The complexity of behaviour: an example from C. elegans

Those who know me know my strong dislike of popular accounts of human neuroethology – you know, those articles that report on some study where college student brains were scanned under different emotions and conclusions are drawn (often made up). Even worse are when the actual studies do this. I’m in no position to say whether behaviour and emotions can be localised to specific brain areas, but what I can tell you is that the human brain is a mess. It’s an inefficient lump of neurons with so many vestiges of evolution and uniquely exaggerated sections – the human brain is one of the most unfit model systems in biology.

But neuroethology itself is a very important subject to study: how neurology causes/affects behaviour. Human brains are of no use. Insect models could work, but they’re also quite derived. The perfect model is Caenorhabditis elegans, arguably the most versatile model organism in all of biology. It’s especially suited for neuroscience: its nervous system consists only of 302 neurons; the development of each individual neuron is know and can be traced using molecular markers. This means that unlike in more complex nervous systems, in C. elegans, we can literally see how every single neuron reacts to different environments, how behaviour is controled, etc.

Whenever I mention this – usually to psych students who have never set foot outside of their anthropology department *cough cough* – I get the same set of questions: Can a thing with 302 neurons even exhibit behaviours? Can it even sense its environment? The italicised parts are usually pronounced with a mixture of shock, awe, disgust and the occasional smug sneer that only an anthropocentric dumbass is capable of producing.

To just give straight-forward answers to those two questions: yes and yes. But I’d like to go one step further and show you an example of C. elegans neuroethology. How about how it can sense and avoid pathogens?

There are several olfactory cues that are hardwired into C. elegans. For example, it is automatically repelled by the pathogenic bacteria Bacillus megaterium (Andrew & Nicholas, 1976) and Microbacterium nematophilum (Yook & Hodgkin, 2007). However, it is also attracted to the pathogenic bacteria Serratia marcescens and Pseudomonas aeruginosa (Zhang et al., 2005), so these built-in preferences can be counterproductive (most likely the result of a selection pressure favouring those bacteria that can attract the worm despite their pathogenicity).

But just because they have innate preferences, it doesn’t mean they don’t have individual behaviour – you know, free will and all that (did I just piss off the philosophers?). When placed in a field of S. marcescens, they will actively try to move away, despite their innate attractedness to the bacterium; this behaviour is referred to as lawn avoidance.
Pradel, E., Zhang, Y., Pujol, N., Matsuyama, T., Bargmann, C., & Ewbank, J. (2007). Detection and avoidance of a natural product from the pathogenic bacterium Serratia marcescens by Caenorhabditis elegans Proceedings of the National Academy of Sciences, 104 (7), 2295-2300 DOI: 10.1073/pnas.0610281104

And this is where this paper comes in. The researchers studied the molecular mechanisms which C. elegans uses to sense and avoid these dangerous bacteria. The bacteria produce a surfactant called serrawettin W2 as part of the colony’s movement mechanism. A specific neuron cluster in C. elegans, AWB, is used just for detecting this surfactant and other potentially dangerous cues (Bargmann et al., 1993). With the detection of the surfactant, lawn avoidance behaviour is induced. Associated with this is the activation of several otherwise dormant biochemical pathways, one of which involves the gene tol-1. But here’s the twist: when the researchers mutated the gene so it doesn’t work anymore, lawn avoidance was still induced. What this means is that serrawettin W2 is not the only cue that C. elegans can use to detect when it’s in a bad spot.

So what does this have to do with my rant at the beginning? It’s simple. This post was spurred by a conversation with an overexcited neuroscience student who was making all sorts of wild claims about how easy it is to predict human behaviour and its molecular underpinnings (you know, dopamine = happiness or some pop psych crap like that). This is merely a tug back to reality for him: we may have simplistic models, but I will wager that for several decades, we won’t even have a working predictive model of human behaviour. I mean, C. elegans has only 302 neurons yet it can display neurologically complex behaviours that we still haven’t fully uncovered. I don’t know the neuron numbers for the human brain, but it’s definitely more than a couple of orders of magnitude more than the worm.

The teaching point is basically this: make generalisations all you want, they may even be true. But know the limitations of your model and of your model organism (in this case, humans). Just because we know that the neocortex is involved in language and that humans have an expanded and specialised neocortex, it doesn’t mean that we suddenly know exactly how language is processed in humans. And yes, that’s exactly the example that this guy gave to me: “neocortex = language; human neocortex is large; therefore we know how language evolved.”

I need to get better conversation partners.


Andrew PA, Nicholas WL. 1976. Effect of bacteria on dispersal of Caenorhabditis elegans (Rhabditidae). Nematologica 22, 451-461.

Bargmann CI, Hartwieg E, Horvitz HR. 1993. Odorant-selective genes and neurons mediate olfaction in C. elegans. Cell 74, 515-527.

Yook K, Hodgkin J. 2007. Mos1 mutagenesis reveals a diversity of mechanisms affecting response of Caenorhabditis elegans to the bacterial pathogen Microbacterium nematophilum. Genetics 175, 681-697.

Zhang Y, Lu H, Bargmann CI. 2005. Pathogenic bacteria induce aversive olfactory learning in Caenorhabditis elegans. Nature 438, 179-184.

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