The DUS1L Knockout Jurkat Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the DUS1L gene in the Jurkat T lymphoblastoid cell line. This polyclonal population enables loss-of-function studies by eliminating DUS1L-mediated tRNA dihydrouridylation without selecting a single clonal isolate, preserving population-level heterogeneity that can reveal broad functional consequences. The gene disruption is achieved through CRISPR/Cas9-mediated genome editing, providing a robust model for investigating the role of this poorly characterized tRNA-modifying enzyme in human T cells.
The host Jurkat cell line is a widely utilized model derived from the peripheral blood of a patient with acute lymphoblastic leukemia (ALL). These cells exhibit an immature T lymphoblastoid phenotype, constitutively active T cell receptor signaling, and high proliferative capacity, making them a standard system for T cell biology, leukemia research, and immune signal transduction studies. The leukemic origin of Jurkat cells additionally positions this knockout model at the intersection of basic tRNA biology and cancer cell pathophysiology.
DUS1L belongs to the dihydrouridine synthase family and is predicted to catalyze the NADPH-dependent reduction of uridine to dihydrouridine at specific positions within tRNA molecules. This modification increases tRNA structural flexibility and may influence codon?Canticodon interactions, translational elongation rates, and overall protein synthesis fidelity. Although the exact tRNA substrates of human DUS1L remain to be defined, its disruption is expected to alter the dihydrouridine landscape of the tRNA pool, potentially affecting translation elongation factors and the efficiency of ribosome transit. In T cells, such translational perturbations could impact the rapid protein synthesis required for activation, proliferation, and effector function.
Given the central role of translational control in immune cell activation, this DUS1L knockout model offers a unique tool to explore how tRNA modifications shape T cell responses. In the Jurkat leukemic context, altered translation may further influence oncogenic signaling networks or stress adaptation, providing insights into the overlapping mechanisms of immune function and malignancy. The polyclonal nature of the knockout population allows for the assessment of phenotype penetrance across a genetically diverse cell pool, increasing the robustness of functional conclusions.
Researchers can employ these cells in a range of experimental applications, including tRNA modification profiling by mass spectrometry or HPLC, polysome profiling to measure global translation efficiency, and flow cytometry-based assays for T cell activation markers. RT-qPCR and western blotting can monitor downstream effects on stress response proteins or translation-related factors. This product is ideally suited for functional genomics screens and mechanistic studies investigating the intersection of tRNA biology, translational control, and immune cell signaling. For custom inquiries or bulk ordering, please contact Ascent Research.
