Abstract text: Uridine diphosphate (UDP)–conjugated glucuronic acid (GlcA) serves as a precursor for several other cell wall–building substrates synthesized in the Golgi apparatus, including UDP-galacturonic acid (GalA), UDP-arabinose (UDP-Ara), and UDP-xylose. These nucleotide sugars are essential components of major cell wall polymers such as pectins, hemicelluloses, and arabinogalactan proteins. In Arabidopsis, the import of UDP-uronic acids into the Golgi apparatus relies on the activity of the UDP-uronic acid transporter 1 (UUAT1) and likely its four homologs. Using the liverwort model organism Marchantia polymorpha, which exhibits significantly reduced genetic redundancy,  this study investigates the physiological consequences of manipulating the expression of the sole UUAT homolog (MpUUAT1). The transport activity of MpUUAT1 was verified in vitro, and preliminary results indicate that loss-of-function mutants may be lethal. In contrast, downregulation of MpUUAT1 via microRNAs leads to abnormal phenotypes in plants accompanied by alterations in their nucleotide sugar composition. Similarly, MpUUAT1 overexpression also causes alterations in the cell wall and changes in the abundance of cell wall epitopes. Taken together, our results provide new insights into the importance of UDP-uronic acids for cell wall biosynthesis and the complex metabolic flux within nucleotide sugar interconversion pathways in plants.