News

PBR's ineptitude meant that 2010 passed almost unnoticed. During 2011 (and forever more) he is to make a concerted effort to keep the website vaguely up to date...

March: Yeserim Yildirim arrives from Istanbul to explore the genetic structure of Pleurobranchia maculata populations, the toxic sea slugs that have caused havoc on North Shore beaches (at least to the dogs that eat them). Heather Hendrickson (who ought to know better) seems hell-bent on three years in Auckland (secretly, we're glad and we hope you don't inherit this). PBR was elected Member of the Max Planck Society and appointed External Scientific Member of the Max Planck Institute for Evolutionary Biology in Ploen, Germany.

February: We feature in two consecutive weeks on Our Changing World (Radio NZ National). PBR on bet hedging (11 Feb), and Eric, Katrin and Caroline (17 Feb) on the evolution of individuality. Available as MP3.

January: We were mostly on holiday, but in-between fishing, the odd G&T, and a little relaxation several of us had the joy of dealing with referees comments.

Susan Bailey (from Rees Kassen's lab in Ottawa) arrived for a four-month stint to work on the ecological causes of diversity. Along with Honour McCann (who arrived in December from Dave Guttman's lab at Toronto to work on plant pathogen evolution), this brings the total number of Canadians fleeing winter to two.

Somehow we managed to convince Peter Lind (who recently completed his PhD with Dan Andersson in Uppsala) that the NZIAS is a great place to holiday. He'll join us mid year on a three-year Marsden-funded project to elucidate rules of genetic evolution.

We also managed to sign up Yuriy Pichiguin a young mathematician from Novosibirsk to work with Eric Libby on the evolution of multicellularity.

Our work and lab environment

2010 (the year that was)

Much happened during 2010... we had visits from Dieter Ebert, John and Shery Roth, Dave Guttman; we said farewell to Joanthan Gauntlet (who now works for Ondek in Perth) and Jenna Gallie (now a post doc with Ben Kerr at U Wash); we managed to do some science, win some grants (including a James Cook Research Fellowship to PBR) and even -- despite the referees -- publish the odd paper. And there was the usual bit of travel. We also managed to get sidetracked with toxic sea slugs and an outbreak of Pseudomonas syringae pv. actinidiae (PSA) in kiwi fruit orchards. PBR's most significant achievement occured in Februrary when he broked into the world of Russian wine where he compares favourably alongside a bottle of Ch Petrus. In January Jenna Gallie successfully defended her thesis and was invited to present her work at the sixth Early Career Scientists Symposium on Experimental Evolution at the University of Michigan.

Read about our latest papers

Rainey, P. B. and Kerr, B. (2010). Cheats as first propagules: A new hypothesis for the evolution of individuality during the transition from single cells to multicellularity. BioEssays 32, 872.

These ideas began to emerge more than five years ago. Why does it take so long to write? The ideas stem from thinking about the possibilty that newly formed cooperative groups of cells (e.g., the mat-forming wrinkly spreader (WS) morphs from our experimental populations) might evolve traits adaptive at the group level. However, one problem immediately looms: newly formed WS groups are not "Darwinian Individuals", i.e., they lack the capacity to leave group off-spring. Lacking Individuality puts pay to the possibility that WS groups (or similar) can evolve by natural selection. Pondering this dilemma led to the realisation that the cheating genotypes that evolve from WS provide a solution. The cheats are able to leave the WS mat, and, by mutation, can regenerate WS: the cheats thus function -- given an appropriate ecological context -- as quasi propagules [voilà(!) Individuality emergences from little other than the tension that exists between levels of selection]. We discuss some interesting aspects and predictions arising from this model, but most importantly, the idea is being realised in experimental studies on the adaptive evolution of WS groups).

Zhang, X.-X., Liu, Y.-H. & Rainey P. B. (2010). CbrAB-dependent regulation of pcnB, a poly(A) polymerase gene involved in polyadenylation of RNA in Pseudomonas fluorescens. Environmental Microbiology 12, 1674.

Arising from our interest in the ecological genetics of histidine uptake and degradation comes a steady flow of work from Xue-Xian (aided in this instance by Yunhao) on the Cbr regulon -- a major player in control of carbon catabolism in Pseudomonas (and there is much yet to publish!). While exploring the possibilty of a small regulatory RNA downstream of the sigma-54 enhancer binding protein encoded by cbrB, Xue-Xian discovered pcnB (a gene encoding a protein involved in mRNA degradation), which he shows is part of the Cbr regulon. Interestingly, pcnB is transcribed from a sigma-70 promoter and not the sigma-54 promoter as expected. However, Xue-Xian did find a sigma-54 promoter, but this turns out to control expression of crcZ, a small anti-sense regulator involved in global regulation of carbon catabolite repression. The bottom line is the connection between mRNA degradation and cellular metabolism: a connection made by Cbr.

Refardt, D. & Rainey, P. B. (2010). Tuning a genetic switch: experimental evolution and natural variation of prophage induction.  Evolution 64, 1086.

This paper marks a departure from our regular work and is the brainchild of Dominik Refardt (now at the ETH in Zurich). Genetic switches have always been a fascination and little studied from an evolutionary perspective. We decided to focus on prophage induction by phage lambda: the classic example of a genetic switch. Dominik shows that the lambda switch can respond rapidly to selection for alteration in threshold and sensitivity. Surprised at the ease with which the switch could be tuned, Dominik turned to a collection of natural lambdoid phages and found that there was considerable variation in sensitivity and threshold of the response function among these isolates. We think that our data provides some insight into the ecology of prophage induction in natural populations of lysogenic phage.

Beaumont et al (2009). Experimental evolution of bet hedging. Nature 462, 90.

This is the first publication arising from an experiment in 'reverse evolution' initiated in 2003 by Bertus Beaumont who until 2007 was a Marsden Funded post doc in New Zealand (He's now back in the Netherlands and strolling through evolution). Although always a possibility, the discovery of bet hedging genotypes (in two of twelve replicate) selection lines, came as a surprise. However, with hindsight, and aided by theory from Eric (manuscript within a whisker or two of submission), it turns out that such genotypes -- assuming they can arise by mutation in the first place -- are highly likely to be fixed under a selection regime that imposes both an exclusion rule (types common in the current environment are assigned a fitness of zero in a future environment) and a population bottleneck. In addition to a description of the bet hedging genotype we show how emergence of the switcher depended on previously fixed mutations; we report the identity of all nine mutations leading to the switcher, but fail to explain why the final mutation has the remarkable effects that it does. Nonetheless, more will be revealed: indeed, the discovery of bet hedging genotypes, the causes of their selective advantage, and much, much more that has arisen from the 2003 experiment (and it goes on) has proved a rich source of fun. Jenna has 'giggled' her way through a PhD on the molecular basis of the switch (a bistable beast based on epigenetic change); Sylke is attempting to explain which mutations really matter in terms of the inevitability of the switcher, Andy continues the selection experiment (and more), and Gayle is engrossed in subsequent evolution of the switch. And there remain many brain-churning, reality-distending projects for the discerning graduate student, or post doc. It's amazing what can be done with a piece of No. 8 fencing wire.

Rainey, P. B. (2009). Arrhythmia of tempo and mode. Nature 461, 1219.

In this News and Views essay Rainey comments on the latest discoveries arising from Rich Lenski's long-term selection experiment with E. coli. The article by Barrick et al (Nature 461, 1243) reports a spectacular plethora of findings that shows just what is possible given both vision and advances in technology; advances barely imaginable a mere five years ago.

McDonald et al (2009). Adaptive divergence in experimental populations of Pseudomonas fluorescens. IV. Genetic constraints guide evolutionary trajectories in a parallel adaptive radiation. Genetics DOI: 10.1534/genetics.109.107110.

This is the fourth paper in a series that tackles the mechanistic details of the evolutionary changes in our experimental Pseudomonas populations. Attention remains focused on the wrinkly spreader (WS) class of niche specialist. Thanks to the monumental efforts of two exceptional students (Mike McDonald (who has just completed his PhD at Massey and is now at SINICA in Taiwan) and Stefanie Gehrig (who completed her D. Phil. at Oxford in 2005)) we describe two new (non-Wsp) mutational routes to WS and show that these two new routes (Aws and Mws), along with Wsp are the three -- and only three -- pathways that evolution follows to generate the WS phenotype. Interestingly, if the Wsp, Aws and Mws pathways are eliminated from the ancestral genotype then WS morphs still evolve, but take much longer to do so. Clearly then, evolution can follow at least one other route (and potentially around thirty additional routes), but does not ordinarily do so. We think the reason that evolution follows just three of many possible routes is due to the fact that the Wsp, Aws and Mws pathways have, on account of particular regulatory connections, a heightened propensity to translate mutation into phenotypic variation, thus biasing the molecular variation presented to selection. We conclude that parallel WS evolution, as we see in our experimental system, is attributable to strong selection, but also genetic (developmental) constraints arising from specific functionalities and regulatory connectivities that lie at the heart of the genotype-to-phenotype map.

Silby et al (2009). Genomic and genetic analyses of diversity and plant interactions of Pseudomonas fluorescens. Genome Biology 10, R51.

At long last the complete genome sequence of our favourite strain of P. fluorescens SBW25 is published. The paper also includes the sequence of strain Pf0-1, along with a detailed comparative analysis, a substantive screen of IVET libraries and a whole lot more. The NCBI entry can be accessed here and the Artemis files are available here.

Zhang & Rainey (2008). Regulation of copper homeostasis in Pseudomonas fluorescens SBW25. Environmental Microbiology 10, 3284.

This paper is an extension of two previous papers (Giddens et al 2007 PNAS and Zhang & Rainey 2007 MPMI) on copper metabolism that brings together knowledge of two different copper systems: one for uptake and one for export; one for scavenging copper when it is scarce and one for exporting copper from the cell when there is too much in the local environment. A curious feature of the copper homeostasis system in SBW25 is that it is something of a hybrid -- being comprised of two separate systems: the well studied CopRS system (but lacking CopAB) and the less well understood CueA system involving a copper transporting P1-type ATPase, a mer-like regulator and copper chaperone. Given the amount of copper dumped on NZ grapevines we ought to be able to use this work to lever some funding!

Dual involvement of CbrAB and NtrBC in the regulation of histidine utilization in Pseudomonas fluorescens SBW25. Genetics 178, 185 [& Genetics 176, 2165].

These two papers are part of a story that began back in the late 1990s with discovery that the histidine uptake and utilization pathway (hut) is activated in the plant rhizosphere. For some years we banged away at more exoctic loci, but frustrated by the lack of phenotypes, we returned to Hut (there is much to be said for being able to take a chemical off the lab shelf, add it to the medium and observe induction!). As progress continues we're become ever more fascinated by the very many facets of this locus. Our journey has taken us to new modes of gene regulation (the HutD governor); sent us to the heart of C:N metabolism, which in terms of regulation is (to borrow from Dr Spock) "like E. coli, but not as we know it". We've also had to face up to the fact that our favourite bug is a gluttonous brute. And then there are the population-level insights, which we've yet to publish, but which reveal substantive polymorphism, for which we think there is a selective explanation. For more on this story see Xue-Xian, Jonathan, Yunhao and Hao's pages.

Rainey (2007). Unity from conflict. Nature 446, 616

Experiments in which groups of cells have been the focus of selection (see Nature 425, 72) has led to the realization that newly emerged groups are incapable of evolving by natural selection because newly emerged groups lack a crucial element of individuality, namely, the capacity to leave collective copies. In observing the dynamic of group emergence and subsequent destruction by cheats, followed by remergence of the group and further destruction by cheats (and so on), the notion of a life cycle emerges in which the group approximates the soma and the cheating cells approximates the germ-line. This perspective, which endows cheats with 'niceness', confers on groups the properties of Darwinian replicators and allows selection experiments to proceed. Stemming from tthis idea is a possible origin of the soma / germ-line distinction and a simple conflict mediation mechanism that relies on nothing more than the tension between higher and lower levels of selection. Rainey is working on a more comprehensive presentation of the ideas with Ben Kerr (their paper will appear soon). Peter Mentjes has begun some selection experiments and will soon be joined by others itching to push the bounds of group-level selection.

Giddens et al (2007). Mutational activation of niche-specific genes provides insight into regulatory networks and bacterial function in a complex environment. PNAS 104, 18247.

The promoter trapping strategy known as IVET identifies genes that are transcriptionally silent in the laboratory, but active in the wild. It is a great tool; and knowing what genes are switched on outside of the laboratory environment stands to tell us a great deal about the lives of bacteria in the wild. The trouble is though, that sooner or later it becomes necessary to understand the biological function of these environment-specific genes and for this it is necessary to be able to express a phenotype in the laboratory. Giddens et al apply some classic genetic approaches (suppressor analysis, albeit genome-enabled) and show how significant progress is possible

Zhang & Rainey (2007). Construction and validation of a neutrally marked strain of Pseudomonas fluorescens SBW25. Journal of Microbiological Methods 71, 71.

Neutrally marked strains are essential for experimental evolution. In the past we have made use of a pantothenate marker, which while useful, is problematic to use. Some time ago Xue-Xian constructed a lacZ-containing derivative of our ancestral bacterium (P. fluorescens SBW25) by introducing a single copy of the marker gene into the chromsome. Extensive analysis of fitness effects in a range of environment (including the plant rhizosphere) revealed no detectable effects. Given the utiliity of this strain we felt it was worth writing up and publishing alongside the fitness data that otherwise might never have seen the light of day.

Fukami et al (2007). Immigration history controls diversification in experimental adaptive radiation. Nature 446, 436.

Ecologists have long known about the principles of island biogeography and the relationship between island size and diversity. Evolutionists think about diversity in terms of adaptive radiation. Tad Fukami's study very nicely brings together the two ideas, shows that they are very much related and shows how the timing of immigration events can profoundly impact on the evolution of diversity.

Kirkelund Hansen et al (2007). Evolution of species interactions in a biofilm community. Nature 445, 533.

Microbial mats, like tropical rain forests, are hot beds of biological diversity.  A glance at either ecosystem shows species that interact with one another in a variety of ways.  So significant and far-reaching are these interactions that it is easy to assume that they are hard-wired.  But it cannot be so: interactions among species must evolve, just as species do. Using a commensal and its host Susse shows that in environments that allow local interactions to form the commensal rapidly adapts to its host, becoming more aggressive, but at the same time forming an intimate and specialized association.  Surprisingly, despite a more exploitative relationship, the health of the community is enhanced.  These results show that species interactions evolve and as they do they affect community function.