After leaving David Horn’s lab almost four years ago in August 2013, when David and his group moved to the University of Dundee, we’re still managing to publish papers together. That’s the consequence of spending ten years in the same small but very productive group that also maintains great collaborative relationships – you get to be involved in multiple projects and, the best part, see them come to fruition! 2016 saw two such papers – Lucy and Seb’s on Vex1, and the NUP2 work by Luke Maishman and colleagues in Mark Field’s group.
Vex1 is a key controller of VSG monoallelic gene expression in Trypanosoma brucei; it localises close to the site of RNA polymerase I mediated VSG transcription, the expression site body. Remarkably, depletion or overexpression of Vex1 leads to loss of monoallelic control, indicating its fundamental role in controlling this process.
NUP2 is a second component of the T. brucei nuclear lamina, which interacts with NUP1 to form a basket-like structure under the nuclear membrane, essential for nuclear integrity and apropriate gene expression regulation. These proteins, though exhibiting functional conservation, are highly divergent from the nuclear lamins of the Ophistokonta, which includes several of the standard model organisms (S. cerevisiae, C. elegans, X. Laevis, D. melanogaster, as well as us!). This is yet another confirmation of the benefit of exploring beyond the narrow confines of the Ophistokonta! Not only can we find many disease-causing organisms in the other groups (Excavata – T. brucei; Alveolates [SAR] – Plasmodium), but we also gain fascinating evolutionary insights through their study.