Choose your conferences wisely

Credit: Jorge Chan,
Credit: Jorge Chan, P.s. Remember to practice! But also not to panic if your talk goes slightly off track.

This year was a mast year of conference-going for me. I hadn’t planned to attend nine conferences (summary of each at the end of the post), but sometimes it is so hard to say no! However, I will not be repeating this schedule in the future, as it has been very hard to keep on top of all the other work I want to/ have to do. So how should I decide on which conferences to attend in the future?

I think the basis for the decision will differ from year to year depending on what I hope to gain, whether I have a new exciting story to present, and whether I am hoping to be inspired and think outside of my usual scientific framework, or hoping to network and build on what I am currently doing. But generally I think meetings break down into three categories:

(A) the large society meetings that feel more like a family reunion than a day at the office;

(B) the specialty meetings where like minds come together and reinforce the momentum of the field, and;

(C) the new topic meetings – either altogether new, or simply new to me – where I spend the entire time brainstorming about what direction I want to move in next and networking is the name of the game.

Each type of meeting has its pros and cons, and I hope to always balance among the three (which means missing the “family reunion” from time to time). Type A acts as a reminder of why I am doing what I do, how much I enjoy my colleagues’ and advisors’ company, and reinforces that I have a terrific support network. These meetings typically have an overwhelming number of talks you could attend (transports me back to the excitement of opening my University course offerings directory each term), are less restrictive in who can give a talk – allowing for early career researchers to present their work, and are highly social. Type B is where I typically gain the most in terms of scientific progress and networking. These meetings often don’t have concurrent sessions, which means that everyone has seen the same set of talks as you, and therefore that dinner conversation topics are easy, even with folks you’ve never met before. This also means you are likely to sit through a talk you wouldn’t have chosen from an abstract book, and learn something unexpectedly relevant to your own interests. Type C are also terrific for networking, as they are often very small and targeted, with a particular goal in mind (synthesizing a field, solving a specific problem, or building collaboration). These meetings are probably the most likely to result in the generation of a new project, and can really solidify a community of researchers. So if you see one on a topic you are interested in getting involved in, there is no better way to put your name on the map than attending!

As you can see, there is no easy choice (especially if you are resource- and/or time- limited). One way to make the decision, especially if you are further on in your career, is to only attend the meetings to which you are invited, either as a plenary speaker or within a symposium. However, if you follow that track you may miss new opportunities for networking, as you are unlikely to be invited to a meeting that is outside your area of expertise. My new plan is to choose one meeting that I want to attend, one meeting that I “should” attend (i.e. based on the table below), and then one that I am invited to, unless that fills either of the two previous niches. I’ll let you know how that pans out next season.

A very broad overview of what's to be gained at each type of conference.
A very broad overview of what’s to be gained at each type of conference.

A bit about this year’s conferences:

First I attended a meeting in Eco-Evolutionary dynamics in Leuven, Belgium which was organized by Ellen Decaestecker and Luc De Meester. The meeting was primarily designed as a networking event for Belgian researchers, but I think all of us invited speakers found it just as useful for networking! The best thing about this meeting was that although it was specific in terms of question being addressed, it was incredibly broad in terms of systems and approaches being used. It was also a great group, with the bulk of the audience representing PhD students. The questions after each talk were very insightful, and it was a warm open atmosphere. The research highlights were hearing about hell breaking loose in three species lab experiments from Nelson Hairston, data presented by Lutz Becks showing increased sexual reproduction with ecological feedbacks, experimental work by Eva Lundstrom indicating that the abiotic environment can select for particular bacterial communities even in the face of 70% dispersal, and a fabulous talk by Jacintha Ellers about trait loss in obligate parasites.

Next I went to the Second International Microbotryum meeting in Amherst, Massachusetts. The meeting was organized by Michael Hood, and focused primarily on using the Silene-Microbotryum system as a model for understanding disease ecology and evolution. However, since many of us have changed paths since studying that system, it included talks from across many plant disease systems. Due to the size of the meeting, everyone presented their work, including some terrific undergraduate students, which meant that we all really gelled and could have great/productive conversation. I had never met Pete Thrall, Tatiana Giraud (although we’ve written a paper together) or Georgiana May, and really enjoyed getting to know each of them. It was an ideal size for a meeting of this sort (20ish), and is even leading to a new publication. Among the highlights and new things I learned were: Emme Bruns explained the use of Aster models for life history (I am definitely going to use these!), Janis Antonovics showed both theory and data on disease spread at the edge of host ranges, Scott McArt taught me about mummy berry disease (very cool!), Britta Buker shared a really great way to identify genes important in host specificity by backcrossing hybridized parasites, Martin Kemler described successful Microbotryum infection of non-host species but no onwards transmission, and Mandy Gibson showed great support for the idea that sexual reproduction is higher in parasitic than free living species of nematodes.

The month of May was a great one for folks studying the evolution and/or ecology of infectious diseases. First, we got to attend a one-day symposium in London organized by Mike Boots on the Evolutionary Ecology of Infectious Diseases (as part of the British Ecological Society’s 100th birthday!) Then we flew over to Pennsylvania State University for the 10th annual Ecology and Evolution of Infectious Disease meeting (and Pete Hudson’s 60th birthday celebration). Both meetings were fabulous! And it became increasingly clear that our understanding of when/how/why disease occurs is dramatically improving. For one thing, there are more researchers working on these questions than ever before; but also, there are some exciting new techniques and approaches being applied, both in generating empirical data and in modeling large datasets. It seems to me that the EEID field has long been lead by theoreticians, with very little data that could be used to test the elegant and clear theory being produced. The new datasets being generated and modeled are pushing the field forward and challenging many of the ideas we thought we had figured out. And this is really exciting – new data leads to new theory leads to leaps and bounds in our ability to manage disease.

The research highlights of these two meetings were much too plentiful to put into this post, but I did live tweet both events, and have collated those here: Tweets from EEIDs. The annual EEID meeting is among my favorites on account of its smallish size, great social events, fabulous and diverse talks, and lively discussions at the end of each session. This time around, the moderators of each session were in charge of shaping the timings for discussion and really got things going by asking provocative and insightful questions. For more highlights from the meetings see: and

Next up was Evolution 2013 in Snowbird Utah. Unfortunately, I missed the opening night and first day, and it took me some time to recover from jet lag and altitude once I arrived. Despite these obstacles, however, it was great fun as always. I was lucky enough to be part of the ASN Vice Presidential symposium on Ecology, Evolution and coevolution of host-parasite interactions, organized by Curt Lively. It was a great experience, and a very supportive group to be part of. Topics ranged from the role parasites play in maintaining sexual reproduction (Curt Lively), bacteriophage adaptation over space and time (myself), self-medicating butterflies (Jaap de Roode), parasite-mediated competition (Meghan Duffy), eco-evolutionary feedbacks in immunity (Andrea Graham), to parasite evolution in immune-compromised hosts (Andrew Read). In the next year or so, you’ll be able to read all about the work presented in a special issue of AmNat.

As always, the meeting was jam-packed with sessions. Unfortunately, it was quite difficult to move among rooms with ease, so I tried to stay through whole sessions. In many ways I prefer this to running around madly, but it did mean I missed many talks I wanted to see. This year’s Evolution meeting also had a new twist: Lightning talks. These 5 minute shorts were a great test of whether a researcher really understood what their work was all about. The best ones typically had only one key point being made; some were funny, others were truly lightning paced, but all were good effort! Overall, the meeting was in a great location (although I didn’t have time to fully exploit it) and was a wonderful opportunity to see many many friendly faces. Again, for more coverage see:

After a three-week break it was on to the Gordon Research Conference on Microbial Population Biology in New Hampshire, organized by Paul Turner. This is my second GRC, and I am sure it won’t be my last. The success of the GRC meetings rests on the quality of the talks and posters (which are almost exclusively on unpublished results), the isolated location of the conference (think summer camp), and the fact that it draws the big names from the field (i.e. great networking opportunities!) Given the confidential nature of the talks – no live tweeting allowed – I will only give vague research highlights here. There were two talks about reconstructing ancestral phenotypes, one by Betul Kacar and one by Eric Gaucher, which really got my imagination going, one about megaplasmids in Pseudomonas syringae by Dave Baltrus, a full session on CRISPRs, including a glimpse into how spacer heterogeneity evolves by Rachel Whitaker and a discussion of the non-random acquisition of protospacers by Rudolpho Barrangou, and an amazing illustration of the evolution of resistance to antibiotics in a Guinness Book of World records-sized agar plate by Roy Kishony.

For those planning to attend the GRC for the first time in coming years, one thing to note: although the meeting can seem “cliquish” at first glance, I’ve found that the meal layout with round tables after a buffet choice is perfect for meeting new people. Whatever you do, don’t stand there looking around for the one person you know. Go to the nearest free seat and ask if you can join. In fact, this should go for every meeting you attend, but it is easier said than done at some.

That brings us up to date, with a nice two-week respite before I head off to the European Society for Evolutionary Biology meeting (ESEB 2013) in Lisbon, Portugal, followed by a desperately needed 10 day holiday in Italy, followed by the Society of General Microbiology meeting in Brighton, UK, followed by two talks (one on science and one public lecture on “what evolution can do for you”) at the 2013 EMPSEB (European Meeting of PhD Students in Evolutionary Biology) meeting organized by our very own PhD students here in Cornwall.

As I said, I won’t be repeating this grueling schedule anytime soon. But it’s been great fun so far!

And the reviews are in….

I really enjoy reading Rosie Redfield’s blog: RRResearch, not least because she’s come up with the brilliant idea of posting the reviews (and her responses) for manuscripts she is publishing. There are a few new journals, such as Faculty of 1000, that are posting the reviews with the manuscripts online. But mostly, the hours and hours of time that go into both writing a review and responding to reviews are only treated as a means to an end- the publication. Given that journal space is at a premium, however, there are often important points that come up during these back-and-forths that don’t make it into the manuscript for one reason or another. Therefore, I am going to follow in Rosie’s footsteps and post reviews of each manuscript once the papers are published (so that readers can understand what the reviewers were talking about!) As a start, here are the reviews and my responses to my new paper in Current Biology. Overall, I thought the referees did a great job. They were tough on me, and made me think very deeply about whether or not to sequence all of my bacterial isolates. In the end, I decided that knowing what species I was dealing with would only confuse matters, as I argue below.

The world is complicated, but we have to start somewhere!

These are reviews and my responses to reviewers for the paper: Koskella, B. (2013) Phage-Mediated Selection
on Microbiota of a Long-Lived Host. Current Biology 23, 1256–1260. (OA)

*Please note that I have excluded all “minor” comments.

First round of review (in response to advisory board at CB):

  • Advisor I. In principle, a study that looks at coevolution among bacteria and phages in nature (especially within one host species) would be a very exciting development.  It seems that the author is addressing both whether bacteria at a certain time point are best adapted to phage from their past and whether phage are best adapted to bacteria from their past.  If we knew that each group (i.e., phage or bacteria) represented a single lineage and that the evolutionary changes within each involved a response to the other, this would be coevolution.  However, it seems that the study by Britt Koskella is much more diffuse, where we are not sure if we are looking at a given pair of bacteria and phage populations over time.  It seems that there could be a great deal of bacterial species sorting involved here, possibly based on actions of the phage and vice versa. 

Response: This is a key point in the paper, and I have now worked to emphasize that the pattern observed is likely a combination of immigration/succession and evolutionary change. In addition, I discuss the likelihood that the observed pattern represents diffuse coevolution. However, the directionality of the pattern observed (that bacteria are most resistant to phages from the past and least resistant to phages from the future) suggests that the bacterial communities are changing in response to the phage and that the phages are then responding to these changes. However, the directionality of the pattern observed (that bacteria are most resistant to phages from the past and least resistant to phages from the future) suggests that the bacterial communities are changing in response to the phage and that the phages are then responding to these changes. The evolutionary response could be driven by immigration of newly resistant/infective types or species (indeed, this is likely a key evolutionary force in these systems), but the pattern clearly does not represent simple species sorting, as this should not lead to the directional change observed. Instead, if new bacterial species were arriving and were facing a competitive advantage due to resistance against local phages, and then new phages were arriving that were able to infect these hosts, we would expect either a peak or a trough (depending on which player was ahead in the coevolutionary race) in resistance at the contemporary time point. The power of these time shift approaches in examining coevolution has been specifically discussed here: Gaba, Sabrina, and Dieter Ebert. “Time-shift experiments as a tool to study antagonistic coevolution.” Trends in ecology & evolution 24.4 (2009): 226-232.

  •  Advisor II. The author does not really know if she sampled the same species/population. The resolution is too low to make this claim and apparently no attempts were done to give convincing arguments. Without making sure that the same populations was sampled several times in time, the study is not convincing. If different populations were sampled the observed patterns have a different meaning.

Response: As mentioned above, I agree that this is both a limitation of the study and also (I think) the strength of the study. We know, based on a myriad of pairwise bacteria-phage experiments in the laboratory, that phages and bacteria can coevolve. However, whether this means they do so under natural settings, given the complexity of all microbial communities examined to date – especially microbiomes – is unclear. My previous work demonstrates that phages are just as infective to bacterial hosts from leaves in other parts of the tree canopy than they are to hosts from the same leaf, but that phages perform poorly on bacterial hosts from leaves of a neighboring tree. This consistent pattern (observed across all eight trees) was my motivation for sampling leaves of the same branch of each tree over the course of the season. It is highly probable that the bacterial community changed dramatically over the season (this is common of most bacterial communities), but the results of this study suggest that the phages are playing a role in this change – as the pattern of resistance to past, present and future phages is directional, rather than highest/lowest for contemporary combinations as would be predicted if this were simply local adaptation across populations/communities that were acting as independent units. I have now worked to emphasize these points in the manuscript.

  • Advisor III. The patterns in the data are simply not that compelling in their support of coevolution; the analysis excludes data and still only reaches marginal significance. Addressing this at the very least requires re-analysis and possibly adding more data and some theory to provide a null hypothesis

Response: The main result (that bacterial resistance depends on whether the phage is from the month prior, same month or future month) has a P-value of 0.008 using a non-parametric test and is robust both to inclusion of the tree with complete resistance and the removal of the tree with a very strong negative slope. These results are now discussed.

  • Conceptually the ms is confused, mainly as regards defining the level of biological organisation that it is studying (i.e. population vs community; see reviewer 3).  Addressing this requires at the very least a complete re-write of the intro/discussion, but to be convincing really requires more data to provide species identifications for the bacterial clones used in the assays

Response: As mentioned above, this has now been taken into account in the revision. As I discuss in more detail below, I am hesitant to sequence the bacterial isolates as (a) the study was designed to examine phenotypic change and therefore the sampling was not exhaustive of the bacterial diversity (which would have required the examination of many fewer tree communities but more isolates), and (b) bacterial species identification is not likely to offer additional information, as resistance can be acquired very quickly under laboratory conditions and thus two genetically unrelated species of bacteria may well share a phage antagonist and therefore follow similar evolutionary responses to phage-mediated selection. To tease apart these possibilities, a very different sampling approach would need to be used and sequencing of multiple loci per isolate would be required (as mentioned by the reviewer below). However, I thank the reviewer for emphasizing that the observed patterns could be explained by multiple levels/mechanisms of coevolution and I have kept this in mind during the revision.

Second round of review:

  • Reviewer I: This paper addresses coevolution of bacteria and phage within a group of horse chestnut trees in a small area.  This is an interesting application of the new method of time-shift experiments, where one can test whether a host becomes resistant to a given pathogen over time and whether a pathogen becomes more capable of infecting a given host species over time.  The results are entirely consistent with a given bacterial species becoming more resistant to a lineage of phage, as well as a given lineage of phage becoming more able to infect a given lineage of host bacteria.  If this conclusion could be nailed down better, I would see this as an extremely important contribution to bacteria-phage evolutionary dynamics and more generally to microbial coevolution.  The catch here is that there is little evidence in the present paper for a continuity of bacteria-phage interactions over time.  It is not clear that the phage from the past (for whom the bacteria are extremely resistant) are from the same phage lineages as those from the present.  This strikes me as essential for the author’s arguments.  As the author acknowledges, this could be a diffuse coevolution where there is no arms race going on between any pair of organisms that co-persist at the study site.  It is important that (as far as I can tell), time-shift experiments up to now have focused on a given host species and its pathogens, which makes it easier to see co-evolution between focus organisms. It seems to me that the paper would be much stronger if the author were to tighten up the evidence that co-evolution is occurring between a given host species and its phage.  This could be demonstrated for the 2-3 most abundant bacterial species over time, as well as for the 2-3 most abundant phage lineages over time.  If the time-shift patterns seen for the whole community hold up for a given taxon or two, I’d be much more convinced.  I should mention that I think the whole-community results are extremely interesting; I just think they need to be supported by carefully demonstrated co-evolution for a couple of bacterial species and their phage.  So, I’d like to see the author sequence the bacterial isolates for 16S, stratify the analysis by bacterial species, identify the predominant phage lineages (not as easy), and see how the time-shift holds up for pairs of host and pathogen.  

Response: I thank the reviewer both for their interest in the results and their comments regarding community-level change. Work in which particular phages and bacteria have been co-cultured in a test tube in the lab have repeatedly demonstrated that coevolution can occur. What I wanted to test here was whether coevolution does occur, given the complexity of the natural environment and the potentially high rate of immigration into the leaf. I have now worked to make clear throughout the manuscript that the results are likely a combination of population and community-level processes, but that the directionality of the data suggest that phages are playing a role in shaping changes in the microbial composition of leaves over time. More broadly, I have also steered the focus away from coevolution per se and more to the selective role of each player in shaping the evolution (which of course includes immigration) of the other.

It is true that the data are not necessarily specific to an interactions between two consecutive lineages, and indeed this is a drawback of all natural studies that include immigration. Demonstrating this would require the use of marked strains released into the tree environment, although would take away from much of the interesting natural history and complexity. One could also sequence all of the isolates, although this would only demonstrate that two isolates are the same species and not that one is derived from the other (given the possibility of immigration). Although this approach would allow me to determine whether the bacterial community was changing over time, and whether common bacterial species were being specifically targeted by phages, it would therefore not provide additional information regarding whether a given phage lineage was coevolving with a given bacterial lineage.

This is true for two reasons: first, because the phages in the horse chestnut phyllosphere can have remarkably broad host ranges, even infecting bacteria across genera (see Koskella and Meaden. 2013. Understanding Bacteriophage Specificity in Natural Microbial Communities. Viruses 5: 806-823); and also because two bacterial isolates from different time points may well be from independent lineages despite being identified as the same species due to immigration. Thus, even if I could identify the bacterial hosts, I could not directly assign a given phage lineage to this host (and indeed the same phage lineage could mutate to broader host range), nor could I clearly link a bacterial isolate from one time point to another. Thus, for the added cost and work involved in sequencing the bacteria and phage isolates I am quite convinced that there would be little if any additional insight gleaned.

Again, I think the idea of focusing on a few common bacterial and phage lineages is good and could yield additional insight to the process, but feel this approach falls outside the scope of this paper and indeed would have required a quite different sampling design, where for example a single tree was followed in great detail over time. This is indeed the plan for a new grant proposal where funding for sequencing is requested.

  • Reviewer II: Koskella reports the findings of a “time-shift” experiment using natural bacteria-phage communities isolated from the leaves of multiple horse chestnut trees. The time-shift approach is powerful, as it allows the change in resistance/infectivity traits to be tracked over time, thereby allowing direct characterisation of reciprocal evolutionary change between interacting species. Time-shifts of both bacteria and phage are performed; these suggest that both resistance and infectivity traits increase with the phase of the time-shift, which the author argues is indicative of directional selection arm-race coevolution. In addition, data is provided on local adaptation, which confirms earlier findings by the same author that phages are locally adapted. Application of the time-shift approach to natural populations is rare, and the application to communities inhabiting a biotic environment is unique and valuable given recently revealed significance of the microbiota to both human health and ecosystem processes. The experiments appear to have been carefully planned and well-executed, and the author does a good job of coping with the inherent ‘messiness’ of field systems. The data are novel and interesting and the analysis is simple, clear and appears robust. The writing is generally OK, but some sections are not terribly easy to follow and the presentation of the data could be improved (see below). I am not entirely convinced by aspects of the interpretation of these data, however. In particular, coevolutionary interpretations are complicated by the fact that resistance/infectivity is measured at the level of the community rather than the population, as is usually the case.  My major concerns are as follows: [1] The major issue is whether one can be confident in the interpretation of coevolution given that no information is provided regarding the identities of the taxa. Without these data it is not possible to distinguish whether the observed patterns are the result of in situ evolutionary change or species sorting or a mix of the two. This matters because species sorting is not coevolution. There are several ways in which this issue could be resolved: [a] The best-case would be to include and analyse taxa ID data. While I appreciate that identifying the taxa is difficult for the phage, where conserved genes are lacking, this information could quite easily be obtained for the bacteria by sequencing the 16s gene. I am assuming that since the information is not provided, the author did not collect these data – if however they did, these data should be included and analysed to test the relative importance of in situ evolution vs. species sorting. [b] The data are still novel and interesting without taxa IDs, however the author should be far more circumspect in their interpretation. Their data are consistent with phage communities imposing selection on bacterial communities, and vice versa, but one cannot be sure whether the observed response to selection is ecological or evolutionary (i.e., species sorting or adaptation, respectively); this will require major re-writing, and obviously the title will need to be changed. I also think the author needs to discuss in rather more detail what is known about the bacterial species richness within HC tree leaves, and how dynamic this is in time (I realise that they do cite 1 or 2 papers on this, but it would help readers to understand the data if they were provided with some idea of roughly how diverse these communities are and what degree of species turnover typically occurs)

Response: I thank the reviewer for their positive comments regarding the novelty of the work and the implications of the data. I appreciate the concern regarding the inability to distinguish phage-mediated selection and reciprocal bacterial-mediated selection at the population versus community level, and the possibility that phages are acting to shape the success of new bacterial immigrants and vice versa. I believe both processes are likely, and I agree that the data were not designed to differentiate between the two processes. Rather, the work was designed to measure whether the phages present in the phyllosphere are playing a significant role in shaping bacterial evolution (including the success of immigrants, as migration is a key mechanism of evolution). The directionality of bacterial resistance to phages from the past, present and future suggest that this is so, and makes a strong case for further examining the nature of coevolution within this, and other host-associated microbial communities.

I have now worked to emphasize the major aims of the study and to discuss the possible role of immigration and species turnover in shaping the observed pattern. I have also changed the title, as suggested.

  • Reviewer III: This study investigates temporal adaptation in bacteria-phage coevolution within horse chestnut trees. I think this is an interesting and straightforward study that merits publication in Current Biology given that it reports considerable advance on previous understanding of bacteria-phage coevolution. Methods and testing sound robust, results obtained as well. Given that a reconstruction was made based on natural populations in the field, the study extrapolates results so far been tested based on laboratory experimental coevolution only.

Response: I thank the reviewer for their support and interest in the study.

  • My only minor comment is that often the author speaks about microbial communities, but that there is no indication of how diverse these communities are (e.g. with respect to OTUs present, would it be possible to characterize those e.g. via pyrosequencing ?).

Response: My previous work has gone some way in characterizing the culturable microbial diversity observed at the end of the season (and I have now discussed this in more detail) but no work has yet been done on assessing diversity at the culture-independent community level. However, there is evidence that leaf-associated microbial communities rank among the environments in large proportion of bacteria are culturable, and this is now discussed. I have also discussed the few other studies that have examined microbial dynamics in the phyllosphere to emphasize the heterogeneity of these communities.

Guest post over at Dynamic Ecology

Jeremy Fox, Meghan Duffy and Brian McGill recently invited me to write a guest post over at their fabulous blog, Dynamic Ecology.

If you’re interested in why I think microcosm experiments are so amazingly cool, go check out the post here.

Not drawn to scale.
Not drawn to scale.

Also, later this week I will finally be posting my review/recap of this year’s EEID meetings (first in London and then at Penn State). They were great!

On dealing with rejection

Rejection is hard for everyone to deal with, but for a scientist, it is both hard and a pervasive part of our everyday lives: we have to deal with many many rejections for every success we achieve. This is true for grant applications, publications, positions we are applying for, promotions within our institutions, and various other competitions in which we take part; the answer is usually no (and when I say usually, I mean upwards of 75% for most journals in Ecology and Evolution, upwards of 94% for grant proposals to the National Science Foundation, and 99.5% for candidates applying for a given faculty position).

rejection letter

These odds can sometimes seem insurmountable. And to overcome them, there are many different strategies. For example, in terms of acquiring a grant you might consider applying for every opportunity that you can. This would surely raise your odds of success, right? Unless of course you are in fact trading off real productivity (i.e., the science you want to and were hired to do) for grant writing and gambling against the odds. Alternatively, you might try the reverse strategy– concentrating on being a productive, focused and dedicated scientist who waits until they have a great idea, some preliminary data, and the time to put together a really clear and exciting proposal (the so-called “eggs in one basket” kind of person). Again, this seems like it should raise your odds of success, given that you are competing against others who are scrambling to write as many proposals as they can. However, there is a component of the system that is truly stochastic (one reviewer who takes a strong dislike to your idea or method can easily sink the success of your proposal), and therefore all of that hard work (either quality or quantity) is not a guarantee.

Unfortunately, this is not a piece offering advice on how to succeed at grant writing – although if that’s what you are looking for, there are some really great ones out there (see here, here, and here).  Instead, I’ll discuss strategies for dealing with rejection and I would love to hear your thoughts/suggestions on others. I would suggest going through the following steps, in whatever order you feel is appropriate:

1) Pat yourself on the back (or hug yourself if you’re flexible). After all, you were brave enough to try! And you can’t succeed if you don’t put yourself out there. It can be very scary to craft your ideas into a proposal or paper and send it off to be torn apart by your competitors/colleagues/idols. You did it. Well done!

2) Scream/curse/cry/kick something – ideally something soft and not alive. You have a right to be angry. You put a lot of time and effort into that proposal/paper/application, and you did it out of love for the field, curiosity and in an attempt to contribute (as opposed to money or fame, since there are little of either available as rewards), and it’s hard to see this wasted.

3) Go commiserate with a friend/colleague. After all, every one of your fellow scientists has dealt with a similar blow and it can really help to know you’re not alone. Don’t worry that they will look down on you or lose respect. Everyone knows it’s part of the job, and it’s no fun.

4) Once you’ve calmed down and are ready, buy a nice coffee/tea/beer and reread your reviews. First look at the positive things that were said. Then think about the negatives. Are any of these good points? Points you could address in your next version? If not, is it because you may have thought the point was too obvious to discuss in your work (in which case, you now know better – there are some real numpties out there, and you need to convince them too).

5) Try and try again! And don’t forget to reflect on your past rejections when you finally do get that paper accepted/job offer/grant funded… you got it against the odds! Go celebrate.

6) Last but not least, we are of course on both sides of this playing field. We are authors, but also reviewers. So when you are dealing with rejection, don’t forget to take some mental notes about how you felt receiving the feedback so you can check back over this the next time you are rejecting someone else; constructive criticism and a spoonful of kind words can go a very long way in making the medicine go down.

Why I dropped out of psychology and became an evolutionary biologist, Part II: Evolution is happening, and it matters.

At about the same time that I was getting very frustrated by my psychology courses, I was taking an Evolution lab course (taught by the ingenious Janis Antonovics) where the theories I had been reading about first began to take shape. It was my first taste of why evolution mattered to me and also of how I could test it experimentally – yes, with controls!

Happy birthday to Charles Darwin. I wonder if he could have imagined how useful his work would be?

During one of our modules (or “labs” as I called them before becoming a Brit), Janis had each of us sample and test our own gut flora for antibiotic resistance. I won’t go into the details of how we did this (it is kind of gross), but instead explain why. When antibiotics are prescribed to kill off an infection caused by one pesky microbe, the entire microbial community is perturbed. What we are doing is imposing very strong selection against all sensitive bacteria in our body, and therefore selection for any bacteria that are able to survive. During treatment, replicating bacterial cells that do not carry resistance to the antibiotic you just took will be killed (want to know how?). This means you are left with much fewer, and a lower diversity of microbes; many of which positively influence your health. This was recently demonstrated using a multi-omic approach [1], where the researchers followed the microbial dynamics of a single patient taking antibiotics (for a nice synthesis of the work see here). They show that, as predicted, microbial diversity in the gut drops during the course of treatment and does not necessarily recover to its previous state after treatment.

One common way bacteria survive antibiotic treatment is by halting reproduction. This works because many antibiotics affect only replicating cells, and therefore any cells in the population that are just hanging about in stationary phase, the so-called “persister cells,” are temporarily resistant. However, just to emphasize how little we know about one of the most important evolutionary phenomena affecting human health: bacteria break even this rule. A recent study out this month in Science [2] has found that a bacterium closely related to the one that causes tuberculosis is able to reproduce, albeit slowly, in the presence of an antiobiotic to which it is not “resistant” (according to the current definition). The ability of this bacterial population to persist in the face of antibiotics is because identically genetic cells are in fact diverse in their behavior; specifically in production of an enzyme with which the antibiotic interacts. This means that some cells, just by chance, are able to survive and reproduce but that their future generations of offspring are just as likely to be killed by the antibiotic as any other cell in the population. In other words, in the absence of heritable genetic change, the population is unable to respond to selection and will not evolve resistance (at least using this mechanism). Unfortunately, this also means that the population will be able to persist and, if it gets lucky, a mutation conferring heritable resistance will pop up. A similar result, albeit without the amazing microfluidics, was found in 1997 [3].

If this result holds true for many more bacterial species, it would suggest yet another way in which our current army of antibiotics are likely to fail. So what does this mean in terms of finishing your course of antibiotics like all good children should? Well, we don’t know. We need data. I could rant about this, but instead I will refer you to a great talk by one of the experts, Andrew Read.

Okay, so evolution happens every time you take your antibiotics. But what about those microbes that aren’t picking fights with their human hosts? Are natural bacterial populations evolving as rapidly? Of course they are! I recently monitored changes in bacterial and bacteriophage populations living within horse chestnut tress in a park near Oxford and found that the bacteria were rapidly evolving resistance against their local phages, and the phages were responding by overcoming this resistance – all within the course of a single season (Paper in review now, so stay tuned). There are also many many examples of bacteria that have evolved incredible adaptations to changing or hostile environments. For example, bacteria are now known to thrive under the Antarctic ice, in thermal vents reaching up to 235°F, and in heavy metal environments. The resilience and adaptability of bacteria is staggering, and we are now learning how bacterial evolution can work in our favor, for example by turning toxic compounds into pure gold, storing our data, protecting against the spread of dengue fever, or making our food.

Rapid bacterial evolution also has major consequences for the fitness of macroscopic organisms with which they interact; our microbiota have important roles in our health (as I blogged about previously), plants associated with salt- and drought-tolerant Rhizobia can increase their fitness under harsh conditions, and emerging disease is often associated with bacterial acquisition of toxins or virulence genes. For example, the strain of Pseudomonas syringae that causes bleeding canker of horse chestnut trees acquired genes that allow it to thrive on woody tissue, presumably allowing for the host shift and subsequent spread.

Much of the great evidence for rapid evolution comes from microbes because of their short generation times and large population sizes, but this certainly does not mean the patterns we observe are restricted to microscopic beings. Indeed, one need look no further than the size of our watermelons and dogs to realize the speed at which an eukaryotic population can response to selection – especially when it is imposed artificially. During my PhD research with Curt Lively, I was able to show that trematode parasites can impose strong selection on populations of their snail hosts over only a few generations in the lab. We evolved experimental snail populations in tanks with and without the sterilizing trematodes and found that, over the five year experiment, trematodes adapted to specifically infect the most common snail genotypes in the tanks and subsequently drove the frequency of these types down [4]. And evidence for such rapid responses during experimental evolution is building. Rowan Barrett recently showed that stickleback populations can evolve cold-tolerance within three generations and Anurag Agrawal demonstrated rapid evolution (over only four years) of flowering time in experimental field populations that were affected by or protected from insect herbivores.

So whether it’s microbes, plants, or animals, there is no question as to whether populations evolve in response to the environment they are in and the species with which they are interacting. Evolution happened, is happening, and will continue to happen. I study evolutionary processes because I believe an understanding of how populations respond to selection is the only way we will be able to produce enough food, fight disease, and protect natural populations.

1 Pérez-Cobas AE, Gosalbes MJ, Friedrichs A, Knecht H, Artacho A, Eismann K, Otto W, Rojo D, Bargiela R, von Bergen M, Neulinger SC, Däumer C, Heinsen FA, Latorre A, Barbas C, Seifert J, Dos Santos VM, Ott SJ, Ferrer M, & Moya A (2012). Gut microbiota disturbance during antibiotic therapy: a multi-omic approach. Gut PMID: 23236009

2Wakamoto Y, Dhar N, Chait R, Schneider K, Signorino-Gelo F, Leibler S, & McKinney JD (2013). Dynamic persistence of antibiotic-stressed mycobacteria. Science (New York, N.Y.), 339 (6115), 91-5 PMID: 23288538

3 Thompson, J. K., et al. “Mutations to antibiotic resistance occur during the stationary phase in Lactobacillus plantarum ATCC 8014.” Microbiology 143.6 (1997): 1941-1949.

4 Koskella, B. and C.M. Lively. 2009. Evidence for negative frequency-dependent selection during experimental coevolution of a freshwater snail and a sterilizing trematode. Evolution, 63(9): 2213-2221.

Your data needed….

Friday night antics. I just recently convinced my husband to try drinking upside down to cure his hiccups. He laughed at me and said, “if that worked, surely everyone would know about it by now.”

So, my first question to you, my replicate samples wonderful readers, is:

Have you ever heard of curing hiccups by drinking upside down? (i.e., top of cup to top lip, lean forward, gulp, swallow).

(Poll now closed)

If so, and only if so, did it work?

(Poll now closed)

Thank you for your help in moving the important field of hiccup-prevention forward.

UPDATE (20 January 2013): Of the 27 participants who took the poll, 21 had tried the treatment. The study revealed that 62% of readers who had tried this method were able to cure their hiccups by drinking upside down. Unfortunately, I was not able to include a placebo group. Indeed, I am very thankful that the results of this study fell out in favor of the treatment working – as I am quite sure the high personal effectiveness of the treatment has a lot to do with my believing that it will work. I still do. 

On a separate note, I came across (via this amazing site where you can see for yourself how publication rates in academia are correlated with gender:

Earlier today, after reading “Self-confidence of women in science and a camel” I started thinking about why women publish less than men. My best guess is that, among other things, women are less likely to be included in large collaborative networks and may have smaller group sizes (postdocs and PhDs) – therefore they are less likely to be in senior authorship positions. Of course, this is going to be confounded with the fact that there is a clear sex * age interaction for gender bias in science, and so we would need to do the appropriate statistics to answer this properly. However, if you use the site to examine authorship in Ecology and Evolution post-1990, the trend is quite clear:

women as first authors

I did not run statistics on this data, partially because I would feel uncomfortable doing so without controlling for career stage, but in line with my hypothesis, women are more likely to be first authors (i.e., they did the work themselves) and very unlikely to be last authors.

The same pattern holds for Molecular and Cell

women as first authors 2I would like to thank the developers of the site and the University of Washington for developing such an insightful and useful tool!

Why I dropped out of psychology and became an evolutionary biologist

Every few months or so, I go through a period of wondering why I am doing what I am doing (as a scientist, that is). It usually happens when I am talking to, or listening to a talk by, another scientist who is studying the mechanism underlying a specific feature of biology. For example, the exact mutations underlying a given disease, the specific cause of a newly emerging disease, or the cascade of interacting hormones that influences a plant’s response to the environment. In other words, when I hear other researchers who are trying to answer questions that have clear-cut answers.

Evolutionary biology is a very stimulating, but often unsatisfying field of study. There are no answers, per se, because we are working to explain phenomena or patterns that are almost certainly the result of multiple interacting factors (and not always in the same way!) We are seeking to describe how selection in the past led to the evolution of the phenotypes we see in the present and ultimately to predict how populations will evolve in response to particular selective forces in the future. Therefore, most of the action either happened well before we were born or will happen well after we are dead, and we are unlikely to find out whether we are “right.”

So why bother? Well, every researcher will have a different answer to this question. But for me, there are (at least) three very exciting reasons. First, because evolution is happening all around us, all the time – we just need to know how to look. Second, because of the new inroads being laid that allow us to understand how our and other genomes evolved millions of years earlier. And third, because experimental evolution allows us to explicitly test how evolution works and what its limits might be. Over the next few posts, I will highlight some of my favorite new work from each of these research avenues and (hopefully) explain why being an evolutionary biologist is not nearly as futile of a task as it might first appear.

Okay, so what does any of this have to do with my decision to change degrees while I was at UVA? Well I thought I wanted to study human psychology; in particular, the role that biology plays in shaping our behavior (oh if my former self could have known that microbes play a role in this, she’d have been too excited to sleep!). I sat through some really great courses, and found the whole field incredibly fascinating. By my third year I had hypotheses… lots of them. I wanted answers. Unfortunately, every paper I read used statistics to attempt to account for confounding factors – like socioeconomic status or how much support a child received from their parents – and I found this very unsatisfying indeed. I wanted to test hypotheses directly. I needed control. Of course, I agree that it is unethical to randomly assign one twin to be raised in one way and another in a different way (or to teach a sick child to be terrified of rabbits), but how else can we satisfy our curiosity? And that is why I dropped out of psychology and became an evolutionary biologist.

Some of my favorite psychology studies:

Two classic studies exploring human cruelty:

1) Stanley Milgrim’s experiment where subjects give electric shocks to others despite their screams.

For a really interesting take on this, with some new insight, I highly recommend the Radiolab podcast:

2) The Stanford prison experiment.

Photo credit:
Photo credit:

3) Why was psychology so much cooler before the advent of ethics committees? (Thanks to Jason Mansel for sharing this!)

4) The broken window effect: exploring when crime begets crime (and this one has great control treatments!)
Keizer, K., Lindenberg, S., & Steg, L. (2008). The Spreading of Disorder Science, 322 (5908), 1681-1685 DOI: 10.1126/science.1161405

And good coverage of the study:

Celebrating Google Scholar

I know there are various theories about Google’s attempts to take over the world and enslave us all in a world of consumption, but I would like to take a moment today to celebrate the unsung hero of Google: Google Scholar.

Unfortunately, Google Scholar has recently dropped from the “more” tab to the “even more” tab, which I find a relatively sad reflection of the world in which we live (replaced by Google offers, wallet, and shopping). But the Google team are still improving the Scholar site everyday.

I was SO excited when they implemented the “cite” link at the bottom of each paper on the search (if you’ve not tried this, you really should!) This feature alone has saved me hours and hours of searching for the correct citation for papers I read. But now they have really gone the extra mile: when you click the cite link, a little box opens as before, and you can add the citation straight to your reference manager (e.g. endnote). This will save so much time and is a terrific service!

So thank you Google Scholar, for making my life easier one search at a time.


Your body is a microbeland

Some people think of their bodies as a temple, others as a wonderland. Me, I think of mine as a petri dish. I am a long-term experiment on microbial community dynamics – with plenty of drama! Love stories, betrayal, war and peace. You name it; it’s going on in here somewhere.

We all think we’re special – and now science is corroborating that idea. My microbes are just as unique as I am. The bacterial community in my nasopharynx is vastly different from that of my gut, which is vastly different from that of my skin, which is vastly different from that of my mouth… and so on1. Furthermore, each of these microbial communities (called ‘microbiota’) is highly dissimilar to that of the person next to me. Although the current evidence suggests that human microbiota fall into three major types (termed ‘enterotypes’)2, the variation in exact microbial abundance and diversity among individuals is staggering; even identical twins harbor significantly different gut microbes than one another3!

I don’t always get along well with my microbiota. There are the odd days, like yesterday, where my microbial populations wreak havoc on my digestive system. Then others, where they cause me to break out in spots4. And still others, where they lend a helpful hand to intruding pathogens by conferring their acquired antibiotic resistances1. But most of the time, I am very happy with my pet microbes. They are constantly working away at alleviating my allergies5, protecting me from infection6, stabilizing my mood7, helping me repel or attract others, including pesky mosquitoes8, and allowing me to make the most of what I eat(even playing a key role in weight gain10).

I have never been particularly germ-conscious. As an evolutionary biologist, I know that a little immigration is good for the body population, fueling the fire of natural selection with a bit more additive genetic variation. So I don’t clean my counters with bleach, and I do let my dog share my bed. There are occasional consequences (I refer again to my illness yesterday), but for the most part I have a fairly healthy immune system. My philosophy is thanks in part to George Carlin’s sermon (, and thanks in part to my studies. But it is also common sense – we are the result of millions of years of evolution. If we were hypersensitive to every bacterium that landed on our kitchen counters, natural selection would have taken us out a long time ago.

I may be weird, but the fact that I am more microbe than me – 10 times more! – is my motivation for taking good care of myself. A sense of responsibility for the health and welfare of all of those microbial cells that are working with me every day to keep us going. They are why I eat right, exercise (occasionally), drink in moderation, and get enough sleep.

So the next time you are scrubbing away at your sinks or dosing yourself with anti-microbials, take a moment to think about all of those commensal bacteria working away to make you… well, you. (and, on that note, keep them to yourself!)

Some food for thought:

1Ecology drives gene exchange within human microbiota:
Smillie CS, Smith MB, Friedman J, Cordero OX, David LA, & Alm EJ (2011). Ecology drives a global network of gene exchange connecting the human microbiome. Nature, 480 (7376), 241-4 PMID: 22037308

2Our microbiota fall into three main categories (with lots of variation!):

3Microbiota of identical twins:

4Have acne? Use phage:

5A potential link between microbiome diversity and allergies:

6It seems the microbes on our skin help warn us about pathogen attack:

7Mind-altering microorganisms:

8Human skin microbiota affects attractiveness to malaria mosquitoes:

 9A nice review on the role of our gut microbes and their recent evolution:

10A core gut microbiome in obese and lean twins:

And a great piece about our microbiome’s in the Economist: