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Tim Tyler

Posted: Mon Feb 12, 2007 9:40 am

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I am not sure if you can have a living organism without
both metabolism and something a /lot/ like replication -
but this recent paper concludes that there is no
substantive evidence for a 'metabolism first' mechanism
for life's emergence:

"Causation and the origin of life. Metabolism or replication first?"

- http://cat.inist.fr/?aModele=afficheN&cpsidt=15525075
--
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Chrisantha

Posted: Tue Feb 13, 2007 6:43 am

Guest

Please take a look at our papers on the origin of metabolism in
compartments and tell us your views.

Szathmary, E, Santos, M, Fernando, C. (2005) Evolutionary Potential
and Requirements for Minimal Protocells. Topics in Current Chemistry
(2005). 23rd August. DOI 10.1007/tcc001 Springr-Verlag Berlin
Heidelberg. Download pdf.

and

Fernando, C., and Rowe, J. (2006) Natural Selection in Chemical
Evolution. (To appear in Journal of Theoretical Biology, accepted
January 2007). See supplementary material here. Submitted paper here

available at

http://www.cogs.susx.ac.uk/users/ctf20/dphil_2005/publications.htm

Yours Sincerely,
Dr. Chrisantha Fernando
Systems Biology Centre
University of Birmingham

Tim Tyler

Posted: Wed Feb 14, 2007 8:49 am

Guest

Chrisantha wrote:

Quote:

Please take a look at our papers on the origin of
metabolism in compartments and tell us your views.

Szathmary, E, Santos, M, Fernando, C. (2005) Evolutionary
Potential and Requirements for Minimal Protocells. Topics
in Current Chemistry (2005). 23rd August. DOI
10.1007/tcc001 Springr-Verlag Berlin Heidelberg. Download
pdf.

and

Fernando, C., and Rowe, J. (2006) Natural Selection in
Chemical Evolution. (To appear in Journal of Theoretical
Biology, accepted January 2007). See supplementary
material here. Submitted paper here

available at

http://www.cogs.susx.ac.uk/users/ctf20/dphil_2005/publications.htm

Those are large documents - and alas, I must be brief:

The first paper is about the origin of lipid-based
organisms.

My own view is that lipid life arrived on the scene late.

The paper acknowledges this possibility:

``We conclude that a lot of evolution must have preceded
the origin of bacterial cells. Some of this evolution may
have taken place even in a pre-cellular phase of
evolution (such as the naked RNA world [8]).''

IMO, whether the first lipid organisms are the product
of organisms produced by an extended period of natural
selection - or not - makes a *big* difference to
theories about how their origin.

Since I'm primarily interested in the origin of
the process of open-ended natural selection, the
origin of lipid-based organisms would only be
of large significance /if/ they came first - which I
consider to be unlikely.

How did the first lipid-based organisms arise? They
arose out of adaptations of existing organisms, and
their metabolic products. We may be able to deduce some
of the details by detective work - or perhaps the details
of what happened will remain a matter of conjecture.

I do not favour the definition of life employed in this
paper. What exactly is a "boundary system", and why is
it important for organisms to have one in order to be
described as being alive?

The second paper describes a computer simulation of
the origin of heritability via a lipid world.

My impression of the underlying hypothesis is that
lipids make unlikely candidates for the first
heritable information systems. They simply lack the
requited characteristics. Their information-carrying
capacity is low. Their fidelity of transmission of
information across generations is also low. They
fail to form a 'thermodynamically-flat' selective -
landscape, instead, some reactions or variants are
significantly thermodynamically favoured - and they have
a 'low information ceiling': they don't scale up.

The most obvious prebiotically-plausible self-organising
system that does not suffer from these drawbacks seems
rather obvious once you think about it - crystallisation
and in particular clay mineral crystals.

Proponents of other candidate systems seem unlikely
to bolster their position via computer models - IMO.

What would help is chemical experiments that show that
lipid materials really do behave in the claimed manner.

As I've mentioned, we can already see that lipids make
unlikely candidates for the first heritable information
systems - so it is not clear whether more experiments
along these lines are worth doing in the first place -
but that seems like the place to start for those who
think that there might be something to a lipid world.

If a computer model helps find the best places to
look all well and good. However, I remain sceptical
that there is anything interesting to find in this area.

The material about entropy production in this paper
is interesting - but that topic has little to do with
the origin of life.
--
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Perplexed in Peoria

Posted: Wed Feb 14, 2007 8:49 am

Guest

"Chrisantha" <ctf20@sussex.ac.uk> wrote in message news:eqsprn$17dh$1@darwin.ediacara.org...

Quote:

Thanks for the links. I will comment on the Szathmary review article
here, and on the Fernando and Rowe article in a later, separate posting.

It is a good review of the 'minimal cell' literature. If I were to
make a general complaint, it would be that it is too committed to the
'chemoton' model. Ganti showed lack of imagination in insisting that
metabolism takes place _within_ the enclosed aquaeous medium. Instead,
he should have simplified his system further by hypothesizing that
the metabolism takes place in the membrane itself. In fact, there are
two symbiotic metabolic systems here - one on the inner leaflet and
one on the outer. A 'minimal life' system consists simply of an
autocatalytic lipid bilayer, or even a mono-layer (oil slick). Ideas
like those of Deamer, that such a system could grow heterotrophically
(by assimilating pre-formed lipid molecules from the environment) are
just silly. Research should focus on identifying a lipid mediated
metabolism for making more lipid (from CO2, CO, or HCN and a source
of reducing power. The enclosed 'cytoplasm' should not be seen as
a store of organic metabolites, but rather as a pool of H+, NH4+, HCO3-,
HS-, and formate at different concentrations on the inside than on the
outside. All the interesting reactions take place on the two hydrophilic
surfaces of the membrane, catalyzed by the membrane molecules themselves.
At least, that is my opinion.

One more detailed comment: The review accepts uncritically Eigen's
assertion that there is an inherent limit on RNA replication fidelity
at around 1 error per 100 bases - in the absense of protein catalysts.
This is simply not so. In fact, there is no tangible limit to the
accuracies which can be achieved, even by simple catalysts, if you are
willing to waste some energy. The mechanism is known as 'kinetic
proofreading'. It involves the kinetic balance between two competing
chemical reactions - a productive one producing template-directed
polymerization from activated monomers; and a destructive one (exonuclease)
degrading polymers to non-activated monomers. Both processes take place
simultaneously. It is assumed that there is some slight preference for
the polymerization process to add the right nucleotide over the wrong one.
It is also assumed that the hydrolytic exonuclease reaction slightly
favors the removal of mispaired monomers. Finally, it is assumed that
the two processes are in a close balance with a slight bias toward net
polymerization. Under these circumstances, replication fidelity can
be arbitrarily high, even with simple catalysts - as long as you are
willing to pay the energy cost of repeatedly reactivating the monomers
which were degraded by the futile cycle. Therefore, I consider your
long review of proposed mechanisms to avert the 'error catastrophe' as
something of a 'red herring'.

Perplexed in Peoria

Posted: Wed Feb 14, 2007 8:49 am

Guest

"Chrisantha" <ctf20@sussex.ac.uk> wrote in message news:eqsprn$17dh$1@darwin.ediacara.org...

Quote:

Again, thanks for the links. I here comment on the Fernando and Rowe
paper.

The paper quotes Wachtershauser:

Abandoning determinism we come to see that chemical reality
covers more than high propensity (“deterministic”) reactions.
In fact, low-propensity ignitions of autocatalytic cycles
(with high-propensity propagations once they have been ignited)
seems to be the very chemical stuff of biochemical evolution.

The paper then attempts to analyze by simulation the implications
of Wachtershauser's vision when wedded to the process of natural
selection at the organism level.

This attempt is very welcome, and very much in alignment with my
own viewpoint on the origin of life. However, as is the case with
all 'in silico' experiments of this kind, the reader is left wondering
just what has been proved. At best we have an illustration of the
concept - you can't call it a 'proof' of concept, because the modeled
'chemistry' is simply a game of reshuffling letter strings. We also
have some suggestive patterns and rules-of-thumb arising out of the
simulation results, but there is no way of knowing whether these are
'real' phenomena or simply a result of the investigator subtly tuning
the parameters of the model until something interesting happens.

Having made that global critique of the whole approach, let me say
again that I am happy that someone is taking Wachtershauser's vision
more seriously than Kauffman's vision. Unrealistic though your
chemistry is, it is at least as realistic as that flowing from the SFI.

But I am left wondering whether it is any better than the SFI models.
You make a big point of how your chemical model is the first to
implement conservation-of-mass. But you are still providing a flow
of foodstuffs for your heterotrophic liposomes, and you arbitrarily
assign product molecules as either hydrophilic (which diffuse away)
or hydrophobic (retained by the liposome). So, I have to ask, how
has your conservation of mass constraint on the reactions themselves
increased the chemical realism of your metabolism? It remains the
case that at the level of metabolism mass is not conserved - in fact,
how could mass be conserved in a model of growth and selection?

I am also left wondering about your decision to compromise with
Wachtershauser's strict autotrophy and to use a model in which a
certain basic level of heterotrophic growth is provided to each
liposome as a "god-given right". Is this just a convenience for
purposes of computation? You still have a 'growth set' of chemical
species which participates in an essential metabolic network. It
seems to me that you are just avoiding having the initial growth
set being unmanageably large. Or do you really doubt the plausibility
of an autotrophic origin?

I have a bit of nervousness about the 'elitism' simplification and
your use of a single modeled liposome in your model of natural selection.
But I will have to think about the situation some more to decide whether
this nervousness can be turned into a real objection.

Again, thanks for sharing. In many ways, this is the best paper on
'in silico' simulation of chemical evolution that I have seen. If
you could email me a preprint of the final version, I would appreciate
it.

Tom Hendricks

Posted: Thu Feb 15, 2007 11:11 am

Guest

Quote:

One more detailed comment: The review accepts uncritically Eigen's
assertion that there is an inherent limit on RNA replication fidelity
at around 1 error per 100 bases - in the absense of protein catalysts.
This is simply not so. In fact, there is no tangible limit to the
accuracies which can be achieved, even by simple catalysts, if you are
willing to waste some energy. The mechanism is known as 'kinetic
proofreading'. It involves the kinetic balance between two competing
chemical reactions - a productive one producing template-directed
polymerization from activated monomers; and a destructive one (exonuclease)
degrading polymers to non-activated monomers. Both processes take place
simultaneously. It is assumed that there is some slight preference for
the polymerization process to add the right nucleotide over the wrong one.
It is also assumed that the hydrolytic exonuclease reaction slightly
favors the removal of mispaired monomers. Finally, it is assumed that
the two processes are in a close balance with a slight bias toward net
polymerization. Under these circumstances, replication fidelity can
be arbitrarily high, even with simple catalysts - as long as you are
willing to pay the energy cost of repeatedly reactivating the monomers
which were degraded by the futile cycle. Therefore, I consider your
long review of proposed mechanisms to avert the 'error catastrophe' as
something of a 'red herring'.

But I think you are missing the bigger picture and the bigger question
-
what is coding for?

Whatever replicant or string of RNA survives IS the selected one,
is the one that codes most correctly, is the one that codes best,
because it codes for stability in that environment or it
would be unstable and wouldn't exist.

Why coding at all? Each and every time to better fit the environment
(that's what all the processes of life are).

There is never a time
when coding would be selected that makes life less stable and
less likely to exist in its environment .

And I'll add the reverse rule.
Coding is always for what is most stable in that environment.

This can be confusing because sometimes some parts of life
are less stable such that overall other life is more stable -
but the stability pluses always outweigh the stability minuses.

Overall every coding is for stability (though over
4 billion years, perhaps the stability is not for that individual
organism or even that single species - but for life overall.)

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