Contact
Massey University
NZIAS
Gate 4, Building 12
Oteha Rohe, Albany
Auckland, New Zealand
+64 9 4140800 ext 41513
gayle.ferguson(at)yahoo.co.nz
Gayle Ferguson, PhD
My research focuses on the evolutionary processes underlying the response of organisms to varying environments
I completed my PhD research with Dr Jack Heinemann at University of Canterbury in 2002, where I demonstrated antibiotic resistance gene-transmission between Salmonella typhimurium when resident within cultured human cells by natural bacterial gene transfer processes - a phenomenon potentially contributory to the spread of antibiotic resistance genes in the gut environment. Following this, I completed a short postdoctoral fellowship with Dr Howard Shuman at Columbia University in New York. Here, I investigated the mechanism of pathogenesis of the bacterium Legionella pneumophila, the causative agent of Legionnaire’s disease, focusing in particular on the mechanism of pathogenic protein translocation from bacteria to human phagocytic cells by Type IV secretion. In 2004 I moved to the UK and took up a position as ‘Teaching Fellow’ in the Faculty of Life Sciences at The University of Manchester.
I joined the Rainey lab in May 2008. My intended research aims to shed light on the mechanics of Pseudomonas fluorescens adaptation to changing environments.
In order to survive widely varying conditions, bacterial populations must possess mechanisms for rapid adaptation through the generation of phenotypic novelty. How differentially fluctuating environments might select between different diversification mechanisms in bacteria has been explored by in silico modelling but has not been addressed empirically. Recent work in the Rainey lab has focussed on the capacity of simple experimental bacterial populations to adapt to repeated bouts of selection in two contrasting environments (A & B). Bacterial populations were required to genetically adapt, by natural selection, to environment A; once achieved, the specific adaptive mutant that evolved in environment A was transferred to environment B (where it is now maladaptive) and required to adapt to this new environment. Once achieved, populations were returned to environment A (thus completing a single cycle of ‘reverse’ evolution) and the process continued. In this way, an evolutionary series of genotypes was built up, where each mutant genotype contained the genetic complement of its immediate ancestor and a single additional mutation (see Christian Kost’s page).
In three out of twelve replicate lines, genotypes have evolved that show high frequency phenotypic switching. That is, they rapidly switch between two phenotypic states, one of which is suited to environment A, the other to environment B (see Jenna Gallie’s page). Emergence of the ‘switcher’ is an interesting experimental outcome as, intuitively, this type of ‘bet-hedging’ strategy circumvents the problems posed by ‘reverse’ evolution: of the nine experimental lines in which ‘switchers’ did not evolve, one lost the capacity for further adaptation after three cycles through environments A and B, most likely due to mutational exhaustion of all genetic routes to realisation of the adaptive phenotype.
Unlike a random mutational mechanism, a locus-specific switch allows the organism to switch (indefinitely) between two beneficial phenotypic states without the need for additional (potentially detrimental) mutations. My proposed experiments aim to explore how environmental fluctuations experienced over differing periods of time might select among different mechanisms for generating diversity. One potential outcome may be the evolution of a deterministic phenotypic switching mechanism from what is currently a stochastic one; another potential outcome may involve “tuning” of the phenotypic switch rate to that of the environment.
Publications from previous work
Ferguson, G.C., Sheader, E.A. and Grady, R.E. (2007) How to assess large numbers of students: a combination of peer- and computer-assisted assessment. ‘Bioscience Education eJournal’, accepted.
Silby, M.W., Ferguson, G.C., Billington, C. and Heinemann, J.A. (2007) Localization of the plasmid-encoded proteins TraI and MobA in eukaryotic cells. Plasmid 57(2): 118-130
Ferguson, G.C., Kennedy, M.A. and Heinemann, J.A. (2002) Gene transfer between Salmonella enterica Serovar Typhimurium inside epithelial cells. J. Bacteriol. 184, 2235-2242.
Ferguson, G.C. and Heinemann, J.A. (2002) A Recent History of Trans-kingdom Conjugation, in ‘Horizontal Gene Transfer’ 2nd Edition, Eds. Syvanen, M. and Kado, C.I. p. 3-17.


