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C-Glycosides are important natural products with various bioactivities. In plant biosynthetic pathways, the C-glycosylation step is usually catalyzed by C-glycosyltransferases (CGTs), and most of them prefer to accept uridine 5′-diphosphate glucose (UDP-Glc) as sugar donor. No CGTs favoring UDP-rhamnose (UDP-Rha) as sugar donor has been reported, thus far. Herein, we report the first selective C-rhamnosyltransferase VtCGTc from the medicinal plant Viola tricolor. VtCGTc could efficiently catalyze C-rhamnosylation of 2-hydroxynaringenin 3-C-glucoside, and exhibited high selectivity towards UDP-Rha. Mechanisms for the sugar donor selectivity of VtCGTc were investigated by molecular dynamics (MD) simulations and molecular mechanics with generalized Born and surface area solvation (MM/GBSA) binding free energy calculations. Val144 played a vital role in recognizing UDP-Rha, and the V144T mutant could efficiently utilize UDP-Glc. This work provides a new and efficient approach to prepare flavonoid C-rhamnosides such as violanthin and iso-violanthin.

Summary: Spatial disorientation (SD) is the main contributor to flight safety risks, but research progress in animals has been limited, impeding a deeper understanding of the underlying mechanisms of SD. This study proposed a method for constructing and evaluating a vestibular SD mouse model, which adopted coupled rotational stimulation with visual occlusion. Physiological parameters were measured alongside behavioral indices to assess the model, and neuronal changes were observed through immunofluorescent staining. The evaluation of the model involved observing decreased colonic temperature and increased arterial blood pressure in mice exposed to SD, along with notable impairments in motor and cognitive function. Our investigation unveiled that vestibular SD stimulation elicited neuronal activation in spatially associated cerebral areas, such as the hippocampus. Furthermore, transcriptomic sequencing and bioinformatics analysis revealed the potential involvement of Slc17a6 in the mechanism of SD. These findings lay a foundation for further investigation into the molecular mechanisms underlying SD.