To investigate how a physical process could come to treat a molecule as information about something else I will employ a different but equally simple model system, but one that makes fundamentally different assumptions about the nature of information than do replicator models.
The model I will use for this purpose is a hypothetical but physically realizable minimally complex molecular process. I first introduced this sort of molecular model in a 2006 paper and have modified it slightly in the years since to ensure that it is both empirically realizable and adequate to its explanatory purpose.
It is modeled after virus structure. In this respect it is not an idealization, just an as yet physically unrealized chemical system. It can be described as a non-parasitic virus that can reproduce autonomously. In this regard it is an autogenic virus, able to autonomously generate copies of itself. A simple virus, like the polio virus, consists of a container or “capsid” shell typically made of protein molecules that assemble themselves into facets of a polyhedral structure that encloses an RNA or DNA molecule. When incorporated into a host cell the viral RNA or DNA commandeers the cell’s systems to make more capsid molecules and more copies of the viral RNA or DNA. Since viral replication requires these complex protein synthesis and polynucleotide synthesis processes, and the molecular machinery to do this involves dozens of molecules arranged in complex structures, viruses replicate parasitically. So a non-parasitic virus would need to use a different and much simpler molecular process to reproduce its parts.
One candidate process is reciprocal catalysis. The simplest form of reciprocal catalysis occurs when one catalytic reaction produces a product that catalyzes a second reaction which produces a product that catalyzes the first, and so on. When provided with appropriate substrate molecules this circular network of catalytic reactions becomes a chain reaction that can rapidly produce large numbers of catalyst molecules. Reciprocal catalysis can involve multiple steps, so long as the circle of reactions is closed, though as we’ll see below, increasing the numbers of interacting molecules is problematic.
Viral capsids self-assemble (as do cell membranes, microtubules, and many other complex molecular structures within cells). Self-assembly is essentially a variant of the process of crystalization. Because of the way that the regular geometries and affinities of these molecules cause them to associate with one another they can spontaneously form into sheets, polyhedrons, or tubes.
These two processes—reciprocal catalysis and self-assembly (depicted in Fig. 1)—are chemically complementary to one another because they each tend to produce conditions that are necessary for the other to occur. So reciprocal catalysis produces high locally asymmetric concentrations of a small number of molecular species while self-assembly requires persistently high local concentrations of a single species of component molecules. Likewise, self-assembly produces constraint on molecular diffusion while reciprocal catalysis requires limited diffusion of interdependent catalysts in order to occur. In this way reciprocal catalysis and self-assembly are molecular processes that each produce the boundary conditions that are critical for supporting each other.
These process can become coupled and their reciprocal relationships linked if one of the molecular side products generated in a reciprocal catalytic process tends to self-assemble into a closed structure. In this case capsid formation will tend occur most effectively where reciprocal catalysis occurs. But this increases the probability that capsids will tend to grow to enclose a sample of the reciprocal catalysts that both produce one another and capsid-forming molecules.
As a result, catalysts that reciprocally depend on one another to be produced will tend to be co-localized, and prevented from diffusing away from one another. While contained, catalysis will quickly cease when substrates are used up, but in the case that the capsid is subsequently damaged and spills its contents, more catalysts and capsid molecules will be synthesized if there are additional substrate molecules nearby. So damage that causes an otherwise inert capsid to spill its catalytic contents into an environment with available substrates will initiate a process that effectively repairs the damage and reconstitutes its inert form. Moreover, depending on the extent of the damage, the distribution of catalytic contents, and the concentrations of substrate molecules the process could potentially produce a second copy of the original from the excess catalyst and capsid molecules that are generated. This makes possible self-repair and even self-reproduction. I will call such an autogenic virus an “autogen” for short (two variants of autogens along with a reaction diagram are shown in Fig. 2).
This constitutes what can be described as an autogenic work cycle. A work cycle consists of a linked sequence of thermodynamic processes that involve transfer of work into and out of a system … and that eventually returns the system to its initial state (paraphrased from Wikipedia). A familiar example is provided by a motor. It is designed to operate continuously when supplied with a constant or periodic throughput of work that changes its configuration through a series of states until the system returns to its initial state. In this way it is able to repeat this cycle again and again. For example, an internal combustion engine uses exploding gasses to move it through a series of configurations so that eventually it expels the exploded gasses and is ready for new fuel and air to be taken in and exploded. The power or (endergonic = “ingoing” + “work”) phase and the exhaust and relaxation (exergonic = “outgoing” + ”work”) phase are matched so that energy doesn’t continually build up within the system.
An autogenic work cycle is similarly composed of two phases distinguished by their difference in chemistry and thermodynamic directionality (see Fig. 3). Catalysis lowers the threshold that must be exceeded in order to initiate a chemical process but once this threshold is crossed an energy gradient difference from reactant to product drives the reaction. Thus the process is endergonic. In contrast, self-assembly (and crystallization in general) enables molecules in a higher energy state in solution to precipitate out of solution into a lattice that absorbs and dissipates this kinetic energy (i.e. of motion, rotation, and vibration) and so spontaneously proceeds from a higher to lower energy state. Thus the process is exergonic.
So, analogous to the two phase cyclic dynamics of an internal combustion engine, the energy that drives the autogenic cycle is provided by energy released by catalysis. This energy—liberated from chemical bonds of the substrate molecules—is the source of work that produces additional catalysts as well as capsid molecules. Self-assembly in turn accumulates the capsid molecules thereby produced and in the process dissipates this energy in the form of heat and an increase in surrounding entropy. But unlike an engine in which the work produced by its changes of state is directed externally to alter some extrinsic state of things, the autogenic work is directed inward, so to speak, to regenerate the very conditions that drive these changes.
This produces a higher order work cycle in which the entire molecular system cycles from disrupted to reconstructed, dynamic to inert, and open to closed. When returned to the reconstructed inert phase the system has been returned to an initial state from which the cycle can again be repeated. At this point the work of self-reconstruction has produced a far-from-equilibrium structure with a relatively high threshold required to dissipate it (in the form of capsid damage). And yet when loss of integrity due to extrinsic damage is sufficient to initiate change toward equilibrium the re-initiation of catalysis and self-assembly works against this.
It is in this way that each of these self-organizing processes produces the extrinsic boundary conditions that the other requires. As a result the critical boundary conditions are internalized and constantly available to channel the work necessary to maintain and reproduce these same constraints. The two self-organizing dynamics are in this sense co-dependent. Each is in effect the permissive environment for the other and in this sense each “contains” the other. This creates an intrinsic source of causal dispositions so that external influences and fixed properties no longer determine its behavior. An autogen is therefore self-individuated by this intrinsic co-dependent dynamical disposition, irrespective of whether it is enclosed or partially dispersed.
Autogens are not only able to self-repair, but because of their cycling from open to closed organization they will also tend to acquire and exchange molecules with their environment. Captured molecules that incidentally share catalytic inter-reactivity with autogen catalysts or capsid molecules will tend to be incorporated and replicated. This will create variant autogen lineages. Those captured molecules that don’t interact with autogen-intrinsic molecules or impede the process without being lethal will tend to get crowded out and eventually passively expelled into the environment in successive reproductions because they are not replicated. This provides a capacity to correct error and to evolve.
So autogenesis provides what amounts to a constraint production and preservation ratchet. During the dynamical phase new components are produced but because of their co-dependent relationships to one another the constraints that provide the reciprocal boundary conditions are also produced as the probability of occurrence of the component self-organizing processes increases. Together these reciprocal and recursive relationships would make autogenic viruses minimally evolvable.