By Dr Matthew Brook, University of Edinburgh
The EMBO conference on ‘Protein Synthesis and Translational Control’, held at EMBL in Heidelberg, Germany in autumn 2015, is without a doubt the main European meeting for the mRNA translation field and as such, is the forum at which it is crucial for Early Career Researchers like myself to present data and gain real-time ‘peer review’ from the world leaders in the field.
However the flip-side to this is that you have to stand and present your data to the world leaders in the field! Most of whom seem to sit in the first two rows of the auditorium! Taken together with the fact that I was presenting data relating to a previously undescribed phenomenon, my talk was a significant departure from the lab’s usual areas of interest and I had to wait until the last day of the conference to speak, hopefully my nerves weren’t too evident!
The talk generated helpful feedback, as hoped, and actually ended up fitting with one of the main emergent themes of the conference: an mRNA can be translationally regulated in a multitude of ways whilst still being associated with multiple ribosomes and appearing translationally ‘active’ when assessed by classical methodologies. I not only got to share my data, but I also came back better equipped to prepare the data for publication.
Over the course of the conference I had the pleasure of hearing Joan Steitz (Yale School of Medicine, USA), Bill Merrick (Case Western Reserve University, USA), Alan Hinnebusch (NIH IRP, USA) and Raul Mendez (IRB Barcelona, Spain) who gave fantastic Keynote lectures. I heard about the cutting-edge developments being made in leading groups around the world and I was able to begin collaborative ventures with some of them.
If I was to comment on a conference highlight, it would be the talks and discussion on the extraordinary power of the increasingly-refined technique of ribosome profiling and how it is revealing entirely new levels of regulation of gene expression. In particular, that the effects of specific usage and ordering of codons (termed ‘codon optimality’) likely spell the end of the ‘silent’ synonymous mutation.