Jason Cawley
Wolfram Science Group
Phoenix, AZ USA
Registered: Aug 2003
Posts: 712 |
Yes, the basic question is about how much can be done by the "raw material of changes and mutation" step alone. I've always appreciated about Gould the fact that he was quite open minded about causes other than natural selection operating within evolution and having important effects. Serendipity being his favorite.
What Wolfram and no doubt others in complexity work have noticed is how many similarities there are between complex forms seen in non-biological systems and in biological ones. There is no serious question of natural selection operating in the non-biological cases - though one can occasionally export some of its concepts, as analogies. If a complex form can arise in weathering or fracture there is no apriori reason to reach for a NS explanation for a similar form seen in a biological system. Common formal factors can be operating in both and give rise to similar outcomes, and since NS is not essential to them in the former there is no reason to assume it is essential in the latter.
What is involved is explaining not life or every phenomenon within it, but specifically complexity, and to a lesser extent, variety. Many biologists have tried to explain both through NS. It is useful to analyse the form of that argument. One sees that it formally imports diversity from outside the biological subsystem, in the form of varied environments acting as separated "attractors". NS explains "homing" on something. That the something homed in on is varied is imported from outside. Coevolution ecosystem studies might get a little more "endogenous" about variety growth. But it is a lot of hacky work to explain variation from NS. It always needs variation in input e.g. from mutation, and also in attractors in "fitness space". If random in and varied out, then NS can sit between and laboriously try to connect one to the other.
But this is not necessary to evolutionary theory. Darwin's original formula was descent with variation as the input to NS. How much variety can be explained by the prior step? Now, from our intuition of complicated systems, prior to our mastering the idea of computation, we might have thought just about any change would "crash", and a lot of special aiming would be needed to "tune" any random input to any noticable variation in output. But when we look at simple enough formal systems this is not what we see.
Instead, point changes in simple programs produce a characteristic diversity of outputs, some simple, many repetitive, many mixed and seemingly random, a few involving semi-periodic persistent structures. So, if some simple program already exists that produces form X, and we imagine untuned random changes thrown at it, we expect a "spray" of forms to come out. If a simple growth process with a few parameters makes a given form, we expect to find "neighboring" forms in the resulting parameter space, before any tuning or any niche-attracting.
Niche-attracting might well then "lock on" to some of the resulting variation and favor this one rather than that, sure. But it is not the underlying cause of the variety, as such. Nor do we formally require some tower of tuned optimizations to arrive at some complex output form, as best fitted for some narrow set of constraints. It is in fact rather difficult to satisfy complicated constraints by successive improvement. But it is quite easy to get complexity from simple programs.
Overall, then, Wolfram thinks he has found some of the principles of an underlying diversity and complexity "motor" that can operate in biology, and feed its results up to NS. NS becomes a winnower and optimizer, expected to prune an already diverse tree of forms. It no longer has to do the job of creating all complexity or all diversity from scratch, so to speak. If you look at the fossil record, this fits rather better in my opinion. Invent a body type "switch" at some point, and you expect a wide variety of body types all at once, followed by slow optimizing pruning. The diversity motor can be algorithmic, the expected result of "poking" an existing body of form-making code.
There is some implicit stuff about the scale of typical effects here. When a progam is very complicated, we tend to expect the impact of a small change to be small, or to "crash" it completely. But when a program is simple, a small change typically "runs" just fine, while producing an output that can be dramatically different from the previous version, or similar to it but different in the details. Essentially, when there aren't that many bits in the formal set up, change to any one of them can have a large effect. While, if that set up is simple enough, the basic surrounding facts about it (what it operates on, the range it can vary things within) may be set by factors external to that bit of the "code". So you expect bounded variation - large changes in a definite aspect, other characteristics (set by other programs, presumably) remaining unchanged.
For those with Mathematica, you can see the typical behavior of all the ECAs that differ from a given ECA at one location in their rule table, using this function -
nearby[rl_] := With[{sample = Flatten[{#, # + Reverse[2^Range[0, 7]] (IntegerDigits[#, 2, 8] /. {1 -> -1, 0 -> 1})}] &@rl, initial = Table[Random[Integer],{50}]}, ArrayPlot[CellularAutomaton[#, initial, 30], PlotLabel -> #] & /@ sample]
Just ask for e.g. nearby[30] to see plots of rule 30 and those of all the rules that differ by one bit in their rule table, from the same initial condition. nearby[45] for the "neighbors" of rule 45 in "mutation space", etc. For those without, the upshot is qualitatively distinct behaviors lie quite close to one another in rule-mutation space, when the form of the rule is simple enough.
The place where this idea has to prove itself is in the micro-study of growth, finding the genetic "switches" involved and seeing how they operate to create this body plan or that pigmentation pattern. Some problems there are easier than others. Shell pigmentation is darn close to a CA in the seen outputs and the known process, as discussed in the book. Leaf shape from L systems and the like is another bit of low hanging fruit. The book has some results there, they can be improved (as I've seen from others working from it, since) and mated more thoroughly to mutation studies and the like.
Another place where people have used CA models in modeling growth is things like models of cell differentiation forming a limb, typically CA style models mixed with growth promoter gradients or diffusion points. Just getting a good formal module that produces the observed effect is the first step. People work on that at e.g. the Biocomplexity Institute at Indiana University, among other places -
http://biocomplexity.indiana.edu/
I hope this helps.
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