The DUS3L Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting DUS3L in the Jurkat T lymphocyte line. This genetically heterogeneous pool contains loss-of-function mutations in DUS3L, enabling functional studies of tRNA dihydrouridine modification. The knockout model is generated via CRISPR/Cas9-mediated gene disruption, providing a resource for dissecting DUS3L biology in immortalized T cells.
The Jurkat cell line is an immortalized human T lymphocyte line derived from peripheral blood of a 14-year-old male with acute lymphoblastic leukemia (ALL). Widely used to study T cell signaling and apoptosis, Jurkat cells exhibit features such as constitutive NF-??B activation and sensitivity to Fas-mediated death. This background offers a context for examining tRNA modifications in T-cell function and leukemogenesis.
DUS3L encodes a putative tRNA dihydrouridine synthase that catalyzes NADPH-dependent reduction of uridine to dihydrouridine at specific tRNA positions. Dihydrouridine modification enhances tRNA flexibility and stability, modulating translation efficiency. DUS3L operates downstream of unknown regulators, possibly general transcription factors or MYC, and produces modified tRNAs that may decode transcripts with specific codon biases. Interacting partners remain uncharacterized, but DUS3L likely associates with other tRNA-modifying enzymes or RNA-binding proteins.
In Jurkat T cells, DUS3L disruption enables investigation of how dihydrouridine-modified tRNAs influence proliferation, apoptosis, and signal transduction pathways such as those downstream of the T-cell receptor. Because Jurkat cells model acute T-cell leukemia, this knockout system may illuminate how tRNA modification imbalances contribute to leukemic cell survival and drug resistance. The polyclonal nature captures a range of mutational outcomes, allowing observation of dominant biological effects.
Researchers can employ these cells for functional dissection of tRNA modification via dihydrouridine profiling by mass spectrometry or HPLC, global translation measurement by puromycin incorporation, and assessment of cell proliferation (WST-8) and apoptosis (Annexin V/PI flow cytometry). Knockout confirmation can be performed by Western blot and RT-qPCR. This model is valuable for screening campaigns to identify genes and pathways sensitive to altered translation control in T-cell leukemia. For more information, please contact Ascent Research.
