Ubiquitination is a post-translational modification carrying broad signal transduction functions in eukaryotic cells. The process is dependent on the attachment of the small protein ubiquitin to a substrate via the catalysis of E3 ubiquitin ligases. Ubiquitin is most commonly conjugated onto substrate protein lysine residues, resulting in a multitude of consequences, for example, substrate degradation, trafficking and association with other proteins. Intriguingly, recent studies demonstrate that specialised E3 ligases can use substrate serine and threonine residues as ubiquitination sites [1, 2]. The repertoire of the ubiquitin machinery is further expanded by the discovery of host cells modifying Salmonella lipopolysaccharide (LPS) with ubiquitin earlier this year [3].
Heme-oxidised IRP2 ubiquitin ligase-1L (HOIL-1L) belongs to the RING-between-RING (RBR) E3 ligase family. HOIL-1L constitutes part of the linear ubiquitin chain assembly complex (LUBAC), a central regulator of innate immune signalling. Recent evidence suggests that HOIL-1L regulates LUBAC activity via ubiquitination of serine or threonine residues[4, 5]. An unpublished study further links HOIL-1L's unconventional ubiquitination activity to non-proteinaceous substrates in vitro [6]. However, deeper understanding of HOIL-1L's catalytic mechanism and function is prohibited by lack of molecular details.
I have established biochemistry methods to investigate different steps of HOIL-1L’s catalytic activity and regulation. Using such methods in combination with mass spectrometry, I have characterised ubiquitination targets by HOIL-1L. I have also obtained molecular information of how HOIL-1L engages ubiquitin for substrate modification using structural biology approaches.