DNM1L Knockout HeLa Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout cell population targeting the DNM1L gene in the HeLa human cervical adenocarcinoma epithelial cell line. This product delivers a heterogeneous loss-of-function model for dynamin-1-like protein (Drp1), a key GTPase mediating mitochondrial and peroxisomal fission. The polyclonal format avoids single-clone selection artifacts and supports pooled functional screening.
The HeLa host line is a classic epithelial cancer model, originally derived from a cervical carcinoma. It is extensively characterized in signal transduction, drug response, and cell cycle studies, providing a reproducible platform for investigating mitochondrial dynamics in a cancer context.
Drp1, encoded by DNM1L, oligomerizes at mitochondrial outer membranes to execute fission, a process critical for network remodeling, mitophagy, and apoptosis. Upstream kinases CDK1, PKA, and CaMKII regulate Drp1 via phosphorylation, while receptors MFF, FIS1, MIEF1, and MIEF2 recruit it to organelles. Modifiers MARCH5 and SENP5 further tune activity. Drp1 assembly constricts mitochondria, and its loss induces elongated mitochondrial networks, impairing cytochrome c release, BAX/BAK activation, and ROS production. Interactions with GDAP1 and BCL2L1 integrate Drp1 into cell death signaling.
In HeLa cells, DNM1L knockout profoundly alters mitochondrial morphology and stress responses. HeLa cells depend on active fission for organelle partitioning during division and metabolic adaptation; disruption yields hyperfused mitochondria, compromising mitophagy and reshaping apoptotic sensitivity. This model serves as a tool for exploring mitochondrial contributions to cancer cell metabolism, drug resistance, and neurodegeneration-related pathways.
Applications include immunofluorescence imaging of mitochondrial networks, flow cytometric ROS measurement with MitoSOX, and ATP quantification for metabolic output. Co-immunoprecipitation assays probe Drp1 interaction with MFF, FIS1, and BAX. Western blotting and RT-qPCR confirm alterations in fission/fusion components such as OPA1, MFN1, and MFN2. The cells support apoptosis assays based on cytochrome c release and caspase activation, as well as chemosensitivity screens targeting mitochondrial function. For additional details, please contact Ascent Research.
