Posted June 16, 2016 by seth & filed under Uncategorized.

In genomic analyses, especially when working with non-model species, we often need to infer gene function based on similarity to other species. This means that lots of people are running the same, or similar, analyses on the same genomes and these can take a really long time to run. Everyone running the same analyses seems a bit silly so I’ve shared some of these results here. If others want to add to the list I’d be happy to include them.

Here I have uploaded the gene ontology analyses of the whole European honeybee (Apis mellifera 4.5) and buff-tailed bumblebee (Bombus terrestris 1.0) transcriptomes which was produced using Annocript. To run the analysis I shortened the names of the sequences to just the NCBI accession number. There is a control file which is the same between the two analyses although point to different fasta files. I have sanitized the control file to remove personal information and if people would like to analyze their data in a similar way they would need to point to the paths for the relevant programs.

The output file for each is a really big table with the NCBI accession number the inferred gene ontology and the sequence. For more info on the output file take a look here.

A quick note about usage. I’m happy for people to use these but please give credit and acknowledge the source of these files.

Downloads again:

Control File

Honeybee results

Bumblebee results

Here are two more bumblebee ontology files shared by Michael Lattorff which came from the now defunct B2G-FAR repository.

Bombus impatiens annot file
Bombus terrestris annot file

These analyses were run at East Carolina University by Seth Barribeau with Dr. Michael Brewer

Posted October 19, 2015 by seth & filed under Uncategorized.

I’m recruiting a PhD student to join the lab!

If want to do a PhD with me, let me know. If you know a great potential PhD student, let them know.

PhD Position in Disease Ecology at East Carolina University (ECU): One Ph.D. position is available in the newly formed lab of Dr. Seth Barribeau in the Department of Biology (http://www.ecu.edu/biology/) at East Carolina University (Greenville, NC). The Barribeau lab focuses on the evolutionary ecology of host-parasite interactions, working mostly with ecologically important insects like bumblebees. There are a number of potential projects available and the successful applicant will have a major role in determining the direction of the research. For detailed information, please see the following websites: http://www.ecu.edu/cs-cas/biology/barribeau_seth.cfm and http://seth.barribeau.com

Enthusiastic, motivated, and curious students are strongly encouraged to apply. Having skills or experience in evolutionary ecology, host-parasite interaction, immunology, or similar areas, as well as proficient writing and speaking skills are preferred. Mad skills in molecular genetics, bioinformatics, or beekeeping would be great, but we will help you work on those. Sense of humor is also a plus. But being a decent, preferably nice, human being is essential. The Department of Biology offers a lively community of researchers to interact with, providing great opportunities for collaboration. Information on the PhD Interdisciplinary Program in Biological Science can be found at http://www.ecu.edu/idpbs/. ECU is the third largest campus in the University of North Carolina system and is situated fairly close to the Atlantic coast and Outer Bank Islands, and the Research Triangle. The department has a strong integrative research program with numerous avenues of student support including student scholarships, travel to conferences, and genomics research. Interested students should send a CV, a brief (less than 500 words) description of research interests, and contact information of two references to Dr. Seth Barribeau (barribeaus14 [at] ecu [dot] edu). Interviews will begin on November 1, 2015 and continue until the positions are filled. Please contact Dr. Barribeau with any questions you may have: Department of Biology, East Carolina University Greenville, NC 27858.

Posted January 14, 2015 by seth & filed under Uncategorized.

I have recently moved to a new position but want to take a moment to thank all the amazing students that I have worked with and all the lovely people I have collaborated with in my time at the ETH in Zürich. It has been a great pleasure and while I am looking forward to the challenges of my new position I will very much miss your ideas, feedback, and encouragement.

Students (in alphabetical order)

Download (PDF, 165KB)

Franziska Brunner

Download (PDF, 165KB)

Mathilde Cathébras

Download (PDF, 165KB)

Robert Dünner

Download (PDF, 165KB)

Alain Reymond

Download (PDF, 165KB)

Eric Seiger

Download (PDF, 165KB)

Chantal Weibel

Download (PDF, 165KB)

Pascal Züger

Friends, Colleagues, & Collaborators

Redacted to avoid incrimination and retaliation.

Posted June 27, 2014 by seth & filed under Bumblebees, Paper, student.

If you imagine a scenario where an individual had unlimited resources, anything that required some investment wouldn’t be a big deal. It would be able to send some of these resources to achieve the required task and go on about its business without worrying about cutting costs elsewhere. When resources are limited, this changes. An individual must allocate resources wisely to make the best of its lot. The immune system is, in my mind, a fairly nebulous concept. It includes all of the normal immune organs and cells that you might expect but, I would argue, also includes behaviours, metabolic pathways, and probably a great deal more than we know at the moment. But while nebulous, the immune system is clearly expensive. Producing immune compounds, or growing organs, or engaging in hygienic behaviours are all expensive and leave fewer resources for other things. In our recent paper Franziska Brunner and I explored how limiting a key component of nutritional resources altered immune responses as measured by gene expression. We found that if we deprived bumblebee workers from pollen, their protein source, for even a fairly short amount of time, they have much weaker immune expression. These bees are really robust, and this wasn’t a greatly stressful condition, but even so, they were unable to upregulate key components of their immune response. It seems that a number of effectors (components of the immune system that are produced to actively kill invading parasites) are protein limited.

We also found that when the bees were protein limited the variance in their immune response reduced. Bees became more similar in their immune responses when they didn’t have enough protein. This can have important consequences because we know that when populations of animals are under stressful conditions there can be outbreaks of diseases. This reduction in expressed immune variation could help explain why diseases are better able to spread in these stressed populations. For instance, imagine a population of individuals that have a distribution of phenotypes (the outcome of the genotype and environment). Parasites that are able to infect common phenotypes do very well since there are many hosts to infect and will thus be selected for.

Download (PDF, 55KB)

Here a parasite has a range of host phenotypes that it can infect but there remain quite a few that it can’t. If, however the population becomes stressed and this shrinks the variation in phenotype, then the parasites are better able to infect a greater proportion of the population.

Download (PDF, 1.03MB)

The variation in immune phenotype might be especially important in social insect colonies, like bumblebees, since workers are very highly related to one another. Because of the haplodiploid sex determination system, and because most bumblebee queens only mate with a single male, all the workers share 75% of their genome. This means that these populations are very homogenous and would be a prime target for invasion by parasites because if a parasite can infect one worker it is very likely able to infect other sister workers. Having workers with diverse immune phenotypes while sharing most of their genome might help buffer bumblebee colonies from parasite outbreaks within the colony. At least, for as long as life isn’t too stressful.

Posted February 18, 2014 by seth & filed under Bumblebees, Paper.

Different parasite strains (of the same species of parasite) are able to infect different individuals (of the same species of host). This is called specificity or can be called a genotype-by-genotype interaction. That is, that some genotypes of parasite are able to infect some genotypes of hosts. In insects, it’s hard to understand how such specificity is generated since insects don’t have the adaptive immune system that is found in vertebrates, which is incredibly flexible, and components of which are known to produce such patterns. Insects have a comparatively modest but very functional immune system. The genes responsible for the recognition of parasites don’t tend to be vary variable (as they are in vertebrates) so it’s hard to see what could produce this pattern of specificity.

The European bumblebee Bombus terrestris is a model for this kind of specificity and we set out to try and understand how this specificity works. Based on some preliminary work it seemed that our bumblebees don’t differ much in candidate immune genes. But we know that different colonies (genotypes of bumblebees) have very different susceptibility to different genotypes of a common gut parasite (Crithidia bombi). In our paper which was just released in PNAS we look at how changes in gene expression might produce this pattern. Genes are turned on and off to achieve certain tasks, and how these genes are regulated, rather than differences in the genes themselves, could play a role in disease resistance.

We found that different parasite clones produced surprisingly different gene expression responses in the bumblebee hosts. We also found that different bumblebee colonies responded to parasite clones in different ways. These results suggest that differences in the way that bees respond to infection through the regulation of genes could also produce specificity without differences in the immune genes themselves. It is important to note that this doesn’t mean that the differences aren’t genetic, but rather that the genetic differences are coded at places other than the immune genes that deal with infection. So, for instance, there might be variation in regulatory genes rather than in antimicrobial peptides which play a major role in fighting infection.

We also found an unexpected result in our data. We found that the parasite clones that were really good at infecting bumblebees produced a different response to the parasite clone that wasn’t very good at infecting. The ‘bad’ parasite clone turned on a lot of what we’d think of as the normal immune response. The ‘good’ parasite clones didn’t. In fact, the infectious parasite clones seem to actively turn off the immune response. Parasites can manipulate all sorts of host responses from complex behaviors, to sleep patterns, and to the functioning of the immune system itself. In this case, it seems that some parasite clones are better able to control the immune system of their hosts, and some hosts are better able to resist this manipulation than others.

///// click below for full text of the paper /////

Barribeau, SM, Sadd, BM, du Plessis, L, & Schmid-Hempel, P (early online) Gene expression differences underlying genotype-by- genotype specificity in a host–parasite system. Proceedings of the National Academy of Science USA. doi/10.1073/pnas.1318628111

What are the costs of and conditions for accelerated reproduction?

Animals have complex ways of dealing with infection. Most of these constitute the immune system, but animals can do other non-immune things to either protect themselves from getting infected, or to help cope with infection (reviewed here with Ben Parker and others). These adaptations might be particularly important for animals with a weak immune system, like pea aphids. In some earlier work with Nicole Gerardo and Dan Sok I found that aphids will crank up reproduction when they detect signs of infection. This process, known as fecundity compensation or terminal investment, helps to ensure that aphids that have a higher risk of death (i.e. because of parasitism) still have some reproductive fitness.

This process of increasing reproduction makes a lot of sense, but what I wondered about is why don’t aphids do this all the time? Aphids already reproduce very quickly. Just ask anyone who finds them on their roses in spring. But they seem to be able to go faster when they are exposed to signs of risk. Surely an aphid that is permanently on this accelerated reproductive rate would outcompete all the other aphids?

To try and understand the conditions which favour fecundity compensation Gabriel Leventhal, Robert Dünner, and I used a combination of models and experiments. We were particularly interested in seeing if we could find costs of fecundity compensation which could explain why this is a plastic trait. Or, in other words, why don’t they always reproduce this quickly. We found that introducing a delay between exposure to a parasite and the onset of virulence (damage) can lead to the evolution of fecundity compensation in our model, even if there is a cost associated with changing reproduction. These costs need to be small though. Our experiment confirmed fecundity compensation in pea aphids when they are given cues of infection but we couldn’t find any costs associated with the reproductive shift, which this falls in line with the model – that costs of fecundity compensation must be small to evolve. Parasites are one factor that will shorten an aphid’s lifetime, but by no means the only factor. It’s likely that a host of conditions alter reproduction to ensure some fitness, such as changes in plant quality, temperature, or predation risk. Being able to manipulate their reproductive schedule according to risk is probably a valuable adaptation to secure fitness in changeable environments.

This paper will be published in The American Naturalist. An accepted draft of the manuscript can be found here.

Posted September 21, 2013 by seth & filed under Uncategorized.

Next year the IUSSI (International Union for the Study of Social Insects) is hosting its meeting in Cairns in Australia. These meetings are held only every four years. I have only been to one of these meetings, which was held in Copenhagen last time, but everyone raves about them. The Copenhagen meeting was excellent and the meeting next year stands to be fantastic again. I am organising a symposium along with Becky Rosengaus about how social insects deal with parasites. The aim of the symposium is to try and bring together the sometimes disparate communities that work on adaptations to parasites. On one side, some groups work on behavioural adaptations that protect social insect colonies, others might work on life history characteristics that influence parasite susceptibility, and on the other side groups are working on the molecular basis of particular resistance mechanisms or using transcriptomics to understand what insects use to protect themselves. I do a bit of both so I’m really excited to see what comes up at this meeting.

The symposium is officially called “Phenotypic phenomena and molecular basis of social insect immunity” and we have a number of confirmed invited speakers including Paul Schmid-Hempel, Sylvia Cremer, Leonard Foster, and Marla Spivak. Abstract submission is now open, so if you’re a researcher working on immunity in social insects we’d love for you to apply. You can find more information about the IUSSI2014 meeting here, and submit your abstract here.

It hardly needs saying, but Cairns is quite far away from most people. To help with the travel costs the IUSSI sections are offering support for students who want to visit Cairns and present their work. So, if you are a student working on social insects, first: join your local branch of the IUSSI, and second: apply for support so you can come to Cairns and show off your work to the world.

Posted September 7, 2013 by seth & filed under Uncategorized.

I have just begun a fellowship at the Wissenschaftskolleg in Berlin. The WIko, or Institute for Advanced Study Berlin, is a place for academics, both junior (me) and senior (me at the end of each day), to focus on a particular project, interact with other researchers, and generally think. It sounds pretty daunting. For one, I now apparently have to do the ambitious project that I suggested. Part of the attraction is not only a chance to retreat from the normal work that can accumulate but also to learn about other researchers, have time to explore new topics, and to spend some small amount of time in one of the great European cities. The Wiko has been fantastically organised in that their staff have answered our avalanche of questions quickly and patiently, have arranged all sorts of details that I would never have thought about.

We arrived last week and almost everything is humming along smoothly. The facilities are fantastic and they even give me intensive German classes which is a great bonus. Work-wise, it’s also really nice to be in Germany. There are a number of groups both around Berlin and further afield which I’ll be able to visit. Some of which have already invited me to go and give seminars. This fall might be quite busy with visits to the Freie University of Berlin, University of Kiel, the Max Planck Institute in Plön, Leipzig for a bee meeting, and the University of Copenhagen. The rest of the year should be exciting!

Things to do while at the Wiko

Learn Python.
Work on my ridiculously ambitious project.
Get a few papers out that have been waiting in the wings.
Improve my German.
Learn Python.
Push forward on some collaborations that have been relegated to the back burner to make time for experiments etc.
Explore Berlin.
Learn Python.
Other stuff.
Also, learn Python.

In case you missed it. I really want to use this time to get better acquainted with Python.

Posted by seth & filed under Paper.

Ben Sadd and I recently wrote a review about heterogeneity in infection outcomes. We were tasked with writing a review about the bumblebee-trypanosome system that we work on, but we wanted to expand the discussion a bit further than simply explaining the workings of our own system. We tried instead to use what is known in our system, which has become something of a model of host-parasite interactions, to explore the causes and consequences of variation in disease resistance that exists in nature. In the review we talk about a great many things but the key point in my mind is that the relationship between parasites and their hosts is complex, infection outcome is rarely certain, and we need to learn why that is the case to make much headway in our understanding of disease dynamics. There are lots of causes of variation in disease outcome, including both the genetic background of the host, and the parasite, the history of the host, the environment, the other microorganisms that it has encountered, both parasitic and beneficial, all play a role in whether that individual gets sick.

When designing experiments, it is often a good idea to reduce variation in order to clearly assess what of the controlled factors are important in whatever it happens to be that you are measuring. This reduces any superfluous noise and allows you to better detect how your factors are involved. But while this approach is very good at finely attributing relationships under controlled conditions it can suffer from being over controlled. This may sound like I’m badmouthing controlled experiments, but I’m not; they are vital. What I am suggesting, and what Ben and I talk about in our review, is that variation on both the host side and the parasite side can be important in determining disease outcome and this variation could also suggest how general the findings are. For instance in my work, we see huge variation in how different families (colonies) of our bumblebee host respond to different clones of our trypanosome parasite species. If we were to base our understanding about how bumblebees interact with trypanosomes based on a single host-parasite genetic combination, we would be missing a huge part of the story.

Posted by seth & filed under Uncategorized, Workshop.

I was recently lucky enough to attend a workshop on the promises and challenges of big data held at the Okinawa Institute of Science and Technology (OIST). I have a personal affinity to Japan after living there for a short time, and had previously visited Okinawa briefly, so I was thrilled to have a chance to return and stock up on Okinawa soba and awamori while learning about the trials and tribulations of dealing with big data. The material was a mix between lectures, covering the visiting speakers’ research and how they interact with big data (from ecology, evolutionary theory, climate change, genomics, and molecular biology), tutorials, and finally group projects.

While there were some hiccups, there were problems with the server and some last minute speaker cancellations, the course was a success. The organisers, speakers, and other participants were fantastic. The topic is, however, as unruly as the data we’re trying to manage, and the organisers did an admirable job given that this was the freshman attempt. I can see the course developing into an even more valuable exercise as both data gets bigger and as the the course works itself through the freshman kinks. The individual projects were a great deal of fun, and the quality of the results produced in such a short time was fantastic.

Beyond spending a huge amount of time in front of speakers, computers, and the beer vending machine, there was also an opportunity to see some natural light, go snorkelling, sample the local awamori (some of which contained a little extra flavor courtesy of the habu pit viper pickled within the bottle) and visit a couple of the local attractions including the aquarium, castle ruins, and some local craftsfolk. As my old friend Koji lives in Okinawa I also had a chance to wander off briefly to catch up and visit a ceramics cooperative where I met the local sensei, and was able to buy a few small, extremely fine, pieces of his work. I would have loved to come away with more, but both funds and a small carry-on suitcases were limiting.

Just north of the OIST was a spectacular cliff with more than a passing resemblance to an elephant.

According to the informational material. Most of the island’s non-human inhabitants were put there solely to kill us. Sadly, we didn’t see a single, non-pickled, habu.

Manga bacteria: sciencey!

Kaito found a frogfish (and a baby pufferfish) and somehow managed to very gently convince it to swim into his water bottle for better viewing. The bottle had sea water in it and the fish was safely returned to the ocean after we all ‘oohed’, ‘aahed’, and ‘kawaiied’ sufficiently. <<< photo from Kaito Kikuchi >>>

Bright blue and delicious looking at the Churaumi aquarium. There was also an amazing dolphin show, but I find those a little weird. Something about watching animals do tricks leaves me impressed and sad at the same time. The manatees, however, looked like they were in heaven quietly munching on veggies in the next display over.

Some of the ceramics that I couldn’t afford or carry. The sensei’s work was incredibly varied, from quite coarse, raw clays and burnt looking glazes, to extremely fine sake cups with delicate celadon glazes.

Even the roadworks were cute! Here the barrier are reflective interpretations of Shisa, protective dog/lions that decorate Okinawan buildings.

OISTers at the castle ruins.

Gene ontology of honeybees and bumblebees

PhD student wanted!

Big thanks!

It’s all about resources

How gene expression can produce specificity

What are the costs of and conditions for accelerated reproduction?

IUSSI 2014 in Cairns and our symposium on immunity in social insects.

A fellowship.

Why infection outcome varies, and why it matters.

The promises of big data, long nights, awamori, and fine porcelain.