Journal club of one: ”Give one species the task to come up with a theory that spans them all: what good can come out of that?”

This paper by Hanna Kokko on human biases in evolutionary biology and behavioural biology is wonderful. The style is great, and it’s full of ideas. The paper asks, pretty much, the question in the title. How much do particularities of human nature limit our thinking when we try to understand other species?

Here are some of the points Kokko comes up with:

The use of introspection and perspective-taking in invention of hypotheses. The paper starts out with a quote from Robert Trivers advocating introspection in hypothesis generation. This is interesting, because I’m sure researchers do this all the time, but to celebrate it in public is another thing. To understand evolutionary hypotheses one often has to take the perspective of an animal, or some other entity like an allele of an enhancer or a transposable element, and imagine what its interests are, or how its situation resembles a social situation such as competition or a conflict of interest.

If this sounds fuzzy or unscientific, we try to justify it by saying that such language is a short-hand, and what we really mean is some impersonal, mechanistic account of variation and natural selection. This is true to some extent; population genetics and behavioural ecology make heavy use of mathematical models that are free of such fuzzy terms. However, the intuitive and allegorical parts of the theory really do play an important role both in invention and in understanding of the research.

While scientists avoid using such anthropomorphizing language (to an extent; see [18,19] for critical views), it would be dishonest to deny that such thoughts are essential for the ease with which we grasp the many dilemmas that individuals of other species face. If the rules of the game change from A to B, the expected behaviours or life-history traits change too, and unless a mathematical model forces us to reconsider, we accept the implicit ‘what would I do if…’ as a powerful hypothesis generation tool. Finding out whether the hypothesized causation is strong enough to leave a trace in the phylogenetic pattern then necessitates much more work. Being forced to examine whether our initial predictions hold water when looking at the circumstances of many species is definitely part of what makes evolutionary and behavioural ecology so exciting.

Bias against hermaphrodites and inbreeding. There is a downside, of course. Two of the examples Kokko gives of human biases possibly hampering evolutionary thought are hermaphroditism and inbreeding — two things that may seem quite strange and surprising from a mammalian perspective, but are the norm in a substantial number of taxa.

Null models and default assumptions. One passage clashes with how I like to think. Kokko brings up null models, or default assumptions, and identifies a correct null assumption with being ”simpler, i.e. more parsimonious”. I tend to think that null models may be occasionally useful for statistical inference, but are a bit suspect in scientific reasoning. Both because there’s an asymmetry in defaulting to one model and putting the burden of proof on any alternative, and because parsimony is quite often in the eye of the beholder, or in the structure of the theories you’ve already accepted. But I may be wrong, at least in this case. If you want to formulate an evolutionary hypothesis about a particular behaviour (in this case, female multiple mating), it really does seem to matter for what needs explaining if the behaviour could be explained by a simple model (bumping into mates randomly and not discriminating between them).

However, I think that in this case, what needs explaining is not actually a question about scope and explanatory power, but about phylogeny. There is an ancestral state and what needs explaining is how it evolved from there.

Group-level and individual-level selection. The most fun part, I think, is the speculation that our human biases may make us particularly prone to think of group-level benefits. I’ll just leave this quote here:

Although I cannot possibly prove the following claim, I consider it an interesting conjecture to think about how living in human societies makes us unusually strongly aware of the group-level consequences of our actions. Whether innate, or frequently enough drilled during upbringing to become part of our psyche, the outcome is clear. By the time a biology student enters university, there is a belief in place that evolution in general produces traits because they benefit entire species. /…/ What follows, then, is that teachers need to point out the flaws in one set of ideas (e.g. ‘individuals die to avoid overpopulation’) much more strongly than the other. After the necessary training, students then graduate with the lesson not only learnt but also generalized, at which point it takes the form ‘as soon as someone evokes group-level thinking, we’ve entered “bad logic territory”’.


Kokko, Hanna. (2017) ”Give one species the task to come up with a theory that spans them all: what good can come out of that?” Proc. R. Soc. B. Vol. 284. No. 1867.

Selected, causal, and relevant

What is ”function”? In discussions about junk DNA people often make the distinction between ”selected effects” and ”causal roles”. Doolittle & Brunet (2017) put it like this:

By the first (selected effect, or SE), the function(s) of trait T is that (those) of its effects E that was (were) selected for in previous generations. They explain why T is there. … [A]ny claim for an SE trait has an etiological justification, invoking a history of selection for its current effect.


ENCODE assumed that measurable effects of various kinds—being transcribed, having putative transcription factor binding sites, exhibiting (as chromatin) DNase hypersensitivity or histone modifications, being methylated or interacting three-dimensionally with other sites — are functions prima facie, thus embracing the second sort of definition of function, which philosophers call causal role …

In other words, their argument goes: a DNA sequence can be without a selected effect while it has, potentially several, causal roles. Therefore, junk DNA isn’t dead.

Two things about these ideas:

First, if we want to know the fraction of the genome that is functional, we’d like to talk about positions in some reference genome, but the selected effect definition really only works for alleles. Positions aren’t adaptive, but alleles can be. They use the word ”trait”, but we can think of an allele as a trait (with really simple genetics — its genetic basis its presence or absence in the genome).

Also, unfortunately for us, selection doesn’t act on alleles in isolation; there is linked selection, where alleles can be affected by selection without causally contributing anything to the adaptive trait. In fact, they may counteract the adaptive trait. It stands to reason that linked variants are not functional in the selected effect sense, but they complicate analysis of recent adaptation.

The authors note that there is a problem with alleles that have not seen positive selection, but only purifying selection (that could happen in constructive neutral evolution, which is when something becomes indispensable through a series of neutral or deleterious substitutions). Imagine a sequence where most mutations are neutral, but deleterious mutations can happen rarely. A realistic example could be the causal mutation for Freidreich’s ataxia: microsatellite repeats in an intron that occasionally expand enough to prevent transcription (Bidichandani et al. 1998, Ohshima et al. 1998; I recently read about it in Nessa Carey’s ”Junk DNA”). In such cases, selection does not preserve any function of the microsatellite. That a thing can break in a dangerous way is not enough to know that it was useful when whole.

Second, these distinctions may be relevant to the junk DNA debate, but for any research into the genetic basis of traits currently or in the future, such as medical genetics or breeding, neither of these perspectives is what we need. The question is not what parts of the genome come from adaptive alleles, nor what parts of the genome have causal roles. The question is what parts of the genome have causal roles that are relevant to the traits we care about.

The same example is relevant. It seems like the Friedriech’s ataxia-associated microsatellite does not fulfill the selected effect criterion. It does, however, have a causal role, and a causal role relevant to human disease, at that.

I do not dare to guess whether the set of sequences with causal roles relevant to human health is bigger or smaller than the set of sequences with selected effects. But they are not identical. And I will dare to guess that the relevant set, like the selected effect set, is a small fraction of the genome.


Doolittle, W. Ford, and Tyler DP Brunet. ”On causal roles and selected effects: our genome is mostly junk.” BMC biology 15.1 (2017): 116.

Johan Frostegård ”Evolutionen och jag”

Jag läste Johan Frostegårds bok om evolutionen och människan över jul. Frostegård är allmänbildad och skriver småtrevligt om lite allt möjligt — lite om människans förhistoria, evolutionära öppna frågor som sexuell fortplantning, altruism, typiskt mänskliga egenskaper, två kapitel om syfilis, plus författarens syn på vetenskaps-, medvetande- och moralfilosofi. Samt Gud och Bob Dylan. Det är kul med en bok om evolution som har så många skönlitterära citat. Det bästa kapitlet är nog kapitel 18, ”Immunologi, evolutionen och jag” som berör hans egen forskning.

Men jag har ett par invändningar. Det går för fort. Jag hänger inte med. Boken stannar aldrig särskilt länge på något ämne. Men det finns ett övergripande tema: att olika ämnen — medicin, moral, nationalekonomi, humaniora — skulle tjäna på en evolutionär analys. Tyvärr är den evolutionära analysen i boken ibland inte särskilt bra. Här är två exempel i detalj:

Så här står det på sidan 89 om färgseende:

Tänk bara på färgblindhet som finns i mycket högre grad hos män än hos kvinnor, och där en rätt rimlig förklaring kan vara att detta ger en fördel när det gäller synförmåga på långa distanser, där den färgblinde anses ha större förmåga att urskilja kontraster, vilket utnyttjats även i moderna arméer. Dess förekomst är statistiskt sett på många håll ungefär som om en i varje jägarlag skulle vara färgblind.

Vad är problemet här?

Det är inte uteslutet att röd–grön-färgblindhet kommer med vissa fördelar också skulle kunna vara föremål för naturligt urval i människor under vissa omständigheter. Som sagt, det finns forskning som tyder på att det finns fördelar och nackdelar med att se två respektive tre färger. Och det är tydligen inte helt ovanligt att primater har variation i färgseende inom arten (Surridge, Osorio & Mundy 2003).

Men frågan är, om det nu är bättre (obs, hypotetiskt) att se två färger och inte tre, varför är inte alla män färgblinda? Det finns flera olika omständigheter när naturligt urval göra så att det finns flera varianter av en gen i en population. Det vill säga: att det fortsätter finnas flera varianter av en gen, efter att den nya varianten uppstått genom mutation. Det händer när en variant är bra ibland, dålig ibland, och kallas balanserande selektion.

Det kan vara så att en genetisk variant har både positiva och negativa egenskaper, som gör att de individer som har en kopia av den (bär den i heterozygot tillstånd) får den bästa balansen av för- och nackdelar. Ett annat alternativ är att en genetisk variant ger fördelar när den är ovanlig i populationen, men är dålig när många andra bär på den.

Men det är också möjligt att färgblindhet uppstår hyfsat ofta genom mutation och att det inte är särskilt skadligt, och kan vara vanligt av den anledningen.

Hur det ligger till är en empirisk fråga. Det räcker inte med en idé om hur något skulle kunna vara en fördel för att ha en bra evolutionär hypotes. Vad tar läsaren med sig från resonemanget om hen inte redan vet vad balanserande selektion är? Jo, en typ av spekulation — om det finns ärftlig variation i egenskap X kanske det beror på att den har en evolutionär fördel — utan vidare data eller bevis, som är vanlig men missvisande.

Exempel 2: Det finns några passager och altruismens evolution och diskussionen om släktskap och gruppselektion.

E.O. Wilson beskriver människosläktets sociala förmåga, kallad eusocialitet, som en central egenskap, och anför till och med gruppselektion som en bakomliggande mekanism, det senare något som blivit mycket ifrågasatt. [38, 53] Gruppselektion innebär att konkurrensen i naturen, som är det naturliga urvalets motor, inte bara sker på individnivå utan även på gruppnivå. (s. 91)


Men en mindre grupp talar för teorin, med nestorn inom sociobiologi, E.O. Wilson, som ett framträdande namn. Han publicerade i den prestigefyllda tidskriften Nature en artikel där han med två medförfattare och matematiska modeller beskrev gruppselektion som en förklaring till social samverkan hos sociala djur som människan [38].

Studien blev genast omdebatterad och hårt kritiserad, bland annat av Richard Dawkins som menar att teorin om gruppselektion bortser från att det är generna som är i centrum för evolutionen, i kraft av att vara replikatorer. Detta förnekar inte heller Wilson. Dock är inte sista ordet sagt, och min gissning är att Wilsons uppfattning kommer vinna mark [37, 256]. (s. 307)

Ja, altruismnördar, referens nummer 38 är ingen mindre än Nowak, Tarnita & Wilson (2010). Nummer 256 är den svarsartikel som 140 evolutionsbiologer skrev i samma tidskrift. Och nej, det tillhör inte direkt vanligheterna att en vetenskaplig tidskrift följs av ett protestupprop i samma tidskrift. (Nummer 37 är en recension som Dawkins skrivit av en av Wilsons böcker.)

Det här är inte en lätt debatt att referera, och den går som synes något djupare än ett meningsutbyte mellan Wilson och Dawkins. Och Nowak, Tarnita & Wilson (2010) är inte någon lätt artikel att läsa. Det är nog inte bara författarnas fel, utan också tidskriftens utrymmesbegränsningars. Den består nämligen av sex sidor ”artikel” och 43 sidor ”supplementary materials” med alla detaljer. Den matematiska modellen får en dryg halv sida i själva artikeln, utan vare sig resultat eller beskrivning av metoden.

Vad kan vi säga om den?

För det första: ”eusocialitet” är inte riktigt ett ord för ”människans speciella sociala natur”. Det är det speciella sociala system där djur lever i kolonier där bara en minoritet reproducerar sig och de andra är sterila. Tänk bisamhällen, myrsamhällen och kolonier av nakenråttor. Författarna tycker uppenbarligen att eusocialitet har tillräckligt gemensamt med arbetsdelning hos människor för att det ska vara en intressant analogi, men det de skriver om människans sociala evolution i artikeln är bara det här:

We have not addressed the evolution of human social behavior here, but parallels with the scenarios of animal eusocial evolution exist, and they are, we believe, well worth examining.

För det andra: det här är en debatt om matematiska modeller. Det är inget fel med det. Matematiska modeller och teoretisk forskning är utmärkt, särskilt om man vill studera något som inte går att observera. I det här fallet hur ett visst beteende uppstod i en sedan länge utdöd förmoder och -fader till en art. Men en diskussion om det bästa sättet att bygga en matematisk modell för ett hypotetiskt scenario blir lätt en smula … teoretisk.

Om vi vill bygga matematiska modeller av hur altruism uppstod finns det lite olika sätt att räkna. Tänk på arbetsbina i ett bisamhälle. Varför har de förlorat förmågan att lägga ägg? Ett sätt är att räkna ut hur många barn de kan få indirekt genom att drottningen, alltså deras mamma, lägger ägg. Om deras arbete gör att drottningen lägger tillräckligt många ägg kan det vara ett effektivare sätt för dem att sprida sina gener än om de skulle ge sig ut i världen och lägga ägg på egen hand. Det är släktskapsselektion (Frostegård beskrier det på s. 304), och sättet att räkna kallas ”inclusive fitness”. ”Fitness” betyder reproduktiv framgång, och ”inclusive fitness” är reproduktiv framgång med släktingarnas bidrag inräknat.

För det tredje så handlar Nowak, Tarnita & Wilson (2010) inte om gruppselektion. Inte direkt, i alla fall. Artikeln är en attack mot släktskapsselektion som förklaring för eusocialitet. De hävdar istället att deras modell, som inte räknar på arbetarnas inclusive fitness, utan istället beskriver hur en mutation som får arbetare att stanna kvar i boet sprider sig i en population, är mer realistisk. Men framför allt verkar de tycka att den är snyggare. Så här skriver de i artikeln:

By formulating a mathematical model of population genetics and family structure, we see that there is no need for inclusive fitness theory. The competition between the eusocial and the solitary allele is described by a standard selection equation. There is no paradoxical altruism, no payoff matrix, no evolutionary game. A ”gene-centered” approach for the evolution of eusociality makes inclusive fitness theory unnecessary.

Och sedan i kommentarer på Nowaks grupps hemsida:

Our paper does not study group selection, and it does not compare group selection
and inclusive fitness. But given the limitations of inclusive fitness it is clear that many models of group selection cannot be analyzed in terms of inclusive fitness. Also note that our model for the evolution of eusociality is not a group selection model; instead it describes selection operating at the level of genes.

Som sagt, den här debatten är rätt teknisk, och på ren svenska en jävla röra. Jag förstår att man inte vill gå in på detaljer i en populärvetenskaplig bok på ämnet. Jag vill inte gå in på detaljer heller. Men än en gång kan man fråga sig om en läsare som inte redan är insatt i ämnet blir något klokare av det här. Vad får vi med oss förutom det felaktiga intrycket att eusocialitet är ”människosläktets sociala förmåga” och ett auktoritetsargument för gruppselektion?


Frostegård, Johan. (2017) Evolutionen och jag. Volante. Stockholm.

Nowak, Martin A., Corina E. Tarnita, Edward O. Wilson. (2010) ”The evolution of eusociality.” Nature 466.7310

Abbot, Patrick, et al. (2011) ”Inclusive fitness theory and eusociality.” Nature 471.7339

Surridge, Alison K., Daniel Osorio, and Nicholas I. Mundy. (2003) ”Evolution and selection of trichromatic vision in primates.” Trends in Ecology & Evolution 18.4

European Society for Evolutionary Biology congress, Groningen, 2017

The European Society for Evolutionary Biology meeting this year took place August 20–25 in Groningen, Netherlands. As usual, the meeting was great, with lots of good talks and posters. I was also happy to meet colleagues, including people from Linköping who I’ve missed a lot since moving.

Here are some of my subjective highlights:

There were several interesting talks in the recombination symposium, spanning from theory to molecular biology and from within-population variation to phylogenetic distances. For example: Irene Tiemann-Boege talked about recombination hotspot evolution from the molecular perspective with mutation bias and GC-biased gene conversion (Arbeithuber & al 2015), while Franciso Úbeda de Torres presented a population genetic model model of recombination hotspots. I would need to pore over the paper to understand what was going on and if the model solves the hotspot paradox (as the title said), and how it is different from his previous model (Úbeda & Wilkins 2011).

There were also talks about young sex chromosomes. Alison Wright talked about recombination suppression on the evolving guppy sex chromosomes (Wright & al 2017), and Bengt Hansson about the autosome–sex chromosome fusion in Sylvioidea birds (Pala & al 2012).

Piter Bijma gave two (!) talks on social genetic effects. That is when your trait value depends not just on your genotype, but on the genotype on others around you, a situation that is probably not at all uncommon. After all, animals often live in groups, and plants have to stay put where they are. One can model this, which leads to a slightly whacky quantitative genetics where heritable variance can be greater than the trait variance, and where the individual and social effects can cancel each other out and prevent response to selection.

I first heard about this at ICQG in Edinburgh a few years ago (if memory serves, it was Bruce Walsh presenting Bijma’s slides?), but have only made a couple of fairly idle and unsuccessful attempts to understand it since. I got the feeling that social genetic effects should have some bearing on debates about kin selection versus multilevel selection, but I’m not sure how it all fits together. It is nice that it comes with a way to estimate effects (given that we know which individuals are in groups together and their relatedness), and there are some compelling case studies (Wade & al 2010). On the other hand, separating social genetic effects from other social effects must be tricky; for example, early social environment effects can look like indirect genetic effects (Canario, Lundeheim & Bijma 2017).

Philipp Gienapp talked about using realised relatedness (i.e. genomic relationships a.k.a. throw all the markers into the model and let partial pooling sort them out) to estimate quantitative genetic parameters in the wild. There is a lot of relevant information in the animal breeding and human genetics literature, but applying these things in the wild comes with challenges that deserves some new research to sort things out. Evolutionary genetics, similar to human genetics, is more interested in parameter estimation than prediction of phenotypes or breeding values. On the other hand, human genetics methods often work on GWAS summary statistics. In this way, evolutionary genetics is probably more similar to breeding. Also, the relatedness structure of the the populations may matter. Evolution happens in all kinds of populations, large and small, structured and well-mixed. Therefore, evolutionary geneticists may work with populations that are different from those in breeding and human genetics.

For example, someone asked about estimating genetic correlations with genomic relationships. There are certainly animal breeding and human genetics papers about realised relatedness and genetic correlation (Jia & Jannik 2012, Visscher & al 2014 etc), because of course, breeders need to deal a lot with correlated traits and human geneticists really like finding genetic correlations between different GWAS traits.

Speaking of population structure, Fst scans are still all the rage. There was a lot of discussion about trying to find regions of the genome that stand out as more differentiated in closely related populations (”genomic islands of speciation/divergence/differentiation”), and as less differentiated in mostly separated populations (introgression, possibly adaptive). But it’s not just Fst outliers. It’s encouraging to see different kinds of quantitative and population genomic methods applied in the same systems. On the hybrid and introgression side of things, Leslie Turner (Turner & Harr 2014) and Jun Kitano (Ravinet & al 2017) gave interesting talks on mice and sticklebacks, respectively. Danièle Filiaut showed an super impressive integrative GWAS and selection mapping study of local adaptation in Swedish Arabidopsis thaliana (Kedaffrec & al 2016).

Susan Johnston spoke about recombination mapping in Soay sheep and Rum deer (Johnston & al 2016, 2017). Given how few large long term genetic studies like this there are, it’s marvelous to be see the same kind of analysis in two parallel systems. Jason Munshi-South gave what seemed like a fascinating talk about rodent evolution in New York City (Harris & Munshi-South 2017). Unfortunately, too many other people thought so too, and I mostly failed to eavesdrop form the corridor.

Finally, Nina Wedell gave a wonderful presidential address about Evolution in the 21th century. ”Because I can. I’m the president now.” Yes!

The talk was about threats to evolutionary biology, examples of it’s usefulness and a series of calls to action. I liked the part about celebrating science much more than the common call to explain science to people. You know, like you hear at seminars and the march for science: We need to ”get out there” (where?) and ”explain what we’re doing” (to whom?). Because if it is true that science and scientists are being questioned, then scientists should speak in a way that works even if they’re not starting by default from a position of authority. Scientists need not just explain the science, but justify why the science is worth listening to in the first place.

”As your current president, I encourage you to celebrate evolution!”

I think this is precisely right, and it made me so happy. Of course, it leaves questions like ”What does that mean?”, ”How do we do it?”, but as a two word slogan, I think it is perfect.

Celebration aligns with sound rhetorical strategy in two ways. First, explanation is fine when someone asks for it, or is otherwise already disposed to listen to an explanation. But otherwise, it is more important to awaken interest and a positive state of mind before laying out the facts. (I can’t claim to be any kind of rhetorics expert. But see Rhetoric: for Herennius, Book I, V-VII for ancient wisdom on the topic.) By the way, I’m sure this is what people who are good at science communication actually do. Second, celebration means concentrating on the excitement and wonder, and the good things science can do. In that way, it prevents the trap of listing all the bad things that will happen if Trumpists, creationists and anti-vaccine activists get their way.

Nina Wedell also gave examples of the usefulness of evolution: biomimicry, directed evolution of enzymes, the power of evolutionary algorithms, plant and animal breeding, and prevention of resistance to herbicides and antibiotics. These are all good, worthy things, but also quite a limited subset of evolutionary biology? Maybe this idea is that evolutionary biology should be a basic science supporting applications like these. In line with that, she brought up how serendipitous useful things can come from studying strange diverse organisms and figuring out how they do things. The example in talk was the CRISPR–Cas system. Similar stories apply to a other proteins used as biomedical and biotechnology tools, such as Taq polymerase and Green fluorescent protein.

I have to question a remark about reproducibility, though. The list of threats included ”critique of the scientific method” and concerns over reproducibility, as if this was something that came from outside of science. I may have misunderstood. It was a very brief comment. But if problems with reproducibility are a threat to science, and I think they can be, then it’s not just a problem of image but a problem with how scientists perform, analyse, and report their science.

Evolutionary biology hasn’t been in the reproducibility crisis news the same way as psychology or behavioural genetics, but I don’t know if that is because of better quality, or just that no one has looked that carefully for the problems. There are certainly contradictory results here too, and the same overly flexible data analysis and selective reporting practices that cause problems elsewhere must be common in evolution too. I can think of some reasons why evolutionary biology may be better off. Parts of the field default to analysing data with multilevel or mixed models. Mixed models are not perfect, but they help with some multiple testing problems by fitting and partially pooling a lot of coefficients in the same model. Also, studies that use classical model organisms may be able to get a lot of replication, low variance, and large sample sizes in a way that is impossible for example with human experiments.

So I don’t know if there is a desperate need for large initiatives for replication of key results, preregistration of studies, and improvement of data analysis practice in evolution; there may or there may not. But wouldn’t it still be wonderful if we had them?

Bingo! I don’t have a ton of photos from Groningen, but here is my conference bingo card. Note what conspicuously isn’t filled in: the poster sessions took place in nice big room, and were not that loud. In retrospect, I probably didn’t go to enough of the non-genetic inheritance talks, and I should’ve put Fisher 1930 instead of 1918.

EBM 2016, Marseille

In September, I went to the 20th Evolutionary Biology Meeting in Marseille. This is a very nice little meeting. I listened to a lot of talks, had some very good conversations, met some people, and presented our effort to map domestication traits in the chicken with quantitative trait locus mapping and gene expression (Johnsson & al 2015, 2016, and some unpublished stuff).

Time for a little conference report. Late, but this time less than a year from the actual conference. Here are some of my highlights:

Richard Cordaux on pill bugs, Wolbachia and sex manipulation — I did not know that Wolbachia, the intracellular parasite superstar of arthropods, had feminization of hosts in its repertoire (Cordaux & al 2004). Not only that, but in some populations of pill bugs, a large chunk of the genome of the feminizing Wolbachia has inserted into the pill bug genome, thus forming a new W chromosome (Leclercq & al 2016, published since the conference). He also told me how this is an example of the importance of preserving genetic resources — the lines of pill bugs have been maintained for a long time, and now they’re able to return to them with genomics tools and continue old lines of research. I think that is seriously cool.

Olaya Rendueles Garcia on positive frequency-dependent selection maintaining diversity in social bacterium Myxococcus xanthus (Rendueles, Amherd & Velicer 2015) — In my opinion, this was the best talk of the conference. It had everything: an interesting phenomenon, a compelling study system, good visuals and presentation. In short: M. xanthus of the same genotype tend to cooperate, inhabit their own little turfs in the soil, and exclude other genotypes. So it seems positive frequency-dependent selection maintains diversity in this case — diversity across patches, that is.

A very nice thing about this kind of meetings is that one gets a look into the amazing diversity of organisms. Or as someone put it: the complete and utter mess. In this department, I was particularly struck by … Sally Leys — sponges; Marie-Claude Marsolier-Kergoat — bison; Richard Dorrell — stramenopile chloroplasts.

I am by no means a transposable elements person. In fact, one might believe I was actively avoiding transposable elements by my choice of study species. But transposable elements are really quite interesting, and seem quite important to genome evolution, both to neutrally evolving and occasionally adaptive sequences. This meeting had a good transposon session, with several interesting talks.

Anton Crombach presented models the gap gene network in Drosophila melanogaster and Megaselia abdita, with some evolutionary perspectives (Crombach & al 2016). A couple of years ago, Marjoram, Zubair & Nuzhdin used the gap gene network as their example model to illustrate the suggestion to combine systems biology models with genetic mapping. I very much doubt (though I may be wrong; it happens a lot) that there is much meaningful variation within populations in the gap gene network. A between-species analysis seems much more fruitful, and leads to the interesting result where the outcome, in terms of gap gene expression along the embryo, is pretty similar but the way that the system gets there is quite different.

If you’ve had a beer with me and talked about the future of quantitative genetics, you’re pretty likely to have heard me talk about how in the bright future, we will not just map variation in phenotypes, but in the parameters of dynamical models. (I also think that the mapping will take place through fully Bayesian hierarchical models where the same posterior can be variously summarized for doing genomic prediction or for mapping the major quantitative trait genes, interactions etc. Of course, setting up and running whole-genome long read sequencing will be as convenient and cheap as an overnight PCR. And generally, there will be pie in the sky etc.) At any rate, what Anton Crombach showed was an example of combining systems biology modelling with variation (between clades). I thought it was exciting.

It was fun to hear Didier Raoult, one of the discoverers of giant viruses, speak. He was somewhat of a quotation machine.

”One of the major problems in biology is that people believe what they’ve learned.”

(About viruses being alive or not) ”People ask: are they alive, are they alive? I don’t care, and they don’t care either”

Very entertaining, and quite fascinating stuff about giant viruses.

If there are any readers out there who worry about social media ruining science by spilling the beans about unpublished results presented at meetings, do not worry. There were a few more cool unpublished things. Conference participants, you probably don’t know who you are, but I eagerly await your papers.

I think this will be the last evolution-themed conference for me in a while. The EBM definitely has a different range of themes than the others I’ve been to: ESEB, or rather: the subset of ESEB I see choosing my adventure through the multiple-session programme, and the Swedish evolution meetings. There was more molecular evolution, more microorganisms and even some orgin of life research.

A year ago in Lund: the panel discussion at Evolution in Sweden 2016

This meeting took place on the 13th and 14th of January 2016 in Lund. It feels a bit odd to write about it now, but my blog is clearly in a state of anachronistic anarchy as well as ett upphöjt tillstånd av språklig förvirring, so that’s okay. It was a nice meeting, spanning quite a lot of things, from mosasaurs to retroviruses. It ended with a panel discussion of sorts that made me want to see more panel discussions at meetings.

The panel consisted of Anna-Liisa Laine, Sergey Gavrilets, Per Lundberg, Niklas Wahlberg, and Charlie Cornwallis, and a lot of people joined in with comments. I don’t know how the participants were chosen (Anna-Liisa Laine and Sergey Gavrilets were the invited speakers, so they seem like obvious choices), or how they were briefed; Per Lundberg served as a moderator and asked the other participants about their predictions about the future of the field (if memory serves me right).

I thought some of the points were interesting. One of Sergey Gavrilets’ three anticipated future developments was links between different levels of organisation; he mentioned systems biology and community ecology in the same breath. This sounded interesting to me, who not so secretly dreams of the day when systems biology, quantitative genetics, and populations genetics can all be brought to bear on the same phenotypes. (The other two directions of research he brought up were cliodynamics and human evolution.) He himself had, earlier in his talk, provided an example where a model of human behaviour shows the possibility of something interesting — that a kind of cooperation or drive for equality can be favoured without anything like kin or group selection. That is, in some circumstances it pays to protect the weak, and thus make sure that they bullies do not get too much ahead. He said something to the effect that now is the time to apply evolutionary biology to humans. I would disagree with that. On the one hand, if you are interested in studying humans, any time is the time. On the other hand, if the claim is that now, evolutionary biology is mature and solid, so one can go out and apply it to help other disciplines to sort out their problems … I think that would be overly optimistic.

A lot of the discussion was about Mats Björklund‘s talk about predicting evolution, or failing to do so. Unfortunately, I think he had already left, and this was the one talk of the conference that I missed (due to dull practical circumstances stemming from a misplaced wallet), so this part of the discussion mostly passed me by.

A commonplace that recurred a few times was jokes about sequencing … this or that will not be solved by sequencing thousands of genomes, or by big data — you know the kind. This is true, of course; massively parallel sequencing is good when you want to 1) make a new reference genome sequence; 2) get lots and lots of genetic markers or 3) quantify sequences in some library. That certainly doesn’t cover all of evolutionary biology, but it is still quite useful. Every time this came up part of me felt like putting my hand up to declare that I do in fact think that sequencing thousands of individuals is a good idea. But I didn’t, so I write it here where even fewer people will read it.

This is (according to my notes) what the whiteboard said at the end of the session:

”It’s complicated …”
”We need more data …”
”Predictions are difficult/impossible”
”We need more models”

Business as usual
Eventually we’ll get there (where?)
Revise assumptions, models, theories, methods, what to measure

Nothing in evolutionary biology makes sense except in the light of ecology phylogeny disease

Everything in evolution makes sense in the light of mangled Dobzhansky quotes.

(Seriously, I get why pastiches of this particular quote are so common: It’s a very good turn of phrase, and one can easily substitute the scientific field and the concept one thinks is particularly important. Nothing in behavioural ecology makes sense except in the light of Zahavi’s handicap principle etc. It is a fun internal joke, but at the same time sounds properly authoritative. Michael Lynch’s version sometimes seems to be quoted in the latter way.)

Paper: ”Feralisation targets different genomic loci to domestication in the chicken”

It is out: Feralisation targets different genomic loci to domestication in the chicken. This is the second of our papers on the Kauai feral and admixed chicken population, and came out a few days ago.

The Kauai chicken population is kind of famous: you can find them for instance on Flickr, or on YouTube. We’ve previously looked at their plumage, listened to the roosters’ crowings, and sequenced mitochondrial DNA to investigate their origins. Based on this, we concur with the common view that the chickens of Kauai probably are a mixture of feral birds of domestic origin and wild Junglefowl. The Kauai chickens look and sound like a mix of wild and domestic, and we found mitochondrial DNA of two haplogroups, one of which (called D) is typical in ancient chicken DNA from Pacific islands (Gering et al 2015).

In this paper, we looked at the rest of the genome of the same chickens — you didn’t think we sequenced the whole thing just to look at the mitochondrion plus a subset of markers, did you? We turn to population genomics, and a family of methods called selective sweep mapping, to search for regions of their genome that show signs of being affected by natural selection. This lets us: 1) draw pretty rainbow plots such as  this one …


(Figure 1a from the paper in question, Johnsson & al 2016. cc:by The chromosomes have been laid out on the horizontal axis with different colours, and split into windows of 40 kb. Each dot represents the heterozygosity of that windows. For all the details, see the paper.)

… 2) highlight a regions of the genome that may have been selected during feralisation on Kauai (these are the icicles in the graph, highligthed by arrows); 3) conclude that the regions that look like they’ve been selected in feralisation overlap very little with the ones that look like they’ve been selected in chicken domestication. Hence the title.

That was the main result, but of course we also look at what genes are highlighted. Mostly we have no idea how they may contribute to feralisation, but a couple of regions overlap with those that we’ve previously found in genetic mapping of comb size and egg laying in our wild-by-domestic intercross. We also compare the potentially selected regions to domestic chicken sequences.

Last year, Ewen Callaway visited Dominic Wright, Eben Gering and Rie Henriksen on the last fieldtrip to Kauai. The article, When chickens go wild, was published in Nature News in January, and it explains a lot of the ideas nicely. This paper was submitted by then, so the samples they gathered on that trip do not feature in it. But, spoiler alert: there is more to come. (I don’t know what role I personally will play, but that is less important.)

As you may have guessed if you looked at the author list, this was a collaboration between quite a lot of people in Linköping, Michigan, London, and Victoria. Thanks to all involved! This was great fun, and for those of you who like this sort of thing, I hope the paper will be an interesting read.


M. Johnsson, E. Gering, P. Willis, S. Lopez, L. Van Dorp, G. Hellenthal, R. Henriksen, U. Friberg & D. Wright. (2016) Feralisation targets different genomic loci to domestication in the chicken. Nature Communications. doi:10.1038/ncomms12950