The DTWD2 Knockout MES-OV Polyclonal Cells product is a heterogeneous population of MES-OV cells engineered via CRISPR/Cas9-mediated disruption of the DTWD2 gene. This polyclonal knockout format captures a diverse array of gene disruptions arising from bulk editing, providing a robust loss-of-function model for studying DTWD2 biology without necessitating clonal isolation. The absence of functional DTWD2 protein enables researchers to interrogate its role in cellular processes in a physiologically relevant genomic context.
MES-OV is a human ovarian serous adenocarcinoma cell line derived from a patient tumor, retaining epithelial characteristics and reflecting the molecular hallmarks of high-grade serous ovarian cancer. It serves as a well-characterized in vitro model for investigating oncogenic signaling, therapeutic resistance, and metastatic behavior. The use of MES-OV as the host for DTWD2 knockout ensures that findings are directly relevant to ovarian tumor biology, providing a disease-specific platform for functional studies.
DTWD2 is predicted to function as a tRNA wybutosine-synthesizing enzyme, specifically modifying phenylalanine tRNA (tRNA-Phe) at position 37. This modification is part of a sequential pathway that includes TYW1, TYW2, TYW3, and TYW4, where DTWD2 acts downstream of TYW1?CTYW3 and upstream of TYW4. By installing the wybutosine moiety, DTWD2 ensures proper codon?Canticodon pairing and translational reading frame maintenance. Disruption of this modification can lead to ribosomal frameshifting and altered translation efficiency of proteins enriched in phenylalanine codons, potentially impacting cellular proteostasis and stress adaptation.
In the context of MES-OV ovarian cancer cells, DTWD2 knockout allows dissection of the contribution of tRNA modifications to malignant phenotypes. Although DTWD2 has not been directly linked to cancer, dysregulation of tRNA modifications is increasingly implicated in tumorigenesis and drug resistance. This model enables the assessment of how loss of wybutosine synthesis affects proliferation, apoptosis, and migration in ovarian carcinoma cells, shedding light on the translational control mechanisms that sustain aggressive cancer cell behavior.
This polyclonal knockout cell population is suitable for a variety of molecular and cellular assays, including RT-qPCR and western blotting to verify DTWD2 disruption, LC-MS for direct measurement of tRNA wybutosine levels, and polysome profiling to monitor translation. Functional assays such as proliferation, apoptosis, and migration tests reveal the phenotypic consequences of DTWD2 loss, while puromycin incorporation provides a global translation readout. The model also accelerates drug discovery efforts targeting the tRNA modification machinery. For technical inquiries and ordering, please contact Ascent Research.
