Staph bacteria. Picture courtesy of Janice Carr/CDC via BBC.

Back to Bacteria page Previous page Next page
*** SUMMARY of Conclusions reached References

Are bacteria truly flexible?

Bacteria, like other organisms, display an impressive repertoire of adaptive behaviour in response to environmental changes. Some of this behaviour qualifies as flexible, according to the definition given above.

Andreas Kilian. Photo courtesy of Fraunhofer Institute for Autonomous Intelligent Systems.

Over the course of time, evolution may modify information pathways in unicellular organisms. Mutations which alter the DNA or RNA of these organisms may give certain individuals a selective advantage. This could be regarded as flexible behaviour of sorts: we might say that over the course of time, a lineage of organisms learn a new pattern of responding. However, Kilian and Muller characterise this as evolutionary adaptation rather than learning, because although the effects of these changes are "reproducible by definition" (as with the ethological definition of learning), they are not "individually acquired during the life-time of the cell" (2001, p. 2) and hence do not qualify as individual learning. Kilian and Muller describe this phenomenon as "phylogenetic 'learning'" (2001, p. 3). Since a lineage of bacteria cannot meaningfully be said to possess mental states (see Conclusion N.5), the mentalistic terminology used here can only be metaphorical, not literal.

However, bacteria can also be very adaptable on an individual level. I propose to examine three aspects of their behaviour - cellular regulation, phenotypic plasticity and gene-swapping - which best exemplify their internal dynamism, and discuss the issue of whether any of them are flexible enough to qualify as evidence for mental states in bacteria.

Cellular regulation in bacteria

Cellular regulation in bacteria is governed by a complex network of interactions between biomolecules and structures inside each cell. Wolf and Arkin (2003) describe how this network can be simplified by identifying recurring regulatory motifs - small regulatory subnetworks that can be classified according to their function, architecture or dynamics:

Regulatory motifs proposed to date ... include switches, amplitude filters, oscillators, frequency filters, noise filters and amplifiers, combinatorial logic, homeostats, rheostats, logic gates and memory elements... (2003, pp. 125-126).

I discuss these motifs at further length in an Appendix. Among these motifs, bistable switches in bacterial cells exhibit the closest thing to truly flexible behaviour in bacteria. These switches have a memory and exhibit a history dependence (known as hysteresis): their pattern of responding to variations in the strength of a signal depends on the initial setting of the switch, and they tend to react slowly to changes in the signal value. There is one pattern of responding when the signal increases in strength (a "going-up" pattern), and another when it decreases (a "coming-down" pattern). I would argue that instead of saying that the switch learns a new pattern as its setting fluctuates, we could more economically describe the "going-up" and "coming-down" patterns as part of a single pattern (the hysteresis loop) which is built into the chemistry of the switch. The value of the output ("on" or "off") can be defined a function of two variables: the strength of the current input signal and that of the previous input signal. Together, these two pieces of information tell us whether the signal is "going-up" or "coming-down". Hysteresis in bacterial cells is a time-lag phenomenon, rather than a learning phenomenon.

I conclude that while cellular regulation in bacteria is built upon an impressive array of inter-locking complex processes, some of which exhibit memory, there is nothing that can properly be described as flexible behaviour, according to the definition of flexible behaviour given above.

Phenotypic plasticity in bacteria

The phenotypic plasticity of bacteria also illustrates their adaptiveness on an individual level. For instance, bacteria are able to switch their genes on and off in response to environmental changes. This ability to regulate gene expression serves a biological function: it allows bacteria to conserve their energy, in order to synthesise products that maximise their growth rate (Bridges, 2002). Because this behaviour serves a biological function, it is amenable to Dennett's intentional stance. Should we, then, interpret this apparent flexibility in bacteria as a mental calculation of the optimal course of action in changing surroundings?

A commonly cited case of phenotypic plasticity in bacteria is the way in which the lac operon is regulated in E. coli bacteria. An operon is a regulatory system found in bacteria, where genes that code for functionally related proteins are bunched together along a strand of DNA, enabling protein synthesis to be controlled in response to the needs of the cell. The lac operon allows E. coli to use lactose as an energy source, and break it up into its constituent sugars: galactose and glucose. An operon may exist in one of two regulatory states: ON or OFF. The lac operon is subject to positive and negative forms of gene regulation. The operon's default state is OFF, but the presence of lactose induces the genes to turn ON (negative regulation). However, if there is glucose in the environment, the lac operon is not expressed, as bacteria prefer glucose to lactose as a source of food (positive regulation).

Impressive as this behaviour is, there are two reasons for not characteristing it in mentalistic terms. First, the behaviour does not meet the criteria for "flexible behaviour" listed in the definition given above. The mechanism (i.e. the relevant program statements) governing the expression of the operon does not vary over time; only the environmental conditions do. Changing conditions correspond to changes in values of the input variables (chemical concentrations). Even in a fixed pattern (see definition above), these values may vary. In other words, the observed response - i.e. the value of the "output" variable - may vary over time, but the underlying pattern, which governs the response, stays the same. As Kilian and Muller (2001) and Beisecker (1999) have argued above, only those processes in which the pattern of responding to external stimuli can be altered over time should be regarded as candidates for mental processes. (See Conclusion N.11 above.)

Second, the behaviour is externally triggered rather than self-initiated: it does not vary in response to internal states. For this reason, it can hardly be said to embody a "decision" on the part of bacterial "agents" regarding which energy source they should use. (See Conclusion N.7 above.) The regulation of the lac operon in bacteria can be better understood using a goal-centred intentional stance rather than an agent-centred stance.

Other, less promising cases of phenotypic plasticity in bacteria (bet hedging, hypermutation and localized elevated mutation rates) are discussed in an Appendix, where I conclude that the impressive adaptability they manifest is not the kind required for the possession of mental states. Additionally, because some of the versatile behaviour (hypermutation) is externally triggered and undirected, I argue that it cannot qualify as an intelligent response to changing circumstances (see Conclusions N.7 and N.8).

Flexible behaviour in bacteria: evidence of mental states?

Gene swapping between individual bacteria is perhaps the most interesting kind of adaptive behaviour, because it informs other bacteria about what is going on, allowing them to adapt to unexpected environmental challenges like toxic mercury. In some ways, this phenomenon appears to be an even better candidate for true learning in bacteria than previous examples. Some bacteria have genes which make them resistant to mercury, as it is a naturally occurring toxin. The most widely studied and sophisticated mechanism for resistance to mercury works by bacteria exchanging transposons, or autonomous mobile sections of their DNA. Some transposons contain genes which confer resistance to mercury, by coding for specialised proteins and enzymes. Bacteria that have (or acquire) these genes can take highly toxic mercury ions into their cytoplasm (cell body) using their specialised carrier proteins, and transfer them to a specialised enzyme. The enzyme reduces ionic mercury to metallic mercury, which is relatively inert and non-toxic, and readily diffuses out of the cell (German Research Centre for Biotechnology, 2002; Petkewich, 2002).

Does the ability of bacteria to acquire genes that allow them to respond to challenges that they were previously unable to cope with constitute true learning? At first glance, the criteria listed by Kilian and Muller above may suggest an affirmative answer to this question. Bacteria which pick up resistance to mercury are acquiring new information from other bacteria about an environmental hazard, and what is more, there is a "reproducible learning effect" here, as Kilian and Muller stipulate (2001, p. 1). Moreover, bacteria which acquire genes for resistance to mercury "can make new substances for new irreversible and reproducible information transfer paths as an answer to a new, formerly not identifiable stimulus" (Kilian and Muller, p. 3).

Additionally, there can be no doubt that the bacteria's changing response to mercury is an instance of truly flexible behaviour. The acquisition of new genes corresponds to a change in the program statement describing the organism's response to mercury, as well as the acquisition of new functions - i.e. new recipes for making specialised proteins and enzymes to handle the toxin. What is more, such gene swapping is a common occurrence among bacteria: for instance, genes which confer resistance to antibiotics can be passed from one species of bacteria to another (Society for General Microbiology, 2003). In fact, gene swapping appears to be a universal trait of organisms, as illustrated by the frequency of lateral gene transfer between different branches of the tree of life.

R.6 All organisms exhibit flexible behaviour, to some degree.

On the other hand, while bacteria can (through gene swapping) acquire new information transfer paths (i.e. new cellular program instructions) that enable them to process stimuli differently, they lack an in-built mechanism for acquiring information that allows them to modify their response to a stimulus. Gene swapping is not so much an exchange of information (i.e. new values of input variables describing events in the environment) between individuals, as a random exchange of information-processing mechanisms (i.e. the acquisition of new cellular program instructions). Bacteria only acquire the ability to respond differently to toxins by acquiring a new genetic processing mechanism from other bacteria. Without such a mechanism, they cannot "tailor their own responsive dispositions to their particular surroundings" (Beisecker, 1999, p. 298).

The program governing a bacterium's response to mercury does not modify itself: it receives new, pre-packaged instructions from an outside source (another bacterium). In the absence of such a source, the bacterium is incapable of changing its response to a stimulus, which remains fixed. Once the bacterium has acquired the instructions that alter its response to a new stimulus, its information processing pathway remains the same until another "gene-swap" occurs. Functional behaviour is still rigidly linked to its goal, as the link between sensors and effectors is still governed by the molecules produced by the cell. One could say that the bacterium has simply acquired a new, more adaptive kind of behavioural rigidity. This suggests that the process of gene swapping, while it qualifies as flexible behaviour, is too externally driven to be regarded as true learning.

Another difference between gene swapping and learning (even the kind ofglearninghdefined as such by psychologists), is that in the former case, the stimulus (mercury) is incapable of modifying the organism's response to it, whereas in the latter case, the change in the organism's behaviour is caused by the stimulus. In gene swapping, it is foreign genes, not the stimulus, that modify the organismfs response to the stimulus. In other words, the causal chain between stimulus and response appears to be fundamentally different from that which occurs in learning.

I should add that if one were to view the acquisition of mercury resistance as true learning, one would have to view all other instances of gene swapping between organisms in the same way.

N.12 Flexible behaviour by an organism must be internally generated (i.e. the organism must be able to modify its patterns of information transfer, by means of an inbuilt mechanism), before it can be regarded as a manifestation of a cognitive mental state.

S.9 The occurrence in an organism of flexible behaviour does not provide a sufficient warrant for the ascription of mental states to it.

L.4 The occurrence in an organism of flexible behaviour is a necessary but not a sufficient condition for learning.

Back to Bacteria page Previous page Next page
*** SUMMARY of Conclusions reached References