Preliminary Steps toward
Artificial Protocell Computation
- DCU Alife Lab:
- Ciarán Kelly
- Darragh O'Brien
- George G. Mitchell
- James Decraene
- Financial support under EU FP6 Integrated Project PACE
Contract number: 002035
- Containment (membrane)
- Information (heredity?)
- It might be at the (proto)-cell level:
- Cell cycle control
- (Differentiation? Apoptosis?)
- It might be at the multi-(proto)-cell level:
- Nervous system
- Immune system
We will concentrate on the single (proto-)cell level.
- Cell signalling networks, CSN
- Genetic regulatory networks, GRN (beyond protocells?)
- Molecular Information Processing:
- Operators: catalysts/enzymes
- Operands: substrates, reactants
- Real time
- Reaction network -- somewhat like term re-writing system
(but no demarcation between rules and messages)
- Reaction network ``closure'' matters (why?)
- Protocell as encapsulated ``replicator world''?
- Concentration matters (as does stoichiometry, thermodynamics,
kinetics, catalysis ...)
- At the protocell level
- Layered on ``replicator'' dynamics at the molecular level
- (AKA ``major transition'')
- Work with an ``artificial chemistry''
- Polymer family composed of two categories of monomer:
labelled 0 and 1 (primary structure is binary
- No thermodynamics (!)
- No material conservation (!!)
- Why does dominant string not take over whole population?
- What is the composition of the rest of the population?
- Why does peak dominant population get progressively smaller?
- (... obviously there is some stuff that has not been
- In this particular ``flow reactor'' system,
longevity and fecundity are exactly, inversely,
coupled, so no evolutionary scope there.
- So: that leaves fidelity -- doesn't it?
- (Think of this as a simple ``experimental control'' or
- Only difference in ``intrinsic'' fitness of the different
replicator species is in ``fidelity'' - and this shows a
progressive, quasi-deterministic, decay.
- Along with this goes reducing concentration of dominant species
(increased mutational load) and consequently reducing fecundity
(albeit with exactly inversely increasing longevity).
- Long term outcome is total distintegration of the original
organisation (progressive - no ``threshold'' effect).
- But this is happens through a sequence of ``short term''
events, each showing perfectly ``darwinian'' selection!?
- Enzymatic ``binding rule'' is ``exact substring match'' (Aaahhhh ...)
- So a ``super-string'' will immediately parasitise any host
sub-string which was previously dominant (think ``hyperline'' rather
than ``hypercycle''!); and will quickly displace it completely.
- All the ``selectional'' events in this particular model are
of this nature: the huge ``parasitic'' gain easily outweighs
each slight, incremental, decrement in fidelity (reducing
- Playing games, not climbing mountains (improbable or otherwise!).
- Bimolecular, ``self-catalysed'', replication has hyperbolic
- Implies density-dependent selection with positive
- Result is ``survival of the common'': invasion is extremely
difficult - even by rivals with much higher intrinsic fitness.
- Very different from classical ``auto-replication''
(mediated by an externally buffered replicase) with exponential
growth rate and yielding straightforward Darwinian selection.
- But that's a different story ...
- ``Yes, it's a little counter-intuitive ...
- ... but it's really just a very very contrived
and peculiar toy system, with no wider ramifications!''
I may not have gone
where I intended to go, but I think I have ended up where I
needed to be. -- Dirk Gently
- At the very least, it underlines that the Dawkins' slogan
(``Longevity, Fecundity, Fidelity'') is wildly over-simplistic.
- We suggest that it was worthwhile to isolate and
characterise this phenomenon clearly before adding
- But best of all: it immediately offers a simple
candidate problem for solution by protocell level selection.
- So stay tuned!
- Presentation slides:
- DCU Alife Laboratory:
- Research Institute for Networks and
Communications Engineering (RINCE):
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