Fractal Geometry in the Natural Selection

Dawkins describes genes as replicators. The suffix “ - or” suggests that genes are in some sense the locus of this replication process (as in a machine designed for a purpose like a refrigerator or an applicator), or else an agent accomplishing some function (such as an investigator or an actor). This connotation is a bit misleading. DNA molecules only get replicated with the aid of quite elaborate molecular machinery, within living cells or specially designed laboratory devices. But there is a sense in which they contribute indirectly to this process: if there is a functional consequence for the organism to which a given DNA nucleotide sequence contributes, it will improve the probability that that sequence will be replicated in future generations. genes as active replicators for this reason, though the word “active” is being used rhetorically...

Replicator theory thus treats the pattern embodied in the sequence of bases along a strand of DNA as information, analogous to the bit strings entered into digital computers to control their operation. Like the bit strings stored in the various media embodying this manuscript, this genetic information can be precisely copied again and again with minimal loss because of its discrete digital organization. This genetic data is transcribed into chemical operations of a body analogous to the way that computer bit strings can be transcribed into electrical operations of computer circuits. In this sense, genes are a bit like organism software.

Replicators are, then, patterns that contribute to getting themselves copied. Where do they get this function? According to the standard interpretation, they get it simply by virtue of the fact that they do get replicated.

The qualifier “active” introduces an interesting sort of self - referential loop, but one that seems to impute this capacity to the pattern itself, despite the fact that any such influence is entirely context - dependent. Indeed, both sources of action — work done to change things in some way — are located outside the reputed replicator. DNA replication depends on an extensive array of cellular molecular mechanisms, and the influence that a given DNA base sequence has on its own probability of replication is mediated by the physiological and behavioral consequences it contributes to in a body, and most importantly how these affect how well that body reproduces in its given environmental context. DNA does not autonomously replicate itself; nor does a given DNA sequence have the intrinsic property of aiding its own replication — indeed, if it did, this would be a serious impediment to its biological usefulness. In fact, there is a curious irony in treating the only two totally passive contributors to natural selection — the genome and the selection environment — as though they were active principles of change.

But where is the organism in this explanation? For Dawkins, the organism is the medium through which genes influence their probability of being replicated. But as many critics have pointed out, this inverts the location of agency and dynamics. Genes are passively involved in the process while the chemistry of organism bodies does the work of acquiring resources and reproducing. The biosemiotician Jesper Hoffmeyer notes that, “As opposed to the organism, selection is a purely external force while mutation is an internal force, engendering variation. And yet mutations are considered to be random phenomena and hence independent of both the organism and its functions.”

By this token the organism becomes, as Claus Emmeche says, “the passive meeting place of forces that are alien to itself.” So the difficulty is not that replicator theory is in error — indeed, highly accurate replication is necessary for evolution by natural selection — it’s that replicators, in the way this concept has generally been used, are inanimate artifacts. Although genetic information is embodied in the sequence of bases along DNA molecules and its replication is fundamental to biological evolution, this is only relevant if this molecular structure is embedded within a dynamical system with certain very special characteristics. DNA molecules are just long, stringy, relatively inert molecules otherwise.The question that is begged by replicator theory, then, is this: What kind of system properties are required to transform a mere physical pattern embedded within that system into information that is both able to play a constitutive role in determining the organization of this system and constraining it to be capable of self - generation, maintenance, and reproduction in its local environment? These properties are external to the patterned artifact being described as a replicator, and are far from trivial... [It] can’t be assumed that a molecule that, under certain very special conditions, can serve as a template for the formation of a replica of itself exhibits these properties. Even if this were to be a trivially possible molecular process, it would still lack the means to maintain the far - from - equilibrium dynamical organization that is required to persistently generate and preserve this capacity. It would be little more than a special case of crystallization.

My question is, has anyone come across ways this is explored as a fractal process?

I think these days it is fairly widely understood, amongst those who have looked into the subject beyond high school biology, that there are selection effects that take place through changes in DNA outside the boundaries of genes. (Gene expression promoting regions of DNA, which are not themselves part of a gene, for example.)

So there is a sense in which definitions of evolution in terms of change in allele frequency over time is simplistic. However, perhaps when looked at on geological time scales, changes in allele frequency over time are such a dominant factor that such simplistic definitions are pragmatic for introducing people to the subject?

Richard Dawkins likes to couch this discussion in terms of replicators and vehicles. Replicators are any entities of which copies are made; selection will favor replicators with the highest replication rate. Vehicles are survival machines: organisms are vehicles for replicators and selection will favor vehicles that are better at propagating the replicators that reside within them. There is a hierarchy of both replicators and vehicles. The key issues are that 1) the "unit" of selection is one that is potentially immortal: organisms die, but their genes could be passed on indefinitely. The heritability of a gene is greater than that of a chromosome is > that of a cell > organism > and so on. But , because of linkage we should not think of individual genes as the units; it is the stretch of chromosome upon which selection can select, given certain rates of recombination. Issue 2) is that selection acts on phenotypes that are the product of the replicators, not on the replicators themselves, but the vehicles have lower heritability and immortality than replicators. What then is the unit of selection? All of them, just of different strengths and effects at different levels.

Charles Darwin conceived of evolution by natural selection without knowing that genes exist. Now mainstream evolutionary theory has come to focus almost exclusively on genetic inheritance and processes that change gene frequencies.

Yet new data pouring out of adjacent fields are starting to undermine this narrow stance. An alternative vision of evolution is beginning to crystallize, in which the processes by which organisms grow and develop are recognized as causes of evolution.

Some of us first met to discuss these advances six years ago. In the time since, as members of an interdisciplinary team, we have worked intensively to develop a broader framework, termed the extended evolutionary synthesis1 (EES), and to flesh out its structure, assumptions and predictions. In essence, this synthesis maintains that important drivers of evolution, ones that cannot be reduced to genes, must be woven into the very fabric of evolutionary theory.

We believe that the EES will shed new light on how evolution works. We hold that organisms are constructed in development, not simply ‘programmed’ to develop by genes. Living things do not evolve to fit into pre-existing environments, but co-construct and coevolve with their environments, in the process changing the structure of ecosystems...

The core of current evolutionary theory was forged in the 1930s and 1940s. It combined natural selection, genetics and other fields into a consensus about how evolution occurs. This ‘modern synthesis’ allowed the evolutionary process to be described mathematically as frequencies of genetic variants in a population change over time — as, for instance, in the spread of genetic resistance to the myxoma virus in rabbits.

In the decades since, evolutionary biology has incorporated developments consistent with the tenets of the modern synthesis. One such is ‘neutral theory’, which emphasizes random events in evolution. However, standard evolutionary theory (SET) largely retains the same assumptions as the original modern synthesis, which continues to channel how people think about evolution.

The story that SET tells is simple: new variation arises through random genetic mutation; inheritance occurs through DNA; and natural selection is the sole cause of adaptation, the process by which organisms become well-suited to their environments. In this view, the complexity of biological development — the changes that occur as an organism grows and ages — are of secondary, even minor, importance.

In our view, this ‘gene-centric’ focus fails to capture the full gamut of processes that direct evolution. Missing pieces include how physical development influences the generation of variation (developmental bias); how the environment directly shapes organisms’ traits (plasticity); how organisms modify environments (niche construction); and how organisms transmit more than genes across generations (extra-genetic inheritance). For SET, these phenomena are just outcomes of evolution. For the EES, they are also causes.

Valuable insight into the causes of adaptation and the appearance of new traits comes from the field of evolutionary developmental biology (‘evo-devo’).Some of its experimental findings are proving tricky to assimilate into SET. Particularly thorny is the observation that much variation is not random because developmental processes generate certain forms more readily than others...



SET explains such parallels as convergent evolution: similar environmental conditions select for random genetic variation with equivalent results. This account requires extraordinary coincidence to explain the multiple parallel forms that evolved independently in each lake. A more succinct hypothesis is that developmental bias and natural selection work together4,5. Rather than selection being free to traverse across any physical possibility, it is guided along specific routes opened up by the processes of development5,6...

Another kind of developmental bias occurs when individuals respond to their environment by changing their form — a phenomenon called plasticity. For instance, leaf shape changes with soil water and chemistry. SET views this plasticity as merely fine-tuning, or even noise. The EES sees it as a plausible first step in adaptive evolution. The key finding here is that plasticity not only allows organisms to cope in new environmental conditions but to generate traits that are well-suited to them. If selection preserves genetic variants that respond effectively when conditions change, then adaptation largely occurs by accumulation of genetic variations that stabilize a trait after its first appearance5,6.In other words, often it is the trait that comes first; genes that cement it follow, sometimes several generations later5.

Studies of fish, birds, amphibians and insects suggest that adaptations that were, initially, environmentally induced may promote colonization of new environments and facilitate speciation5,6. Some of the best-studied examples of this are in fishes, such as sticklebacks and Arctic char. Differences in the diets and conditions of fish living at the bottom and in open water have induced distinct body forms, which seem to be evolving reproductive isolation, a stage in forming new species. The number of species in a lineage does not depend solely on how random genetic variation is winnowed through different environmental sieves. It also hangs on developmental properties that contribute to the lineage’s ‘evolvability’.

In essence, SET treats the environment as a ‘background condition’, which may trigger or modify selection, but is not itself part of the evolutionary process. It does not differentiate between how termites become adapted to mounds that they construct and, say, how organisms adapt to volcanic eruptions. We view these cases as fundamentally different7...

Finally, diluting what Laland and colleagues deride as a ‘gene-centric’ view would de-emphasize the most powerfully predictive, broadly applicable and empirically validated component of evolutionary theory. Changes in the hereditary material are an essential part of adaptation and speciation. The precise genetic basis for countless adaptations has been documented in detail, ranging from antibiotic resistance in bacteria to camouflage coloration in deer mice, to lactose tolerance in humans.

That said, arguments about selection on the basis of form, defined broadly as "developing echolocation," or "developing the ability to fly" do seem fairly controversial. At least part of the fear here is that it introduces too much teleology in to biology, making it seem like purposeful development.