ArticleBiotechnology journal2026
Xylt2 Knockout Eliminates O-Xylosylation and Enhances Bone Morphogenetic Protein 2 Production in Chinese Hamster Ovary Cells.
Article in Biotechnology journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
O-xylosylation of glycine-serine (GS) linkers in multispecific antibodies or fusion proteins introduces product heterogeneity, posing critical challenges for biomanufacturing quality control and elevating potential immunogenicity risks. This post-translational modification is primarily catalyzed by xylosyltransferase 2 (Xylt2) in chinese hamster ovary (CHO) cells. To address this, we generated Xylt2-deficient CHO cells via both clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9) and zinc finger nuclease (ZFN)-mediated gene knockout, which resulted in the complete elimination of O-xylosylation as verified by mass spectrometry in a GS linker-containing bispecific antibody. Furthermore, because heparan sulfate proteoglycans (HSPGs), key cell-surface receptors for ligand binding and internalization, rely on O-xylosylation for their proper biosynthesis and function, the Xylt2 knockout also enhanced the titer of human bone morphogenetic protein 2 (hBMP2), which undergoes HSPG-dependent cellular uptake, with up to a 2.5-fold increase from 9.62 to 34.09 µg/mL in engineered cells compared to wild-type CHO controls. Collectively, our results demonstrate that Xylt2-deficient cell lines provide a genetic approach to produce recombinant proteins without O-xylosylation, as well as for enhancing the titer of hBMP2.
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