Ch 12: extract 5

More reasons we are not like machines: only room for one today (but it is a big one) ... more tomorrow

If yesterday’s extract seemed to be missing a few crucial lines, that’s because it was. I haven’t experienced this before, but the program randomly ditched a few sentences - if I’d known it could do that, I’d have proofread it more carefully. For those who want to read the text as it should have been, you can find it here.

I can imagine some readers want a change of diet. I promise to offer one as soon as I have posted the rest of the argument of this chapter, on the difference between living organisms and machines. I think the topic is of crucial importance, and, well - topical. But it is one of many strands of thinking I’d like to pursue.

I suspect the missing phrases yesterday were caused by it being a long piece - and today’s is, if anything, longer. Today’s is about the question of the influence of the whole, and so is a relatively long subsection. It's either that or I take even longer to post! Apologies for not being a particularly adept ‘substacker’ …. yet …

6. The influence of the whole

While a machine has clearly defined parts, this is not, then, the case in an organism.^[1] A process arguably has no parts and is, in reality, an indivisible unity. As Scott Turner puts it, ‘integrity and seamlessness seem to be the essence of an organism’.^[2] To the extent that one can speak of an organism as having ‘parts’ at all, we find them by dismantling the whole in an inevitably somewhat arbitrary fashion. They are ultimately a product of human attention, a function of the way we choose to attend to the organism for a particular end of our own, and the parts we choose to define change depending on our focus of interest at the time.

Let us assume, however, for the sake of argument, that there are identifiable parts. These parts are unlike machine parts – and not just because they constantly change. For such parts do not, as those of a machine do, exist prior to the whole that they make up, but come about at the same time as the making of the whole. They are further examples of ‘mutual constitution’. They are not pre-existing entities put together, but instead distinguish themselves in the process of self-differentiation of a living whole: thus the liver, the heart, the kidneys are not assembled, but come into ever more defined being as the whole living organism grows. And the relationships between the parts don’t go to make up the whole, but derive from the existence of the whole. They are handy post factum mental representations. ‘Parts’ are inextricably involved with their context, without which they are both impotent and unpredictable; and neither the parts, nor even the local interactions of the parts on their own, account for the qualities of the whole organism that we observe.^[3]

Lower levels of an organism are not straightforwardly explanatory of the higher levels. Microscopic findings do not predict macroscopic outcomes, nor vice versa. Walsh writes that ‘as physical systems take on new configurations, they bring new phenomena into existence’.^[4] These phenomena are not easily accounted for in terms of phenomena at some more reduced level. Examples given by him include atomic nuclei, magnets, superconductors, excitable media, fluids and tissues, and organic agents.^[5] As always, we are dealing with Gestalten, not with constructions.

In explaining a multicellular organism’s stability, the intrinsic properties of what we see as the parts are of little significance compared with ‘the dynamic relationships among parts at different levels of the organisational hierarchy.’^[6] Note, dynamic relationships among parts at different levels. The existence of emergent properties at every level throughout the natural world suggests, too, that we are on the wrong track when we try to account for what we find in terms of things rather than processes. It would be like trying to account for the unique quality, the power and, yes, the life of a piece of music by examining each note, or at most a phrase, in ever greater detail, outside the flow of the whole work, in the hope that by this ‘drilling down’, as we say, there at last we will find the secret. We cannot account for a phenomenon at the topmost level merely by a concatenation of elements at the lowest level. We are dealing with a Gestalt. That is to say the ‘betweenness’ is more important than the ‘things’ we believe we discern within it. Relationships are prior to relata, a topic I will return to in Part III.

An aside on terminology. When I use the word ‘betweenness’, I refer, not just to what happens between two or more ‘things’, but to the unique whole in which we might later come to identify ‘things’ and the relationship between them. Thus an electrical current resides not in the negative pole or the positive pole, nor the space between the poles, but in the sum of all of these, plus, crucially, the wholly new element that comes about from ‘adding them together’ (which, of course, never happens except in our theoretical post factum reconstruction). There is no hitherto existing adequate word for this idea in English, but the concept is important, so ‘betweenness’ will have to do. It is close to Sharma’s ‘interdependent mutual constitution’.

Molecular structures are good examples of entities that cannot be reduced to their parts: according to biochemist Ross Stein, ‘the essential nature of the compound subject transcends, and cannot be reduced to, the simples from which it is composed … Complex objects are no mere aggregates, but possess a defining unity.’^[7] And at the phenomenological level we see this all the time. As molecules form new wholes, utterly new qualities, unpredictable from the apparent constituent parts, emerge: so a tasty white crystalline substance – table salt – emerges from the compound of sodium, a dullish grey, malleable metal, and chlorine, an evil-smelling, poisonous, greenish-yellow gas.

Writing about the ways in which living systems display characteristics not to be found in their constituent parts, cell biologists Sophie Dumont and Manu Prakash observe that:

subtle variations in parameters (energy expenditure, architecture, and temporal dynamics) can dramatically change the mechanics of the resulting structure in ways we do not understand … Emergent structures exhibit properties that their smaller building blocks (air molecules or sand grains) do not … It is very likely the case that these mechanical design principles will be fundamentally new and as such may not have a known analogue in nonliving physical systems.^[8]

The expected conventional terminology of mechanics here seems awkward, and with good reason. For, if ‘mechanics’ are dramatically changed in ways we do not understand – and I have no doubt that they are – in what sense are they still mechanics? If the ‘mechanical design principles’ are ‘fundamentally new’, and have no ‘known analogue in non-living physical systems’, surely the comparison of organisms with machines (still implicit in the language with which, I quite understand, the researchers must write their paper if they wish to get it published) is self-confuting.

‘The astonishing plasticity of organisms contrasts with the brittleness of machines’, writes Nicholson,

which tend to stop working when their parts break or are damaged. Of course, redundancy and self-repair can be built into the design of machines to some extent, and although this can make their operation more robust and more reliable, the inherent limitations of their fixed architecture remain.^[9]

Here the question arises, how the part can have that sense of the whole to which it belongs, of which Barbara McClintock spoke. A machine as a whole typically does not adapt in response to parts becoming worn or defective, nor invent a solution at a local level that will further the purpose of the overall machine.

Carl Woese again:

Machines are stable and accurate because they are designed and built to be so. The stability of an organism lies in resilience, the homoeostatic capacity to re-establish itself. While a machine is a mere collection of parts, some sort of ‘sense of the whole’ inheres in the organism, a quality that becomes particularly apparent in phenomena such as regeneration in amphibians and certain invertebrates and in the homoeorhesis [see note] exhibited by developing embryos.^[10]

To quote Ford, ‘Although we now recognise that experiential input can bring about epigenetic modification of the cell nucleus, there must be undivined mechanisms that relate the experiences of the entire multicellular organism back to the cell.’^[11] And even the single cell seems to have what the biochemist Jesper Hoffmeyer describes as ‘tacit knowledge’ that is ‘inherent within the cellular organization and must be presupposed by, rather than materially built into, the DNA description.’^[12] Hence Shapiro’s claim that ‘life requires cognition at all levels’.

As yet, we have little idea of how the ‘parts’ seem to ‘know’ what whole they belong to, and how it should be shaped: it is an ancient question, to which no-one has ever given a satisfactory answer. One answer worth considering is that the part quite simply does not exist: the being can only be considered as a whole. As John Haldane noted:

From a consideration of the general characteristics which distinguish a living organism from a machine I had become convinced that a living organism cannot be correctly studied piece by piece separately as the parts of a machine can be studied, the working of the whole machine being deduced synthetically from the separate study of each of the parts. A living organism is constantly showing itself to be a self-maintaining whole, and each part must therefore always be behaving as a part of such a self-maintaining whole.^[13]

The question, by the way, is not ‘by what immediate mechanism?’ – to be answered at the molecular level by speaking of, say, electrical gradients affecting the direction of diffusion of polarised molecules; an account which is at best a first step towards a description, hardly itself an explanation, let alone an understanding.^[14] That is like trying to understand a ballet by measuring the impact of ATP hydrolysis on myosin in the dancer’s skeletal muscle fibres. In the words of Ford,

Knowing how the intricate mechanisms within the cell perform tells us nothing of the entire cell, just as studying the hormone fluctuations and changes of blood pressure in a human subject would reveal little of why they were late for work in the first place … It is as though we have clamoured for the most intimate insights into the minutest workings of the telephone exchange, while disregarding the subscribers – who they are, why they choose to speak, or what they are saying.

When they are injured, organisms – from simple bacteria, to trees, to complex vertebrates – are often able to heal themselves and repair the damage, regaining the form that was lost. Some organisms (eg, axolotls and salamanders) can regenerate entire body parts, including limbs, parts of the brain, and even the heart. Lobsters can regrow claws, spiders can regrow legs, and rabbits and certain species of mice can regenerate a number of their organs.^[16] Although antler growth is peculiarly shielded from environmental influences, and although no two sets of antlers are the same, any one animal’s antlers are perfect mirror images of one another, and, if both are cut off, will regain the same shape from memory.^[17] Trees and plants, of course, have a multitude of individual and characteristic forms of their own, which are not principally moulded by the environment, and which they will strive to regain if their form is damaged (see Plates 13[c] & 13[d]).

Indeed, some relatively complex creatures, such as flatworms, can regenerate the entire body including their centralised brain, from a fragment of the original animal.^[18] This was noted by Charles Darwin’s grandfather Erasmus Darwin.^[19] In one case a planarian, a type of flatworm, was cut into 279 pieces, each of which proved capable of generating a new body within a few weeks.^[20] Each part appears to know what it lacks, and can thus regenerate a new whole. What is still more extraordinary is that if flatworms – the ‘first’ class of organism to have a centralised brain with true synaptic transmission,^[21] and to share the majority of neurotransmitters that occur in vertebrate brains^[22] – are decapitated, they not only regrow a head, but retain their memories; for example, which way to turn in a maze they had previously ‘solved’ before their heads were chopped off.^[23] A body is a moulded river indeed.

The preservation of form does not depend on trotting out ‘pre-programmed’ developmental blueprints.^[24] For example, the face of a tadpole is quite different from that of a frog; in order to produce the typical adult frog’s face, a series of deformations must be carried out, and, along with it, various organs and tissues relocated. Surely, then, it follows the steps of a programme? Not in any obvious sense of the word. When developmental defects were artificially induced in a tadpole, subsequent development was able to adjust accordingly, apparently making corrections towards what it seemed to sense was its ultimate goal, the adult frog’s face, despite there being no ‘programme’ or previously known mechanism to direct it.^[25] Michael Levin, a prominent geneticist at Tufts, writes:

Most organs were still placed into the right final positions, using movements quite unlike the normal events of metamorphosis, showing that what is encoded is not a hardwired set of tissue movements but rather a flexible, dynamic program that is able to recognize deviations, perform appropriate actions to minimize those deviations, and stop rearranging at the right time.

The question is ‘where is the information?’ That is to say, the in-form-ation. Where is the overall form or shape of the being stored, as a whole, in service of which any mechanisms we can detect and measure would be acting?

We should remember that evolution, and indeed the reproduction of organisms, is not a flow of ‘information’ only in the abstract sense of that word – that of, eg, ‘information technology’. We should remember that information is not a thing: it is the capacity for a channel to create a new link between two processes. Evolution is a physical, embodied process, not reducible to pieces of data. Organisms flow down the ages by reproduction and by evolution, literally mingling bodies – their forms – at a moment in time and from generation to generation, something no machine does: every embodied reproduction is evolution in action, and every evolutionary advance is an embodied reproduction. Offspring of organisms, from single cell to homo sapiens, are not separately engineered from new material externally, but emerge as new whole forms from the material forms of the bodies of their parents. The flow is embodied and seamless.

Barbara McClintock discovered, in experiments conducted in the 1940s, and therefore before the structure of DNA had been determined, that the genome is not a static entity, but subject to rearrangement, and moreover that there were heritable changes in gene expression not caused by changes to DNA sequences: what we now call epigenetics. She reflected that a genome must repeatedly face ‘shocks’ of various kinds, for some of which it is prepared and to which it can respond in a ‘pre-programmed manner’. As she says, some sensing mechanism must be present in these instances to alert the cell to imminent danger, and to set in motion the orderly sequence of events that will mitigate this danger. That is in itself remarkable. But she saw something still more remarkable:

there are also responses of genomes to unanticipated challenges that are not so precisely programmed. The genome is unprepared for these shocks. Nevertheless, they are sensed, and the genome responds in a discernible but initially unforeseen manner … in most known instances of such challenges the types of response are not predictable in advance of initial observations of them

These responses appear to be, as C.H. Waddington believed they were, due to information in the organism as a whole, not just localised to specific pre-existing, temporarily silenced, genetic mutations.^[28] To quote Noble, ‘organisms seem to be very resourceful when challenged with knockouts, blockers or absence of nutrients. If we look for that ingenuity at the molecular level we may not find it.’ On McClintock’s discoveries, he comments:

She could not have anticipated the extent to which her idea would be confirmed by the sequencing of whole genomes … [implying] the movement of whole functional domains. This is far from the idea of slow progressive accumulation of point mutations … the rearrangement of whole domains including the functionality of those domains in response to stress could have been the origin of creativity in the evolutionary process … This is why McClintock characterised the genome as a highly sensitive organ of the cell. ^[29]

From all of this it would seem that an organism is not just driven from the bottom up. Decisions seem to be taken by the organism – even a single cell – as a whole; what’s more, intelligent decisions – ones that are creative and ‘hand-tailored’, not just selected from a predetermined repertoire – which in itself would require a (lower) level of intelligence. Considering a number of accounts of intelligence, Ford writes that common to the ‘different definitions of intelligence there is one concept on which all seem to focus: the ability to deal constructively with the unforeseen’:

The definitive demonstration of intelligence, must observe the cell encountering a situation which it cannot have previously experienced; it needs to demonstrate abnormal behaviour specifically in response; and the cell must act remedially to restore normality to its abnormal predicament.

Cells pass each of these tests with flying colours. And they do so, often, in an awe-inspiring balance between autonomy and co-operation that a human society might envy.

Everywhere we can observe this proclivity for ingenuity. When a surgical suture is secured with staples, the resulting repair is conspicuous and crude. Within weeks, the scar is healed, smooth, and scarcely visible. The cells at the site of the incision have identified the nature of the surgical trauma and have initiated manoeuvres to restore it. Capillaries re-form so that the microcirculation is restored, innervation is reinstated, and the many epidermal layers are properly reconstituted. None of this we understand. These complex processes are invisible to the brain, and are not controlled by cerebral activity, neither are they subject to regulatory intervention by circulating hormones. The cells are the decision-makers … No computer model comes close to emulating the mechanisms manifested by an amoeba, as it seeks its way ahead, selects which food substances are suitable for ingestion, modifies its cell membrane to accommodate the situation and moves on in a direction it has motivationally selected. A team based at Sapporo, Japan, have even shown that amoebae have memory for events. .^[30] This takes us deeper into the realities of living cells than current conceptions of memory as the propensity only of cell aggregates. Single cells can take decisions; single cells can plan responses; single cells contain memory.^[31]

I will have more to say about all this in Chapter 25.

Another interesting example relates to the nervous system of animals, and concerns the well-known principle that ‘what fires together wires together’. Such plasticity (known as Hebbian, after Donald Hebb, the Canadian psychologist, who posited it) is widely considered to be the mechanism by which information can be coded and retained in neurones in the brain. ‘The general idea is an old one’, wrote Hebb, ‘that any two cells or systems of cells that are repeatedly active at the same time will tend to become “associated”, so that activity in one facilitates activity in the other.’^[33] With continued use, changes at the synaptic cleft mean that such neuronal sequences are preferred, and may even become semi-automatic, in a process known as kindling. This is well established, and is a process of positive feedback: more leads to more. So far, so good. Recently, however, we have become aware that Hebbian adaptations are just one of three possible changes that may occur with use. A second is the opposite. It is homoeostatic: in other words, up-regulation causes a compensatory down-regulation – negative feedback: more leads to less. But even more interestingly, we now know there is a process called neurotransmitter switching, whereby the neurotransmitter involved at the synapse is swapped for another:

Significantly, transmitter switching often reverses the sign of the synapse: an excitatory transmitter is replaced by an inhibitory one or vice versa. These reversals in synaptic sign change the function of the circuits in which they occur, complicating the interpretation of the connectome … ‘Neurons that fire together, wire together’ encapsulates Hebbian plasticity. ‘Neurons with chronic firing, reverse wiring’ summarizes the impact of transmitter switching.

‘Complicating the interpretation of the connectome’ looks like an understatement. Not for the first time we are brought to ask, what is causality? Certainly we cannot just close our eyes to what we are seeing and hold to conventional bottom-up (ie, from parts to whole) causation only, as the machine model suggests. (A bottom-up approach starts, in any case, only from what is presumed to be ‘the bottom’.) In organisms the whole is also necessary for the functioning of the parts: the part is apparently able to access information about the whole, and act on it in service of the whole. We may not know how, but that is not grounds for denying that it happens. One solution might be to accept that there are no parts as such, and that what we see is simply the action of a whole, as a whole: the problem lies in our perception.

If a cell is placed in a slightly acid medium, its mitochondria break up into small spherical beads. But, amazingly, on return of the cell to a normal medium, they merge again into strings, and eventually take on once more the appearance and internal structure of normal mitochondria.^[35] Further, let us suppose you cut a developing limb bud out of an amphibian embryo, shake the cells loose from each other, and then allow them to aggregate once more into a random lump. You then replace the random lump in the embryo. What happens? A normal leg develops. The form of the limb as a whole dictates, according to Lewontin, the rearrangement of the cells:

Unlike a machine whose totality is created by the juxtaposition of bits and pieces with different functions and properties, the bits and pieces of a developing organism seem to come into existence as a consequence of their spatial position at critical moments in the embryo’s development. Such an object is less like a machine than it is like a language whose elements … take unique meaning from their context.

Or like a dynamic field. ‘If the organism was simply its substance we would not be able to recognise it from one day to another’, wrote Lawrence Edwards, an expert in plant morphology. ‘Yet its being and largely its form are invariant from one moment to another, and from one day to another. The form can live within the flux. Something greater than the substance takes it up, moulds it, uses it, and then casts it away.’^[37]

Again, unlike in a machine, no two limb buds in a developing embryo are ever exactly the same; the buds of formative, mesenchymal cells develop each in their own way. The result is in each case a normal, fully formed limb of the kind dictated by its position. But not just its ‘predestined’ position: the same cell group in a limb bud can nonetheless, though destined to form the pattern of, say, a right limb, give rise to the mirror image, a left limb, with the opposite symmetry, simply by being transplanted to the opposite side of the embryo.^[38]

Another example of the whole somehow overruling the parts comes from fascinating experiments on the fruit fly, Drosophila. The absence of a gene, homologous to Pax6 (see above), causes the fly to develop without eyes. However, if such flies are interbred, they have been found soon to develop eyes – despite not having the gene in question.^[39] Indeed, after ‘knocking out’ (disabling) both copies of a gene that had a normally important role in the development of a mouse, molecular biologists found that in many cases the mouse seemed unimpaired, and functioned normally.^[40] In certain strains of mice, mutations in the Kit gene cause white patches on the tail and feet; if a mouse has one normal Kit gene and one mutated one, it will have the patches. Yet some of the offspring of such mice, who inherit two normal Kit genes, still have the white tail.^[41] Resistance to viral infection in a nematode worm was achieved by some of the population having DNA that produced a viral-silencing RNA sequence; when cross-bred with worms who lacked this DNA, some of the offspring inherited the antiviral mechanism and some didn’t. All as one might expect. However, subsequent generations inherited the antiviral mechanism even if they lacked the required DNA. This non-DNA inheritance was followed successfully for 100 generations.^[42] Similarly ‘adaptive mutation’ dictates that if a strain of bacteria is unable to utilise lactose, and is placed in a lactose-rich medium, 20% of its cells will quickly mutate into a form that enables them to process lactose: the mutation is then inherited by subsequent generations.^[43]

Organisms don’t just passively wait, then, for a lucky accident or resign themselves to dying out, but actively remodel themselves in response to changes in their environment.

As mentioned, changes in DNA are no longer thought to be mere accidents.^[44] Indeed Darwin himself wrote:

I have hitherto sometimes spoken as if the variations … were due to chance. This, of course is a wholly incorrect expression … Some authors believe it to be as much the function of the reproductive system to produce individual differences, or slight deviations of structure, as to make the child like its parents.

Another idea that perhaps does not square too well with the idea of genes bent on preserving themselves at all costs.

Everything depends on an organism’s capacity to be flexible and responsive to its environment, just as the environment, both living and non-living, is responsive to organisms. It is this combination of interlocking responses that ensures stability. ‘There is now good experimental evidence’, write Jablonka and Lamb, ‘as well as theoretical reasons, for thinking that the generation of mutations and other types of genetic variation is not a totally unregulated process.’^[46] A seminal paper asserts that ‘not all genome changes occur at random and that cells possess specific mechanisms to optimize their genome in response to the environment’^[47] – not even the gene actively optimising the cell, but the cell actively optimising its genes. In a now famous paper in Nature it was claimed that ‘cells may have ways of choosing which mutations occur’, and they can ‘learn from experience’.^[48] Another has shown that ‘bacteria that have lost their flagella through deletion of the relevant DNA sequence can evolve the regulatory networks required to restore flagella and so restore motility in response to a stressful environment within just four days’.^[49]

In Shapiro’s phrase, cells and organisms have evolved to become, ‘cognitive (sentient) entities that act and interact purposefully to ensure survival, growth and proliferation’.^[50] Evolution itself is an ‘intelligent’ process (he describes it as not only ‘cognitive’ and ‘sentient’, but ‘thoughtful’). According to him, a twenty-first-century view of evolution implies

a shift from thinking about gradual selection of localized random changes to sudden genome structuring by sensory network-influenced cell systems … It replaces the ‘invisible hands’ of geological time and natural selection with cognitive networks and cellular functions of self-modification. The emphasis is systemic rather than atomistic, and information-based rather than stochastic [random].

This is not only plausible, but no form of ‘heresy’. According to Denis Noble, Darwin ‘was concerned that he did not know the origin of variation and he acknowledged the existence of other mechanisms, including the inheritance of acquired characteristics.’^[52] In The Origin of Species, he had written:

I placed in a most conspicuous position – namely, at the close of the Introduction – the following words: ‘I am convinced that natural selection has been the main but not the exclusive means of modification.’ This has been of no avail. Great is the power of steady misrepresentation; but the history of science shows that fortunately this power does not long endure.

On the last point, however, he was sadly mistaken.

Cell biologist Bruce Lipton writes of the immune system, producing antibodies, that it

employs an amazing mechanism called affinity maturation, that enables the cell to perfectly adjust the final shape of its antibody protein. Activated immune cells make hundreds of copies of the original antibody gene. However, each new version of the gene is slightly mutated so that it will encode a slightly different shaped antibody protein. The cell selects the variant gene that makes the best fitting antibody.^[53]

This is further sculpted (by a mechanism known as somatic hypermutation) to become the perfect physical complement of the virus that it is to neutralise. What’s more, the cell remembers this antibody shape and passes on the memory to its daughter cells.

In the late nineteenth century, Hans Driesch separated the two cells produced by the first division of a fertilised sea urchin egg and observed that each of these, which would normally have produced half of an organism, actually produced a complete Pluteus larva, the initial free-living form of the species. Each of these larvae was half the size of the normal Pluteus, but was complete in every detail and grew into perfectly normal adults.^[55] ‘How’, asks Brian Goodwin, ‘is the system organised so that when these two cells remain part of one embryo each produces half the future organism, but when they are separated, each produces a whole?’^[56] Interestingly, Driesch compared the phenomenon with the bar magnet, which if divided produces two magnets, each with two poles.

One way of looking at multicellular organisms, including, of course, ourselves, is that we are historically an aggregate of single cell organisms that gave up their autonomy and co-operated, so as better to survive: we are ancient societies. Signals released by cells into the environment allowed for the co-ordination of a dispersed population of unicellular organisms. This enhanced the survival of single cells by providing them with the opportunity to live as a primitive ‘community’.^[57] Even the individual cell is itself the result of collaboration of many parts, including elements such as mitochondria which were originally bacteria that took up residence in the intracellular environment. The trillions of cells that go to compose our bodies, like the millions of people who live in a large city, share common purposes served by the adoption of widely different roles. And so do the trillions of commensal organisms – bacteria, mainly, on which our bodies depend for healthy functioning. Until recently, bacteria were largely viewed as opportunistic inhabitants of the comfortable environment offered by the gut, but they are now known not just to be vital for digestion, but for the nervous system, the immune system and even for normal development at all.^[58] They belong to the wider conception of ourselves as organisms: ‘commensal’ means sitting at a shared table: we couldn’t dine without their company. What counts as an individual – not just a part – depends on the question being asked, and the focus of our interest.

As has often been pointed out, bees, ants and termites behave like parts of a whole so tightly organised that they seem to act as if parts of one large organism. ‘A single termite is unintelligible’, writes Brian Henning,

apart from the collective organism of which it is a member … as a single superorganism, the termite colony is extended in space and time, without clearly defined boundaries or a skin to define where the environment stops and the superorganism begins … a single termite is no more an individual than a single cell in a petri dish solution.’^[59]

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^[1] See, eg, Dupré & Nicholson 2018.

^[2] Turner 2007 (90).

^[3] ‘It is utterly impossible for human reason’, wrote Kant in The Critique of Judgment, ‘to hope to understand the generation even of a blade of grass from mere mechanical causes’(Kant 2007, 238; Part II, div 2, §77). An understanding relying on such causation is confuted, he believed, by the self-organising nature of Nature: ‘In such a natural product as this, every part is thought as owing its presence to the agency of all the remaining parts, and also as existing for the sake of the others and of the whole, that is as an instrument, or organ’ (ibid, 201; Part II, div 1, §65).

^[4] Walsh 2018 (172).

^[5] Batterman 2015 (133); quoted in Walsh op cit (172).

^[6] Bertolaso & Dupré 2018 (327).

^[7] Stein 2004.

^[8] Dumont & Prakash 2014.

^[9] Nicholson 2018 (147).

^[10] Woese 2004 (176). ‘Homoeorhesis’ is a term coined by Waddington in 1957 meaning steady flow, the processual equivalent of ‘homoeostasis’, which implies returning to a steady state.

^[11] Ford 2017.

^[12] Hoffmeyer 2008 (82).

^[13] JS Haldane 1917 (14: emphasis added).

^[14] For instance, Tseng & Levin (2013) report that ‘bioelectric cues function alongside chemical gradients, transcriptional networks, and haptic/tensile cues as part of the morphogenetic field that orchestrates individual cell behavior into large-scale anatomical pattern formation’. This is a rough description of the small part we observe to happen, but it doesn’t seem to me to get us closer to an explanation of what a morphogenetic field is, or where it is. I don’t have an answer, either, of course; so my target is neither the positing of a morphogenetic field in the first place, which seems an intelligent hypothesis, nor the failure to provide an explanation of where or what it is, but rather the implication that one’s favoured mechanism provides even a partial answer. See also Levin 2012; and Burr & Northrop 1935.

^[15] Ford 2017.

^[16] Birnbaum & Sánchez Alvarado 2008.

^[17] For further discussion, see Turner 2007 (79–87). See also Goss 1983 (esp 218–30); and Lincoln 1992.

^[18] Reddien & Sánchez Alvarado 2004.

^[19] E Darwin 1809 (419).

^[20] Handberg-Thorsager, Fernandez & Salo 2008.

^[21] Sarnat & Netsky 1985.

^[22] Buttarelli, Pellicano & Pontieri 2008.

^[23] Shomrat & Levin 2013. At least one group has been able to ‘demonstrate conclusively that associative memory survives metamorphosis in Lepidoptera’. What that implies is that, despite the dissolution of the caterpillar’s nervous system, memories that were imprinted in the caterpillar are nonetheless present in the imago (Blackiston, Silva Casey & Weiss 2008).

^[24] Voskoboynik, Simon-Blecher, Soen et al 2007.

^[25] Vandenberg, Adams & Levin 2012.

^[26] Levin 2012 (247).

^[27] McClintock 1984 (792).

^[28] Fabris 2018 (259).

^[29] Noble 2017 (emphasis in original).

^[30] Ford 2017.

^[31] Saigusa, Tero, Nakagaki et al 2008.

^[32] Ford op cit.

^[33] Hebb 1949 (70).

^[34] Spitzer 2017.

^[35] Weiss 1970.

^[36] Lewontin 1983.

^[37] Edwards 1993 (40: emphasis in original). There is a strong correlation between a bud’s closeness to the ideal form – whether measured by closest fit to the perfect mathematical curve-form, or simply as the mean of all examples – and the amount of sap in the bud, as an index of its vitality (203ff). Did the level of vitality dictate the form, or the form dictate the level of vitality? ‘We have here two possible ways of looking at the world. One sees form as a necessary adjunct of matter. The substance is there, therefore it must have a form of some sort or another. The form is there because of the substance. The other sees form as the primary reality, which can only then become visible to our eyes when it takes up substance and moulds it to its purpose. The substance is there because of the form’ (209). I imagine it could be both: an accident of form, due to say wind or weather, is therefore inhibited in vitality, which means that in turn it is less open to being moulded in the form to which it should go – and vice versa.

^[38] Weiss 1971.

^[39] Webster & Goodwin 2011 (87 & 240); Leiserson, Bonini & Benzer 1994. I readily acknowledge that there are other mechanisms involved in the production of eyes, in which several genes interact (Iyer, Singh, Jensen et al 2018; McCammon, Blaker-Lee, Chen et al 2017). What remains of interest is that the whole senses that the parts need to change in order that a certain apparently foreseen outcome should be achieved for the whole, despite the normal mechanism’s failure. Merely showing that a different mechanism comes into play does not address this issue.

^[40] Barbaric, Miller & Dear 2007.

^[41] Rassoulzadegan, Grandjean, Gounon et al 2006.

^[42] Rechavi, Minevish & Hobert 2011.

^[43] Foster 2000. I am indebted to Steve Taylor for this information.

^[44] Talbott 2011b (44). See Caporale 2006, especially Doyle, Csete, & Caporale 2006. See also King & Kashi 2007; King 2011.

^[45] Darwin 1859 (131).

^[46] Jablonka & Lamb 2005 (80).

^[47] Jack, Cruz, Hull et al 2015 (emphasis added).

^[48] Cairns, Overbaugh & Miller 1988. See also Foster 1998; and Goodwin 1994.

^[49] Taylor, Mulley, Dills et al 2015. The paper is cited by Noble (2017), who continues: ‘Specifically, Taylor et al show that deletion of FleQ (Flagellar transcriptional regulator) in Pseudomonas fluorescens, and starvation of the bacteria, produces mutations that enable the regulatory role to be taken over by a different pathway, normally involved in nitrogen uptake and assimilation. The genes required to produce flagella are then reactivated by the new regulatory pathway. The authors interpret their work as showing how selection can rapidly produce this kind of substitution to restore activation of flagella genes. But, equally clearly, the mutations are targeted in a remarkably precise way. They are not randomly occurring anywhere in the genome’ (emphasis added).

^[50] Shapiro 2011 (143).

^[51] ibid (146).

^[52] Noble 2017.

^[53] Darwin 1872 (421).

^[54] Lipton 2005 (8).

^[55] Driesch 1964. See below.

^[56] Goodwin 1994 (226).

^[57] Lipton op cit (100).

^[58] Dupré 2017b.

^[59] Henning 2013 (240–1). See also Turner 2000.