Universal senescence



T

Tim Tyler

Guest
Here's my "Universal senescence" essay.

It can be found on the web - at:

--> http://alife.co.uk/misc/universal_senescence/ <--

To offer a brief synopsis:

I suggest that the tendency of many sorts of object to fall
to bits represents a general rule of complex systems.

This rule is distinct from the second law of
thermodynamics, and - unlike the second law - can be
applied to open systems.

The aging of biological organisms represents a particular
instance of this rule.

I think the idea is a pretty obvious one - and I'd be
suprised if it originated with me. Any references to prior
work would be gratefully received.

Universal senescence
====================

An increasing tendency to fall to bits
--------------------------------------
A naive interpretation of the second law of thermodynamics
describes it as an increasing tendency of things to fall to
bits as time passes.

This isn't what the second law /actually/ says - but the
idea /does/ have a sort of intuitive appeal - since it
/does/ seem that many common objects /do/ eventually
fall to bits.

Could it be that this tendency deserves to be described as a
universal aspect of complex systems?

Occasional disintegration
-------------------------
Complex adaptive systems follow lawful behaviour just like
other objects do - though in many cases the rules they
follow may not yet be entirely clear.

These laws are best regarded as /additional/ rules of
thermodynamics designed to deal with complex adaptive
systems.

By far the most obvious rule is the statment of how such
systems affect entropy - which I have previously attempted
to describe [snip reference to my "bright light" essay].

Here I would like to propose that the phenomenon of
senescence is a common feature of a range of complex
adaptive systems - and can be characterised by the
occasional disintegration of such systems.

The suggested rule is different from the second law of
thermodynamics. That also suggests that complex systems tend
to fall to bits - but it can only be used to make that
prediction in closed environments.

The proposed rule does not have that restriction - the
intention is that it can also be applied to self-organising
systems in open environments.

Subjects of senescence
----------------------
Probably the most familiar senescing objects are biological
organisms.

Senescence is common in biology, and - among more complex
organisms - it is / nearly/ universal.

However, other sorts of system also exhibit senescence.

In particular, complex pieces of machinery also exhibit
limited lifespans - and often have lifespan curves
suggesting that progressive degradation followed by
catastrophic collapse is occurring - the signature of
senescence.

To gives some concrete examples, I claim this is true of
cars, houses, computers, stereos, clocks, motors, hyraulics
and companies.

Causes of senescence
--------------------
Why do complex things tend to fall to bits?

It appears that there are many reasons - and that different
ones can apply to different sorts of system:

- *Environmental damage* - complex systems are exposed
to damage from their environment. Often no individual
bit of damage it worth repairing - but the cumulative
long-term effects of the damage is that the system
degrades over time
- and eventually stops functioning.

- *High repair costs* - complex systems are often
difficult to repair. They can need specialist knowledge
to locate the problem and specialised tools to fix it.
This can mean that some problems are more cheaply fixed
with a new model.

- *High cost of durable components* - one simple strategy
aimed at preventing things from falling to bits is to
build them out of strong, durable materials.
Unfortunately, these are often expensive and difficult
to machine.

- *Planned senescense* - some things fall to bits simply
because they were / designed/ to fall to bits. A broken
piece of machinery often creates demand for a replacement.
Sometimes, there is little incentive for manufacturers to
build long-lived components - since doing so destroys
their future market.

- *Disposable soma* - reproductive and maintenance processes
can compete for resources. Reproducing early has many
advantages - and is consequently somatic tissue
maintenance programs do not receive sufficient investment
to support indefinite survival.

- *Antagonistic pleiotropy* - this is the idea that genes
that /delay/ the expression of other deleterious genes
are favoured.

More generally, it suggests that genes may be favoured
if they have beneficial early effects but deleterious
later effects.

- *Cumulative parasite load* - systems accumulate parasites
faster than they succeed in ridding themselves of them.
The result is progressive loss of function - followed by
catastrophic collapse.

- *Obsolescence* - in a rapidly changing environment systems
may be discarded because they are out of date. This effect
is commonly seen in computer systems - but also arises
among organisms who are in combat with parasites which
evolve to adapt to common host genotypes - where older
genotypes are more likely to encounter parasites that have
evolved the capability of exploiting their resources.

The role of complexity
----------------------
Complex systems are often more expensive to replace than
corresponding simpler ones. This makes replacing them more
expensive.

However, they also have more different bits to go wrong. It
is harder to identify the cause of problems - and it
typically require an engineer with more spare parts and
specialised knowledge to fix.

The case of companies
---------------------
The theory of "universal senescence" suggests that companies
exhibit senescence.

However - as far as I am aware - this theory has never
been tested.

It should not be too difficult to test - and the results may
be of some interest.

In theory, a number of mechanisms of senescence ought to
apply to companies.

In particular, companies:

- ...are vulnerable to environmental damage;

- ...can grow large, become unable to manoeuvre properly -
and then crash;

- can accumulate garbage in their components in the form of
well-disguised dud employees or poorly-designed systems -
in a way that makes the problem difficult to repair;

- ...can reach a size where they become attractive to
predators - and vulnerable to being swallowed up and
destructively digested - in a merger with a larger
company;

- ...that have been around longer have increased chances of
attracting parasites - either agents inside the company
who do not have its best interests at heart or externally-
run protection rackets - and the like.

Companies are an interesting case - since most companies are
still very young - and have not directly descended from
other senescing companies. Thus - unlike most complex
organisms with substantial genomes - they are not "built to
senesce". However the theory suggests that they will -
nontheless - exhibit senescence - and that the effect will
/probably/ be big enough and visible enough to be evident
from their lifespan curves.

Unfortunately, companies /also/ exhibit the equivalent of
"large infant mortality" - and the effect is a substantial
one. This may act to obscure the effect of senescence over
the lifespan of the majority of companies.

This may make company senescence more difficult to detect.

Modularity
----------
Can senescence be defended against using modularity? It
seems that - by using a modular design and "unit tests" that
failures in individual modules can be identified, isolated
and repaired - without large-scale failures necessarily
being involved.

Modularity is - without doubt - a major weapon aganist
senescence.

However there are a few drawbacks:

- Modularity is a design constraint that conflicts with
efficiency. This is probably why (for example) we don't
have twelve hearts - one heart simply works better;

- Unit tests - and the time spent executing them - also
represent something of a burden;

Also, modularity doesn't /completely/ fix the problem. There
is still the issue of connections between the modules. These
themselves senesce - and may not be so easy to diagnose
problems in.

There are also the possibilty of unplanned-for failure
scenarios within modules - failures that cause unit tests
to mis-report, failures that knock out whole modules -
and so on.

Exceptions
----------
There are a few complex organisms that don't senesce. How do
those fit into the idea of "universal senescence"?

Not very well, it must be said. However, they are not very
common - and the theory doesn't suggest that /all/ long-
lived organisms must senesce - it merely provides reasons
why most of them might.

One way to ensure you have good repair mechanisms is to make
sure finding a mate and reproducing is very, very difficult
- so that it can take a very, very long time.

Under such circumstances, selection will favour very long
lifespans.

I am happy to agree that selection is powerful enough to
produce organisms with extremely long lifespans. However I
am inclined to doubt whether that sort of selection will
ever be acting very frequently.
--
__________
|im |yler http://timtyler.org/ [email protected] Remove
lock to reply.
 
Tim Tyler wrote:
>

[snip}

> Here I would like to propose that the phenomenon of
> senescence is a common feature of a range of complex
> adaptive systems - and can be characterised by the
> occasional disintegration of such systems.
>

The earth's biosphere, a vast, complex adaptive system, has
lasted for some 3.5 billion years without senescing. It
fact, it has grown more complex as the life and ecosystems
within it have evolved, and has been able to continually
renew itself.

Of course, it could be argued that one of its subcomponents
-- the human one -- is malfunctioning like a cancer and may
bring the rest of the biosphere to an end someday.

[snip]

[email protected]
 
Tim Tyler <[email protected]> wrote in message news:<[email protected]>...
> Here's my "Universal senescence" essay.
>
> It can be found on the web - at:
>
> --> http://alife.co.uk/misc/universal_senescence/ <--
>
> To offer a brief synopsis:
>
> I suggest that the tendency of many sorts of object to
> fall to bits represents a general rule of complex systems.
> [snip] Senescence is common in biology, and - among more
> complex organisms - it is / nearly/ universal.
>
> However, other sorts of system also exhibit senescence.
> [snip] Exceptions
> ----------
> There are a few complex organisms that don't senesce. How
> do those fit into the idea of "universal senescence"?
>
> Not very well, it must be said. However, they are not very
> common - and the theory doesn't suggest that /all/ long-
> lived organisms must senesce - it merely provides reasons
> why most of them might.
>
> One way to ensure you have good repair mechanisms is to
> make sure finding a mate and reproducing is very, very
> difficult
> - so that it can take a very, very long time.
>
> Under such circumstances, selection will favour very long
> lifespans.
>
> I am happy to agree that selection is powerful enough to
> produce organisms with extremely long lifespans. However I
> am inclined to doubt whether that sort of selection will
> ever be acting very frequently.

The glaring exception to your rule of universal senescence
of complex

I think that this is one of those situations in which the
explanation of the exception "proves the rule". Given your
oft stated beliefs that

incorporate this into your essay.
 
dkomo <[email protected]> wrote or quoted:
> Tim Tyler wrote:

> > Here I would like to propose that the phenomenon of
> > senescence is a common feature of a range of complex
> > adaptive systems - and can be characterised by the
> > occasional disintegration of such systems.
>
> The earth's biosphere, a vast, complex adaptive system,
> has lasted for some 3.5 billion years without senescing.
> It fact, it has grown more complex as the life and
> ecosystems within it have evolved, and has been able to
> continually renew itself. [...]

The version of the essay on my web page discusses the case
of the earth's biosphere (under "Forces opposing senescence"
and "The Earth").

My conclusions about how it fits into the theory are not
easy to express concisely - but I suggest that the biosphere
is still early on in its developmental process. In
particular, it has not yet learned how to reproduce - and so
is best regarded as not yet being reproductively mature.

On http://alife.co.uk/misc/universal_senescence/ I suggest
that the biosphere's apparent lack of a tendency for the
probability of large-scale catastrophic failure to rise as
time passes is likely is likely to come to an end when it
ultimately faces competiton from its offspring after
reproducing.
--
__________
|im |yler http://timtyler.org/ [email protected] Remove
lock to reply.
 
Jim Menegay <[email protected]> wrote or quoted:
> Tim Tyler <[email protected]> wrote:

> > Here's my "Universal senescence" essay.
> >
> > It can be found on the web - at:
> >
> > --> http://alife.co.uk/misc/universal_senescence/ <--
> >
> > To offer a brief synopsis:
> >
> > I suggest that the tendency of many sorts of object to
> > fall to bits represents a general rule of complex
> > systems.

[...]

> > Exceptions

[...]

> The glaring exception to your rule of universal senescence
> of complex

I'm sceptical ;-)

> I think that this is one of those situations in which the
> explanation of the exception "proves the rule". Given your
> oft stated beliefs that

> incorporate this into your essay.

of an error-correcting mechanisms - if I were forced to
choose between that theory and the "Red Queen" theory of
Hamilton/Jaenike/Van

then the Queen would get my vote.

A possibility for the reason why I failed to mention the
possibility of phylogeronty (species senescence) is that I
had already written a previous essay expressing my approval
of the idea:

http://alife.co.uk/misc/species_senescence/

...and did not want to repeat myself too much.

Unfortunately, this essay can be criticised on the grounds
that it is basically armchair speculation.

Species senescence is a testable theory - but a reasonable
empirical test would probably represent some work.

Until this is done, hand-waving arguments about species
attracting parasites as they age - and about how the
"disposable soma" arguments about prioritising reproduction
over longevity are likely to be a consequence of species-
level selection (assuming that exists) are the sort of thing
I can offer.
--
__________
|im |yler http://timtyler.org/ [email protected] Remove
lock to reply.
 
Tim Tyler wrote:
>
> dkomo <[email protected]> wrote or quoted:
> > Tim Tyler wrote:
>
> > > Here I would like to propose that the phenomenon of
> > > senescence is a common feature of a range of complex
> > > adaptive systems - and can be characterised by the
> > > occasional disintegration of such systems.
> >
> > The earth's biosphere, a vast, complex adaptive system,
> > has lasted for some 3.5 billion years without senescing.
> > It fact, it has grown more complex as the life and
> > ecosystems within it have evolved, and has been able to
> > continually renew itself. [...]
>
> The version of the essay on my web page discusses the case
> of the earth's biosphere (under "Forces opposing
> senescence" and "The Earth").
>
> My conclusions about how it fits into the theory are not
> easy to express concisely - but I suggest that the
> biosphere is still early on in its developmental
> process. In particular, it has not yet learned how to
> reproduce - and so is best regarded as not yet being
> reproductively mature.
>
> On http://alife.co.uk/misc/universal_senescence/ I suggest
> that the biosphere's apparent lack of a tendency for the
> probability of large-scale catastrophic failure to rise as
> time passes is likely is likely to come to an end when it
> ultimately faces competiton from its offspring after
> reproducing.

Ok, I need some more time to read the essay out there, but
in the meantime, since turnaround time on sbe is so long,
let me put my next question regarding your idea of complex
adaptive systems having inherent senesence: why don't
bacteria senesence? Aren't they complex adaptive systems
(simple relative to others perhaps, but complex enough to
be alive)?

In previous discussions about aging, I favored the idea
that senesence is *programmed* into multicelluar eukaryotic
life by evolution, and hence is not something that is
necessarily an intrinsic property of life or complex
adaptive systems in general.

[email protected]
 
On 2004-03-10, Tim Tyler <[email protected]> wrote:
> Here's my "Universal senescence" essay.
>
> It can be found on the web - at:
>
> --> http://alife.co.uk/misc/universal_senescence/ <--
>
> To offer a brief synopsis:
>
> I suggest that the tendency of many sorts of object to
> fall to bits represents a general rule of complex systems.
>
> This rule is distinct from the second law of
> thermodynamics, and - unlike the second law - can be
> applied to open systems.
>
> The aging of biological organisms represents a particular
> instance of this rule.
>
> I think the idea is a pretty obvious one - and I'd be
> suprised if it originated with me. Any references to prior
> work would be gratefully received.
>
> Universal senescence

[snip]

Nice article, and I'm sympathetic to its general thesis.
However, there are some challenging exceptions. For
examples, some reptiles, e.g. tortoises, are very long-
lived. If it be objected that these have a slow metabolism
and therefore age very slowly, what about birds such as
parrots? Churchill's parrot is still alive at the age of
103. And, very significantly, a centenarian parrot looks no
different from a young one. Does the theory apply more to
mammals than to birds or reptiles?

AC

--
Using Linux GNU/Debian - Windows-free zone
http://www.acampbell.org.uk (book reviews and articles)
Email: replace "www." with "ac@"
 
Anthony Campbell <[email protected]> wrote or quoted:
> On 2004-03-10, Tim Tyler <[email protected]> wrote:

> > Here's my "Universal senescence" essay.
> >
> > It can be found on the web - at:
> >
> > --> http://alife.co.uk/misc/universal_senescence/ <--

[snip]

> Nice article, and I'm sympathetic to its general thesis.
> However, there are some challenging exceptions. For
> examples, some reptiles, e.g. tortoises, are very long-
> lived. If it be objected that these have a slow metabolism
> and therefore age very slowly, what about birds such as
> parrots? Churchill's parrot is still alive at the age of
> 103. And, very significantly, a centenarian parrot looks
> no different from a young one. Does the theory apply
> more to mammals than to birds or reptiles?

The animals and plants which exhibit "negligible senescence"
are mostly - I suspect - the product of selection for long
lifespans - and good self-repair mechanisms.

I suspect that the force driving such selection is most
frequently difficulty in reproduction - caused by problems
finding a mate, difficulty in dispersing seeds to other
fertile areas - and so on. It does seem that such selection
can prolong natural lifespans to a very large extent.

Selection for long lifespans can be very effective - it
seems - but the effect seems destined to be confined to rare
species - or species in obscure habitits.

Regarding how far such longevity can be taken:

http://www.research.utas.edu.au/reports/1998/clone.htm ...is
an article about the world's oldest known living thing.

It weighs in at 43,600 years old.

A vegetative growth pattern which allows an individual to
spread over a wide area - combined with an effective defense
against predation seems like it has been a fairly successful
strategy for living for a long time in that case.

It is interesting to note that the plant is sterile. Maybe
by only appearing in one place on the planet, it manages to
avoid the attention of most parasites and predators.
--
__________
|im |yler http://timtyler.org/ [email protected] Remove
lock to reply.
 
dkomo <[email protected]> wrote or quoted:

[http://alife.co.uk/misc/universal_senescence/]

> Ok, I need some more time to read the essay out there, but
> in the meantime, since turnaround time on sbe is so long,
> let me put my next question regarding your idea of complex
> adaptive systems having inherent senesence: why don't
> bacteria senesence? Aren't they complex adaptive systems
> (simple relative to others perhaps, but complex enough to
> be alive)?

The "simplicity" is significant in the case of bacteria.
*Complex* systems are the ones which have the most
difficulty building self-repair mechanisms - and the
relative simplicity of bacteria means that they have fewer
parts to go wrong - and that environmental damage stands a
high chance of killing them outright - and a low chance of
merely damaging one of their components.

However, my answer to the question is to doubt the premise.
It is commonly believed that many small micro-organisms
don't senesce and die - but the view is mistaken. They /do/
senesce - albeit slowly.

Follow an individual bacterium through multiple cell
divisions (choosing at random when it divides) and after a
while the bacterium you are looking at will die. Do this
lots of times, plot the resulting lifespans on a graph - and
bacteria will be seen to have infant mortality and
senescence like most other organisms.

Senescence will arise because not *all* mutations and
environmental damage that can happen to a bacterium are
neutral or fatal. Some are deleterious - and these will
accumulate and ultimately kill their bearers - resulting in
an increased probability of death as time passes.

However, perhaps most bacteria will die of starvation,
asphyxiation problems dividing or accidents before they have
had much time to senesce.

No doubt the next point will be about bacterial colonies.
Even if individual bacteria age and die isn't the *colony*
potentially-immortal - and lacking in senescence?

This is much more reasonable - at least for planet-spanning
bacterial populations - but I will not admit it ;-)

Instead of recognising their indefinite longevity I have a
prediction of doom for most of today's bacterial colonies.

Though there are a few ocean-dwellers which may have lasted
reasonably well from ancient times to the present day, I
reckon - in the next billion years - they will all be
effectively wiped out - and replaced by engineered creations
- probably using different genetic substrates and phenotype-
construction technology.

Will we *ever* see the bacterial equivalent of a "wheel" -
i.e. a fairly simple self-reproducing design that beats off
all comers within its niche - and lasts indefinitely? It's a
difficult question - and at the moment I'm not prepared to
rule the possibility out - but I suspect we are talking
about far-future events here.

> In previous discussions about aging, I favored the idea
> that senesence is *programmed* into multicelluar
> eukaryotic life by evolution, and hence is not something
> that is necessarily an intrinsic property of life or
> complex adaptive systems in general.

Senesence /is/ (to some extent) programmed into multicelluar
life by evolution - but that doesn't mean it is not also an
intrinsic property of complex adaptive systems.

The latter effect is best seen as the underlying cause - and
the adaptations which influence the aging rate in complex
organisms are a response to it.
--
__________
|im |yler http://timtyler.org/ [email protected] Remove
lock to reply.
 
in article [email protected], dkomo at [email protected]
wrote on 3/11/04 10:10 PM:

> Ok, I need some more time to read the essay out there, but
> in the meantime, since turnaround time on sbe is so long,
> let me put my next question regarding your idea of complex
> adaptive systems having inherent senesence: why don't
> bacteria senesence? Aren't they complex adaptive systems
> (simple relative to others perhaps, but complex enough to
> be alive)?

I am very skeptical of the claim that bacteria don't
senesce, because I share Tim's view that every kind of
dynamical system in the universe must senesce. However, this
also makes me very interested in any evidence that might
exist supporting the claim that bacteria don't senesce. It
would dramatically alter my views if I could be convinced
that this was even possible. So, what is the evidence that
bacteria don't senesce?

Guy
 
Guy Hoelzer wrote:
> in article [email protected], dkomo at
> [email protected] wrote on 3/11/04 10:10 PM:
>
>
>>Ok, I need some more time to read the essay out there, but
>>in the meantime, since turnaround time on sbe is so long,
>>let me put my next question regarding your idea of complex
>>adaptive systems having inherent senesence: why don't
>>bacteria senesence? Aren't they complex adaptive systems
>>(simple relative to others perhaps, but complex enough to
>>be alive)?
>
>
> I am very skeptical of the claim that bacteria don't
> senesce, because I share Tim's view that every kind of
> dynamical system in the universe must senesce. However,
> this also makes me very interested in any evidence that
> might exist supporting the claim that bacteria don't
> senesce. It would dramatically alter my views if I could
> be convinced that this was even possible. So, what is the
> evidence that bacteria don't senesce?
>
> Guy
>
>

you may or may not find this interesting, was at
pubmed at found this:

"1: Exp Gerontol. 2001 Apr;36(4-6):675-85. Related
Articles, Links

Does bristlecone pine senesce?

Lanner RM, Connor KF.

Institute of Forest Genetics, USDA Forest Service,
Placerville, CA 95667, USA.

We evaluated hypotheses of senescence in old trees by
comparing putative biomarkers of aging in Great Basin
bristlecone pine (Pinus longaeva) ranging in age from
23 to 4713 years. To test a hypothesis that water and
nutrient conduction is impaired in old trees we
examined cambial products in the xylem and phloem. We
found no statistically significant age-related changes
in tracheid diameter, or in several other parameters of
xylem and phloem related to cambial function. The
hypothesis of continuously declining annual shoot
growth increments was tested by comparing trees of
varying ages in regard to stem unit production and
elongation. No statistically significant age-related
differences were found. The hypothesis that aging
results from an accumulation of deleterious mutations
was addressed by comparing pollen viability, seed
weight, seed germinability, seedling biomass
accumulation, and frequency of putative mutations, in
trees of varying ages. None of these parameters had a
statistically significant relationship to tree age.
Thus, we found no evidence of mutational aging. It
appears that the great longevity attained by some Great
Basin bristlecone pines is unaccompanied by
deterioration of meristem function in embryos,
seedlings, or mature trees, an intuitively necessary
manifestation of senescence. We conclude that the
concept of senescence does not apply to these trees.

Publication Types:

* Review
* Review, Tutorial

PMID: 11295507 [PubMed - indexed for MEDLINE]

07>

g

--
Europe will never be like America. Europe is a product of
history. America is a product of philosophy. -- Margaret
Thatcher (1925 - )
 
Tim Tyler wrote:
>
> dkomo <[email protected]> wrote or quoted:
>
> [http://alife.co.uk/misc/universal_senescence/]
>
> > Ok, I need some more time to read the essay out there,
> > but in the meantime, since turnaround time on sbe is so
> > long, let me put my next question regarding your idea of
> > complex adaptive systems having inherent senesence: why
> > don't bacteria senesence? Aren't they complex adaptive
> > systems (simple relative to others perhaps, but complex
> > enough to be alive)?
>
> The "simplicity" is significant in the case of bacteria.
> *Complex* systems are the ones which have the most
> difficulty building self-repair mechanisms - and the
> relative simplicity of bacteria means that they have fewer
> parts to go wrong - and that environmental damage stands a
> high chance of killing them outright - and a low chance of
> merely damaging one of their components.
>
> However, my answer to the question is to doubt the
> premise. It is commonly believed that many small micro-
> organisms don't senesce and die - but the view is
> mistaken. They /do/ senesce - albeit slowly.
>
> Follow an individual bacterium through multiple cell
> divisions (choosing at random when it divides) and after a
> while the bacterium you are looking at will die.

I'm not sure this makes sense. When a bacterium fissions
into two bacteria, how do you tell which one is the mother
cell and which the daughter by observing the action from the
outside with a microscope? Remember that during mitosis the
DNA is replicated, then divided equally between the two
cells. Properly, the mother cell is the one with the
original DNA after mitosis. I don't think you can easily
determine this unless that DNA is marked in some way.

If you say, are you kidding? Just keep a careful eye on the
original cell during division and you should be able to keep
track of that cell during the entire mitosis. Yes, but
because of the way the DNA is replicated and partitioned
between the two cells, what you thought was the original
cell could receive the replicated DNA instead of the
original DNA. And it is in this replicated DNA that most
mutations occur.

Thus, it is useless to speak of a single bacterium's
lifespan or whether it senesces or not. This is not an
observable. You have to talk of the senescence of the
bacterial colony as a whole.

> Do this lots of times, plot the resulting lifespans on a
> graph - and bacteria will be seen to have infant
> mortality and senescence like most other organisms.
>

Many bacteria will die, but the colony will remain healthy
and thriving unless threatened by external conditions.

> Senescence will arise because not *all* mutations and
> environmental damage that can happen to a bacterium are
> neutral or fatal. Some are deleterious - and these will
> accumulate and ultimately kill their bearers - resulting
> in an increased probability of death as time passes.
>

Maybe. But it is only those mutated bacteria that become
sickly or infertile or die. The ones without mutations will
more than make up for these because of the incredible
"fertility" of bacteria.

Consider a single healthy bacterium. When it fissions, one
daughter cell receives the original DNA, the other the
relicated DNA. Mutations will mostly occur in the replicated
DNA. If any of these are deleterious, that daughter cell's
line will be threatened. However, the other daughter cell
will go on and start a line of descendants numbering in the
billions and trillions. In the fullness of time that
deleterious mutation didn't matter in the least.

> However, perhaps most bacteria will die of starvation,
> asphyxiation problems dividing or accidents before they
> have had much time to senesce.
>

Even if most do, the colony can still thrive because of the
high reproductive rate.

> No doubt the next point will be about bacterial colonies.
> Even if individual bacteria age and die isn't the *colony*
> potentially-immortal - and lacking in senescence?
>

Already made this point.

> This is much more reasonable - at least for planet-
> spanning bacterial populations - but I will not
> admit it ;-)
>
> Instead of recognising their indefinite longevity I have a
> prediction of doom for most of today's bacterial colonies.
>
> Though there are a few ocean-dwellers which may have
> lasted reasonably well from ancient times to the present
> day, I reckon - in the next billion years - they will all
> be effectively wiped out - and replaced by engineered
> creations - probably using different genetic substrates
> and phenotype-construction technology.
>
> Will we *ever* see the bacterial equivalent of a "wheel" -
> i.e. a fairly simple self-reproducing design that beats
> off all comers within its niche - and lasts indefinitely?
> It's a difficult question - and at the moment I'm not
> prepared to rule the possibility out - but I suspect we
> are talking about far-future events here.
>
> > In previous discussions about aging, I favored the idea
> > that senesence is *programmed* into multicelluar
> > eukaryotic life by evolution, and hence is not something
> > that is necessarily an intrinsic property of life or
> > complex adaptive systems in general.
>
> Senesence /is/ (to some extent) programmed into
> multicelluar life by evolution - but that doesn't mean it
> is not also an intrinsic property of complex adaptive
> systems.
>
> The latter effect is best seen as the underlying cause -
> and the adaptations which influence the aging rate in
> complex organisms are a response to it.
> --
> __________
> |im |yler http://timtyler.org/ [email protected] Remove
> lock to reply.

[email protected]
 
Guy Hoelzer wrote:
>
> in article [email protected], dkomo at
> [email protected] wrote on 3/11/04 10:10 PM:
>
> > Ok, I need some more time to read the essay out there,
> > but in the meantime, since turnaround time on sbe is so
> > long, let me put my next question regarding your idea of
> > complex adaptive systems having inherent senesence: why
> > don't bacteria senesence? Aren't they complex adaptive
> > systems (simple relative to others perhaps, but complex
> > enough to be alive)?
>
> I am very skeptical of the claim that bacteria don't
> senesce, because I share Tim's view that every kind of
> dynamical system in the universe must senesce. However,
> this also makes me very interested in any evidence that
> might exist supporting the claim that bacteria don't
> senesce. It would dramatically alter my views if I could
> be convinced that this was even possible. So, what is the
> evidence that bacteria don't senesce?
>
> Guy

Let's start here:

http://www.chelationtherapyonline.com/articles/p190.htm

I did a google on "bacteria immortal". Most of the web pages
I came up with repeat the assertion "bacteria are immortal."
I didn't have time to view all the pages. If you're looking
for counter-evidence, I believe one article mentioned that
*some* bacteria appear to age.

I repeat what I said in today's followup to Tim Tyler: it
doesn't make sense to talk about the lifespan of a single
bacterium. We need to talk about bacterial colonies when
discussing senescence.

Consider the following experiment. Culture a colony of
bacteria under carefully controlled conditions of light,
temperature, humidity and nutrients. In other others, give
them suckers the best of tender loving care to make sure
they don't die from external causes. Periodically cull the
colony so that it doesn't suffer from overcrowding.

Now, do you really believe that after X number of months,
years or decades you'll come into the lab some day and find
the colony dead from no other apparent cause than old age?

Also, if you believe this, do you also believe that all
those many batches of Hela cells around the world which have
been reproducing happily for decades now will begin someday
dying of old age? Yes, I know I've switched the playing
field to eukaryotes here, but the principle is the same as
with bacteria.

[email protected]
 
D:- I repeat what I said in today's followup to Tim Tyler:
it doesn't make sense to talk about the lifespan of a
single bacterium. We need to talk about bacterial colonies
when discussing senescence.

JE:- Your argument is classically group selective. If you
only look at populations of assumed Darwinian selectee's
(fertile forms) then everything alive becomes immortal
except that such grouped immortal forms can change over time
into a different species. Where does this get you? Now you
have to explain how this evolution occurs. To do this you
have to acknowledge the fitnesses of the individuals
concerned. Immediately you do this, the non senescent group
as one selectee disappears before your very eyes. You have
to acknowledge that Darwinian forms must live, reproduce and
die. If you delete any one of these, then none the others
make any sense.

Regards,

John Edser Independent Researcher

PO Box 266 Church Pt NSW 2105 Australia

[email protected]
 
On Mon, 15 Mar 2004 00:48:02 +0000 (UTC), dkomo <[email protected]>
wrote:

>Tim Tyler wrote:
>>
>> dkomo <[email protected]> wrote or quoted:
>>
>> [http://alife.co.uk/misc/universal_senescence/]
>>
>> > Ok, I need some more time to read the essay out there,
>> > but in the meantime, since turnaround time on sbe is so
>> > long, let me put my next question regarding your idea
>> > of complex adaptive systems having inherent senesence:
>> > why don't bacteria senesence? Aren't they complex
>> > adaptive systems (simple relative to others perhaps,
>> > but complex enough to be alive)?
>>
>> The "simplicity" is significant in the case of bacteria.
>> *Complex* systems are the ones which have the most
>> difficulty building self-repair mechanisms - and the
>> relative simplicity of bacteria means that they have
>> fewer parts to go wrong - and that environmental damage
>> stands a high chance of killing them outright - and a low
>> chance of merely damaging one of their components.
>>
>> However, my answer to the question is to doubt the
>> premise. It is commonly believed that many small micro-
>> organisms don't senesce and die - but the view is
>> mistaken. They /do/ senesce - albeit slowly.
>>
>> Follow an individual bacterium through multiple cell
>> divisions (choosing at random when it divides) and after
>> a while the bacterium you are looking at will die.
>
>I'm not sure this makes sense. When a bacterium fissions
>into two bacteria, how do you tell which one is the mother
>cell and which the daughter by observing the action from
>the outside with a microscope? Remember that during mitosis
>the DNA is replicated, then divided equally between the two
>cells. Properly, the mother cell is the one with the
>original DNA after mitosis. I don't think you can easily
>determine this unless that DNA is marked in some way.
>
>If you say, are you kidding? Just keep a careful eye on the
>original cell during division and you should be able to
>keep track of that cell during the entire mitosis. Yes, but
>because of the way the DNA is replicated and partitioned
>between the two cells, what you thought was the original
>cell could receive the replicated DNA instead of the
>original DNA. And it is in this replicated DNA that most
>mutations occur.
>
>Thus, it is useless to speak of a single bacterium's
>lifespan or whether it senesces or not. This is not an
>observable. You have to talk of the senescence of the
>bacterial colony as a whole.
>

This is not the way that DNA works. The replication is semi-
conservative. That is, the two strands separate and each
serves as the template for the new second strand. As a
result, there is no "original" DNA vs. the "replicated" DNA.
Each of the two new DNA molecules contains an original
strand and a replicated strand. Nor is it true that one
strand contains the genes -- some are on one strand, others
are on the opposite strand. Mutations are equally likely in
either daughter.

Also, when a bacterium replicates, there is no telomere to
shorten since the DNA is ordinarily a circle and there are
no ends. Therefore there is no DNA senescence. Cell
structures are in constant turnover (there are no
independent mitochondria or plastids or other complex
organelles). So at the time of binary fission, the "life" of
each daughter cell is considered to start from zero; the
clock is reset and the cells are rejuvenated by fission.
Even eukaryotes that reproduce

telomeres are reconstituted by passing through the
gamete/zygote stage which resets the aging clock.
 
dkomo <[email protected]> wrote in message news:<[email protected]>...
> [snip] Now, do you really believe that after X number of
> months, years or decades you'll come into the lab some day
> and find the colony dead from no other apparent cause than
> old age?
>
> Also, if you believe this, do you also believe that all
> those many batches of Hela cells around the world which
> have been reproducing happily for decades now will begin
> someday dying of old age? Yes, I know I've switched the
> playing field to eukaryotes here, but the principle is the
> same as with bacteria.
>
> [email protected]

Actually, HeLa may be an exception that helps to prove Tim's
rule, at least for eukariotes. I believe I have read that
Henrietta is now famous because her carcinoma is (or was)
the only immortal human cell culture. Almost all other
attempts at metazoan cell cultures senesce after a few dozen
generations, and die out.
 
dkomo <[email protected]> wrote or quoted:
> Tim Tyler wrote:
> > dkomo <[email protected]> wrote or quoted:

> > [http://alife.co.uk/misc/universal_senescence/]
> >
> > > Ok, I need some more time to read the essay out there,
> > > but in the meantime, since turnaround time on sbe is
> > > so long, let me put my next question regarding your
> > > idea of complex adaptive systems having inherent
> > > senesence: why don't bacteria senesence? Aren't they
> > > complex adaptive systems (simple relative to others
> > > perhaps, but complex enough to be alive)?
> >
> > The "simplicity" is significant in the case of bacteria.
> > *Complex* systems are the ones which have the most
> > difficulty building self-repair mechanisms - and the
> > relative simplicity of bacteria means that they have
> > fewer parts to go wrong - and that environmental damage
> > stands a high chance of killing them outright - and a
> > low chance of merely damaging one of their components.
> >
> > However, my answer to the question is to doubt the
> > premise. It is commonly believed that many small micro-
> > organisms don't senesce and die - but the view is
> > mistaken. They /do/ senesce - albeit slowly.
> >
> > Follow an individual bacterium through multiple cell
> > divisions (choosing at random when it divides) and after
> > a while the bacterium you are looking at will die.
>
> I'm not sure this makes sense. When a bacterium fissions
> into two bacteria, how do you tell which one is the mother
> cell and which the daughter by observing the action from
> the outside with a microscope?

As I said, by choosing at random when it divides.

> Remember that during mitosis the DNA is replicated, then
> divided equally between the two cells. Properly, the
> mother cell is the one with the original DNA after
> mitosis. I don't think you can easily determine this
> unless that DNA is marked in some way.

You /could/ mark the DNA - if you were *really* keen.

> Thus, it is useless to speak of a single bacterium's
> lifespan or whether it senesces or not. This is not an
> observable. [...]

I don't agree.

You can get a good idea of a bacterium's average lifespan by
holding a bacterial colony in steady state (by limiting its
nutrient supply) - and measuring the death rate - and the
size of the colony.

Another approach would be to limit the nutrient supply - to
a degree that allowed maintenance of a few individuals - but
did not allow reproduction. Tricky, perhaps - but not
impossible.

> Maybe. But it is only those mutated bacteria that become
> sickly or infertile or die. The ones without mutations
> will more than make up for these because of the incredible
> "fertility" of bacteria.
>
> Consider a single healthy bacterium. When it fissions, one
> daughter cell receives the original DNA, the other the
> relicated DNA. Mutations will mostly occur in the
> replicated DNA. If any of these are deleterious, that
> daughter cell's line will be threatened. However, the
> other daughter cell will go on and start a line of
> descendants numbering in the billions and trillions. In
> the fullness of time that deleterious mutation didn't
> matter in the least.

I admit on my page that the ability to run an evolutionary
process can sometimes protect systems from senescence.
However I also suggest that self-reproducing systems which
face competiton from their offspring are likely to senesce
nontheless. That is normally the case with bacterial
colonies - and so I would expect them to senesce - i.e. for
the probability of them catastrophically failing to increase
over time.

If you fail to distinguish between a colony and its
(genetically different and quite likely physically
separated) offspring then you may not be able to identify
death - but it (or an analogous process) is happening
nontheless - whole strains of bacteria are continually being
completely wiped out and replaced by their descendants.

The most common mechanism that allows descendants to be
fitter is disease resistance. Most bacteria are preyed upon
by bacteriophages - and disease resistance continually
offers advantages to new strains - and penalises
established ones.
--
__________
|im |yler http://timtyler.org/ [email protected] Remove
lock to reply.
 
in article [email protected], dkomo at [email protected]
wrote on 3/14/04 4:48 PM:

> Guy Hoelzer wrote:
>>
>> in article [email protected], dkomo at
>> [email protected] wrote on 3/11/04 10:10 PM:
>>
>>> Ok, I need some more time to read the essay out there,
>>> but in the meantime, since turnaround time on sbe is so
>>> long, let me put my next question regarding your idea of
>>> complex adaptive systems having inherent senesence: why
>>> don't bacteria senesence? Aren't they complex adaptive
>>> systems (simple relative to others perhaps, but complex
>>> enough to be alive)?
>>
>> I am very skeptical of the claim that bacteria don't
>> senesce, because I share Tim's view that every kind of
>> dynamical system in the universe must senesce. However,
>> this also makes me very interested in any evidence that
>> might exist supporting the claim that bacteria don't
>> senesce. It would dramatically alter my views if I could
>> be convinced that this was even possible. So, what is the
>> evidence that bacteria don't senesce?
>>
>> Guy
>
> Let's start here:
>
> http://www.chelationtherapyonline.com/articles/p190.htm

I found no evidence whatsoever at this web site supporting
the claim that there is such a thing as a cell that does not
senesce. The term "immortal cell" used on this web site
refers to a claim that some cell lineages are able to
support cellular reproduction for a very long time (perhaps
forever). I don't see the relevance.

> I did a google on "bacteria immortal". Most of the web
> pages I came up with repeat the assertion "bacteria are
> immortal." I didn't have time to view all the pages.

Me either. And I don't see what good it does for anyone to
repeat the claim that bacteria can be immortal in the
absence of any evidence or theoretical support for the
claim. I remain interested in potential evidence for
immortality or (more to the point) the absence of senescence
for any kind of organism. I become a little more confident
that such a thing does not exist every time an advocate of
the immortality view fails in to produce evidence when
challenged.

> If you're looking for counter-evidence, I believe one
> article mentioned that *some* bacteria appear to age.

Thanks. I find this sort of evidence about as interesting as
further support for the phenomenon of gravity, but it might
be illuminating for someone who believes that all bacteria
are immortal.

> I repeat what I said in today's followup to Tim Tyler: it
> doesn't make sense to talk about the lifespan of a single
> bacterium. We need to talk about bacterial colonies when
> discussing senescence.

I agree that it is generally worthwhile to track lineages
rather than focusing on individuals, but that does not mean
that bacteria don't have lifespans. The confusion over the
distinction between cell division and death can be
circumvented by studying death in cells that is not
confounded by cell division. I predict that preventing any
cell from dividing will eventually reveal their paths to
senescence.

> Consider the following experiment. Culture a colony of
> bacteria under carefully controlled conditions of light,
> temperature, humidity and nutrients. In other others, give
> them suckers the best of tender loving care to make sure
> they don't die from external causes. Periodically cull the
> colony so that it doesn't suffer from overcrowding.

OK. This is done in labs every day.

> Now, do you really believe that after X number of months,
> years or decades you'll come into the lab some day and
> find the colony dead from no other apparent cause than
> old age?

I would predict that this would be inevitable if you could
track the experiment for long enough. I think that more work
on the theory side needs to be done so that we can predict
the temporal scale of life history for any particular kind
of system before we try to do the experiment.

> Also, if you believe this, do you also believe that all
> those many batches of Hela cells around the world which
> have been reproducing happily for decades now will begin
> someday dying of old age? Yes, I know I've switched the
> playing field to eukaryotes here, but the principle is the
> same as with bacteria.

The switch makes no difference to me, because I am
considering the issue of senescence from a completely
general point of view. I don't know enough to answer your
question with any confidence. While I am persuaded by the
"Stan Salthe" view of universal life history paths, I also
recognize that there are mechanisms which compromise the
existences of systems while rejuvenating the system's life
history stage. This is essentially how I think of biological
reproduction, and it is IMHO the source of confusion over

share the fundamental pattern of the DISINTEGRATION of an
old, functional system(s) followed by the "prefab"
integration of a new system. We are familiar with the notion
in Biology that such a process leads to the re-setting of
the organismal life-history clock. It may be that some of
the lab tricks that have been developed to maintain cell
lines, like the HELA cell lines, have similar effects. I am
certainly not prepared to assume that all of the HELA cells
in the world currently constitute a single, coherent system
of any kind.

Guy
 
"Guy Hoelzer" <[email protected]> wrote in message
news:[email protected]...
> in article [email protected], dkomo at
[email protected]
> wrote on 3/14/04 4:48 PM:
>
> > Guy Hoelzer wrote:
> >>
[snippage]

> The switch makes no difference to me, because I am
considering the issue of
> senescence from a completely general point of view. I
don't know enough to
> answer your question with any confidence. While I am
persuaded by the "Stan
> Salthe" view of universal life history paths, I also
recognize that there
> are mechanisms which compromise the existences of systems
while rejuvenating
> the system's life history stage. This is essentially how
I think of
> biological reproduction, and it is IMHO the source of
confusion over

> share the fundamental pattern of the DISINTEGRATION of an
old, functional
> system(s) followed by the "prefab" integration of a new
system. We are
> familiar with the notion in Biology that such a process
leads to the
> re-setting of the organismal life-history clock. It may
be that some of the
> lab tricks that have been developed to maintain cell
lines, like the HELA
> cell lines, have similar effects. I am certainly not
prepared to assume
> that all of the HELA cells in the world currently
constitute a single,
> coherent system of any kind.
>
> Guy

I like your phrasing as to disintegration and
(re)integration. It seems to me that what we know about
thermodynamics and non-linear dynamic systems (chaos thy)
all works to result in the ultimite _disintegration_ of
highly complex systems--the former, even if unlimited
energy/resource input is presumed over all time, and the
latter, if energy/resources are ultimately limited. All the
common chaotic systems we know ultimately decay, including
chemical clocks, atmospheric storms (Jupiter's Red Spot
hasn't yet, but will, in time) cometary orbits (ditto for
some), and even stars--should cells be different? ....tonyC
 
in article [email protected], Anthony Cerrato at
[email protected] wrote on 3/19/04 8:27 PM:

> "Guy Hoelzer" <[email protected]> wrote in message
> news:[email protected]...
>> in article [email protected], dkomo at
> [email protected]
>> wrote on 3/14/04 4:48 PM:
>>
>>> Guy Hoelzer wrote:
>>>>
> [snippage]
>
>> The switch makes no difference to me, because I am
>> considering the issue of senescence from a completely
>> general point of view. I don't know enough to answer your
>> question with any confidence. While I am persuaded by the
>> "Stan Salthe" view of universal life history paths, I
>> also recognize that there are mechanisms which compromise
>> the existences of systems while rejuvenating the system's
>> life history stage. This is essentially how I think of
>> biological reproduction, and it is IMHO the source of
>> confusion over birth/death in

>> fundamental pattern of the DISINTEGRATION of an old,
>> functional system(s) followed by the "prefab" integration
>> of a new system. We are familiar with the notion in
>> Biology that such a process leads to the re-setting of
>> the organismal life-history clock. It may be that some of
>> the lab tricks that have been developed to maintain cell
>> lines, like the HELA cell lines, have similar effects. I
>> am certainly not prepared to assume that all of the HELA
>> cells in the world currently constitute a single,
>> coherent system of any kind.
>>
>> Guy
>
> I like your phrasing as to disintegration and
> (re)integration. It seems to me that what we know about
> thermodynamics and non-linear dynamic systems (chaos thy)
> all works to result in the ultimite _disintegration_ of
> highly complex systems--the former, even if unlimited
> energy/resource input is presumed over all time, and the
> latter, if energy/resources are ultimately limited. All
> the common chaotic systems we know ultimately decay,
> including chemical clocks, atmospheric storms (Jupiter's
> Red Spot hasn't yet, but will, in time) cometary orbits
> (ditto for some), and even stars--should cells be
> different?

Nope. That was the point I tried to make earlier.

Cheers,

Guy