Current Research Projects

The main research theme of our group is the evolution of translation. We currently have projects on the evolution of tRNA gene sets and mature tRNA pools, and the evolution of codon usage. We are also interested in the lon-term survival of bacteria.

The evolution of tRNA sets

Fig 1. During tranlsation tRNAs match codons to amino acids. Some (alpha) tRNAs are essential, while other (beta) tRNAs are not. Image credit Jenna Gallie.

Transfer RNAs (tRNAs) are adapter molecules that match codons with amino acids during translation (Figure 1). There are 61 theoretically possible types of tRNAs – one matching each of 61 codons that code for amino acids. In practice, organisms use 61 codons but carry far fewer corresponding tRNA types. This is possible because some tRNAs translate more than one codon (through wobble base pairing). Intriguingly, which tRNA types are present in an organism differs considerably across the tree of life.

In our laboratory, we are interested in exploring the evolutionary basis of tRNA set composition. We have a number of projects in this area, including:

- Mathematical modelling of tRNA gene sets (with Dr Hye Jin Park, Dept of Evol Theory)
- Analysis of tRNA genes in the model bacterium Pseudomonas fluorescens SBW25
- Experimental evolution to compensate for suboptimal tRNA gene sets in bacteria
- The evolution of biased codon usage in Pseudomonas fluorescens
Adaptation and application of mature tRNA pool sequencing (YAMAT-seq, Shigematsu et al., 2017) for use in bacteria

Shigematsu et al., 2017. Nucl. Acids. Res: 45.

Long-term survival: the evolution of bacteria in starved batch culture

Fig 2. Survival/extinction of E. coli and P. fluorescens in minimal medium over 6 weeks. Image credit Saul Pierotti.

In addition to our research on the evolution of translation, we have a growing interest in mechanisms of long-term survival in bacteria. In a typical laboratory experiment, bacteria are grown under conditions that – at least at first – support rapid and plentiful growth. However, survival in many natural environments is likely to require persistence through substantial periods of hardship. A number of laboratory-based experiments mimicking long term persistence have been performed (starved batch cultures), resulting in the identification of a variety of mutational classes that can provide a growth advantage in stationary phase (GASP mutants; reviewed in Zinser and Kolter, 2004). These include point mutations, small deletions, and larger genomic rearrangements.

We are interested in the long-term survival of our favourite model organism, Pseudomonas fluorescens SBW25 compared with E. coli. We are performing evolution experiments in starved batch culture with these species (Fig. 2, left), with the aim of elucidating the population genetics underpinning survival (or extinction) in each lineage.

Zinser and Kolter, 2004. Res Microbiol: 155.

Long term survival: the evolution of a bacterial bet hedging strategy

This recently-completed projected was peformed in collaboration with Paul Rainey (Department of Microbial Population Dynamics, MPI), Frederic Bertels (Microbial Molecular Evoluiton, MPI), Philippe Remigi (INRA-CNRS, France) and Gayle Ferguson (Massey University, NZ).

Fig 3. Colony (left) and cell (right) level switching in Line 6. Image credit Jenna Gallie.

Bet hedging – stochastic switching between phenotypes – is a widespread evolutionary adaptation that facilitates survival in unpredictable environments. There are many examples of bet hedging behaviour in nature, ranging from microbes to humans. However, very little is known about how bet hedging strategies emerge. An experiment in Paul Rainey’s laboratory saw the evolution of a bet hedging strategy in two parallel, independent evolutionary lineages of the bacterium P. fluorescens SBW25 (Beaumont et al., 2009). In both cases, the evolved bet hedging type produces colonies of two distinct phenotypes, with each type rapidly giving rise to both itself and the opposite type. This phenotype switching is mirrored at the cellular level by the production of capsulated and non-capsulated cells (Fig. 3, right).

The first of these two bet hedging types (Line 1), including the phenotype, genotype and evolutionary history has been extensively characterized; bet hedging emerges as a consequence of a non-synonymous point mutation in the central metabolic gene carB (Beaumont et al., 2009; Gallie et al., 2015; Remigi et al., 2019). In the second lineage (Line 6), bet hedging is caused by a non-synonymous mutation in the housekeeping transcription factor, rpoD. In our recent paper, we show how mutations in genes as seemingly distantly related as carB and rpoD can reconcile at the molecular level to generate a very similar phenoytpe (Gallie et al., 2019).

Gallie et al. (2019). Mol Biol Evol
Remigi et al. (2019). Mol Biol Evol
Gallie et al. (2015). PLoS Biol
Rainey et al. (2010). Microbial Cell Fact
Beaumont et al. (2009). Nature


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