Structural insights into the Urm1-Uba4 pathway and its biological roles
Ubiquitin-related modifier 1 (Urm1) is a unique and evolutionarily conserved member of the ubiquitin-like protein (UBL) family that represents a molecular link between ancestral sulfur carrier proteins (SCPs) and canonical eukaryotic UBLs. Urm1 is required for the thiolation of tRNAs and a non-canonical post-translational modification, called 'urmylation'. Activation of Urm1 by its E1-like enzyme, ubiquitin-like protein activator 4 (Uba4), involves the sequential adenylation, thioesterification, and thiocarboxylation of Urm1's C-terminus. Thereby, Urm1 can provide sulfur for the tRNA modification reaction or catalyze its conjugation to target proteins through a mechanism that is independent of E2-conjugating enzymes and E3 ligases. Recent structural studies have resolved several key intermediates of the fungal Uba4-Urm1 system, shedding light onto its two distinct subdomains and their dynamical interplay. Notably, Urm1 also interacts with several additional up- or downstream partners of the two pathways. Foremost, urmylation couples an UBL-conjugation reaction with the persulfidation of a cysteine residue in the target proteins. This protective oxidative post-translational modification underscores Urm1's central role in redox regulation and cellular stress responses. Here, we aim to summarize the most recent mechanistic insights and structural advances in the eukaryotic Urm1-Uba4 pathway.
Authors
- Anna Biela (ORCID: https://orcid.org/0000-0001-6142-6759)
- Keerthiraju Ethiraju Ravichandran (ORCID: https://orcid.org/0000-0003-2568-1343)
- Dominika Kwaśna (ORCID: https://orcid.org/0000-0002-6792-7703)
- Sebastian Glatt
Institutions
- Jagiellonian University (PL)
- University of Veterinary Medicine Vienna (AT)
- Postgraduate School of Molecular Medicine (PL)
Publication Details
- Journal
- Essays in Biochemistry
- Published
- 2025-12-01
- DOI
- https://doi.org/10.1042/ebc20253041
- Primary Topic
- RNA modifications and cancer
- Type
- article
- Field-Weighted Citation Impact
- 0.00