinoma of a female patient and exhibit an adherent epithelial morphology with the capacity for both enterocytic and mucous differentiation. This cell line is widely employed as an intestinal epithelial model for studying epithelial differentiation, mucus secretion, and colorectal cancer progression. Its established genetic background and well-characterized signaling networks make it a relevant host for targeted gene disruption, allowing dissection of molecular pathways that govern microtubule organization and tumor cell behavior in a gastrointestinal malignancy context.
KATNAL1 encodes the catalytic subunit of the katanin complex, a microtubule-severing AAA ATPase that actively remodels the cytoskeleton. KATNAL1 is regulated by mitotic kinases including CDK1, Aurora A, and PLK1, which control its severing activity during cell cycle progression. It interacts with KATNB1, the katanin regulatory subunit, and microtubule-associated proteins such as ASPM, to localize severing at mitotic spindles, ciliary axonemes, and throughout the cytoplasmic microtubule network. Downstream, KATNAL1 activity impacts microtubule organization, mitotic spindle formation, ciliary disassembly, and overall cellular morphology. Representative pathway components linking KATNAL1 to microtubule dynamics include ??/??-tubulin, KATNB1, CDK1, Aurora A, PLK1, and ASPM.
In HT29 colorectal cancer cells, knockout of KATNAL1 is expected to impair microtubule severing, thereby disrupting mitotic spindle assembly, cytokinesis, and ciliogenesis. Given the ability of HT29 cells to undergo enterocytic and mucous differentiation, KATNAL1 loss may also alter epithelial polarization and secretory functions that depend on microtubule-based transport and signaling. This model provides a physiologically relevant platform for dissecting how microtubule-severing activity contributes to colorectal cancer cell division, motility, and the cytoskeletal remodeling that underlies tumor progression and metastasis.
This polyclonal knockout cell population is suited for a variety of experimental approaches to interrogate KATNAL1 function. Researchers can employ immunofluorescence microscopy to examine microtubule and spindle morphology, live-cell imaging to track mitotic progression, and flow cytometry for cell cycle analysis. Additional methods such as microtubule sedimentation assays, ciliogenesis induction and quantification, western blotting, and functional assays for cell migration, invasion, and proliferation allow comprehensive functional characterization. These applications position the KATNAL1 Knockout HT29 Polyclonal Cells as a valuable tool for mechanistic studies and drug discovery targeting microtubule regulators in colorectal cancer. For additional information or technical support, please contact Ascent Research.
