Let there be life

[From Bill Powers (970801.0815 MDT)]

Bruce Abbott (970731.0915 EST)--

Some added comments after a good night's sleep.

The main doubt I think I'm raising is whether this "sifting process" is
sufficient to account for the changes we see.

It seems to me that the "sifting process" is the same in your account and
the traditional one. Where they differ is in the "variation process." In
the traditional account, the rate of variation is essentially constant,
whereas in your account it is tied to error in essential variables.

I think it's just the other way around: the "variation" process in both
cases is a random change in system parameters in which all possible changes
have equal probability before any single mutation. The sifting process,
however, is very different. In traditional natural selection, if one
lineage encounters an unfavorable mutation, it stops there: it dies out.
That's the only selection mechanism. In the PCT model, an unfavorable
mutation simply shortens the interval (the number of generations that
appear) before the next mutation, so that lineage gets a second, and third,
and so on chance. It dies out only if a whole series of "chances" leads to
worse and worse conditions.

In the traditional model, "survival of the fittest" is a qualitative idea.
The only choices are survival or death. In the PCT version, "fitness" is a
continuous variable with many dimensions, and organisms can go on
reproducing even if they have less than maximum fitness. It's this ability
to go on reproducing that gives them multiple chances to mutate in
favorable directions. The assumption, of course, is that most mutations
have small effects, so that while a given mutation may reduce fitness, it
doesn't reduce it very much. The species doesn't die out instantly, in the
very next generation. The "unfitness" will show up only over many
generations, in comparison with other lineages: it is a relative measure.
And as a result, the least fit species will mutate sooner than the more
fit, giving it a chance to recover its relative position or head off in
another direction that reduces competition with other species, or both.

ยทยทยท

-----------------------------------
You have characterized the E. coli method as simply causing a higher
mutation frequency, thus given a apecies "more chances" to find a favorable
mutation. But that isn't quite right. The "decision" as to whether to
mutate again is made continuously during the interval between mutations. If
the result of a mutation is to reduce intrinsic error, the time to the next
mutation is stretched out; if intrinsic error increases, it is shortened.
During the interval, the error signal can fluctuate so the cutoff time can
be changing up and down, but of course the actual delay time isn't
determined until the total elapsed time since the last mutation becomes
longer than the current value of the delay time, tm0 - k*e. It's what
happens during _each cycle_ that matters. If you start thinking in terms of
"increased frequency" of mutation, you're considering many cycles, in a
sort of averaging approach. But in the E. coli method, each cycle is
independent of the others; the critical relationships are found in the
interval between one mutation and the next.

One way of modeling this process is to define a variable that increases
continuously at a rate determined by intrinsic error. When this variable
reaches a fixed upper limit, it is reset and a "tumble" occurs. Obviously,
if intrinsic error is small, this accumulating variable will take a long
time to reach the fixed upper limit, so the next tumble will be delayed,
and so forth. At zero error, the delay will become infinite.

This _sort_ of mechanism is quite probable in the real E. coli's means of
steering. The rotation of the flagellae is driven by some chemical process.
What seems to be the case is that there is a very narrow region over which
the rotational velocity is proportional to chemical concentration, with a
_reversal of rotation_ occurring somewhere within this region. If the six
or seven flagellae have slightly different settings for the zero-rotation
state, there will come a point where some of the flagellae reverse while
some are still turning in the forward direction. This is what creates a
tumble. What Koshland found was that if the rate of change of concentration
were made abnormally large, _all_ the flagellae would reverse, and the
bacterium would actually start backing up. Between the "all reversed" and
the "all forward" conditions, tumbling occurs. The randomness would be
created by the phase relations between the rotating flagellae at the moment
a reversal occurs. It's not really random, of course, but apparently the
result is random enough that the spatial orientations after a tumble are
evenly distributed.

Here, the interval between tumbles would be determined by how rapidly the
chemical driving the forward rotation _decreases_ in concentration after a
tumble (when it is presumably reset). But it's the same idea.

The main reason for going through that was to show how a mechanism could
exist that makes the interval between mutations depend on processes
occurring during each interval. That's the appropriate way to think of the
E. coli principle.
----------------------------------
One more thought. In the standard theory of natural selection, we can think
of the long-term probabilities of changes in different directions as being
equal. In two dimensions (two variables being mutated) the probabilities of
changing in particular directions would be represented by a circle centered
on the origin, the radius being the probability density. When we close the
loop, so that some function of the two variables determines the probability
density in each direction, the circle becomes something like an ellipse
with the origin at one focus. The long axis of the ellipse points in the
direction of most probable change.

On top of this diagram, we could draw another ellipse indicating the
long-term survival rate as a function of change in a given direction. This
would be another figure something like an ellipse, with the long axis
pointing in the direction of the best adaptation. This second ellipse would
correspond to the "natural selection" theory. Organisms that mutated the
two variables in the right proportions would have the maximum survival
potential, while all other combinations would lead to lower fitness.

This shows the difference between natural selection and E. coli selection
in a different way. If the function of the two variables x and y that is
determining the direction of most likely change is not aligned exactly with
the long axis of the ellipse showing the greatest probability of survival,
then the directed evolution will not be optimized. In other words, the
intrinsic variable that is being sensed as the basis for varying the
interval between mutations is not exactly the right one for maximizing
survival rates. The best possible case is the one in which the most likely
direction of change is aligned with the direction of highest survival rates.

From this schematic picture we can draw several conclusions about fitness

from the effect of any one variable on fitness. The best direction of
change for survival is a function of many variables. Looking at the effect
of one variable on fitness does not tell us what the optimal value of that
variable is; _all_ the variables on which fitness depends have to be
considered. If we can imagine an increase of fitness as a result of
increasing one variable, this does not mean that maximum fitness is
achieved by maximizing that variable. Maximizing any variable would
probably take us well off the long axis of the ellipse.

Another conclusion would be that even if the E. Coli type of selection
criterion caused the long axis of the "change" ellipse to point in the
wrong direction, natural selection itself would eventually align its long
axis with the long axis of the "survival" ellipse!

The same would hold for the _shape_ of the "change" ellipse. If this
ellipse were originally a circle, meaning that there are no feedback
effects to make any direction of change more likely than any other, natural
selection would, or at least could, result in acquiring an E. coli type of
mechanism that would change the circle to a modest ellipse, then gradually
increase its eccentricity, and finally align its long axis with the
direction of maximum survival rate.

Of course the net survival rate would be the product of the radii of the
two ellipses in each direction. I think this shows the relationship between
natural selection and directed evolution very neatly.
------------------------------
One final thought that popped up during an absence from the keyboard.
Long-term survival is not the same thing as maximum short-term reproductive
success (I'm sure this has been said before). As ecological studies
clearly show, a species that reproduces too fast can be as doomed to
extinction as one that reproduces too slowly. The predator can eat up all
the prey and starve to death.

The rate of reproduction per generation is simply another variable in the
equation for long-term survival of a species. And long-term survival of a
species is not really the ultimate criterion, either. If conditions change,
species evolve so that _life_ continues. It does not matter to living
systems, and particularly not to the basic biochemical processes that I
presume drive evolution, what the physical form of an organism is. The
basic picture is that living systems, by varying their forms and functions
in whatever way is necessary, continue to live. The first declaration is
not "Let there be light." It is "Let there be life."

Best,

Bill P.

[From Bruce Abbott (970802.0745 EST)]

Bill Powers (970801.0815 MDT) --

I'll be out of town the rest of today, but here are a few brief comments to
think about until I return.

It seems to me that the "sifting process" is the same in your account and
the traditional one. Where they differ is in the "variation process." In
the traditional account, the rate of variation is essentially constant,
whereas in your account it is tied to error in essential variables.

I think it's just the other way around: the "variation" process in both
cases is a random change in system parameters in which all possible changes
have equal probability before any single mutation. The sifting process,
however, is very different.

The process of variation is what is directly affected by the linkage with
error in intrinsic variables: its rate is no longer assumed to be roughly
constant. Natural selection is still natural selection: those organisms
with more of the "right stuff" (given current conditions) contribute a
greater proportion of their genes to the next generation than those with
less of it.

In traditional natural selection, if one
lineage encounters an unfavorable mutation, it stops there: it dies out.
That's the only selection mechanism. In the PCT model, an unfavorable
mutation simply shortens the interval (the number of generations that
appear) before the next mutation, so that lineage gets a second, and third,
and so on chance. It dies out only if a whole series of "chances" leads to
worse and worse conditions.

This is an incorrect description of the conventional view. In the
conventional view, even changes that have small effects on reproductive
success will alter the frequency-mix of genes in the next generation. Death
without reproduction is only the severest possible consequence of inheriting
an unfavorable mutation, not the only consequence. Thus, even in the
conventional view, a lineage normally will die out only after a whole series
of "chances" fail to bring about improvement. Reproductive fitness is a
quantitative variable.

In the traditional model, "survival of the fittest" is a qualitative idea.
The only choices are survival or death. In the PCT version, "fitness" is a
continuous variable with many dimensions, and organisms can go on
reproducing even if they have less than maximum fitness. It's this ability
to go on reproducing that gives them multiple chances to mutate in
favorable directions. The assumption, of course, is that most mutations
have small effects, so that while a given mutation may reduce fitness, it
doesn't reduce it very much. The species doesn't die out instantly, in the
very next generation. The "unfitness" will show up only over many
generations, in comparison with other lineages: it is a relative measure.
And as a result, the least fit species will mutate sooner than the more
fit, giving it a chance to recover its relative position or head off in
another direction that reduces competition with other species, or both.

See above. What you have described applies to the conventional model.

You have characterized the E. coli method as simply causing a higher
mutation frequency, thus given a apecies "more chances" to find a favorable
mutation. But that isn't quite right. The "decision" as to whether to
mutate again is made continuously during the interval between mutations. If
the result of a mutation is to reduce intrinsic error, the time to the next
mutation is stretched out; if intrinsic error increases, it is shortened.
. . .

I was careful to describe how mutation rate (the inverse of mutation delay)
changes with the size of intrinsic error, so your suggestion that my
description "isn't quite right" isn't quite right. I focused on _rate_
because the conventional view of mutation makes an assumption about
mutational rate, and I wanted to compare the two views in this regard to
show how they differ. For the purpose of describing your proposed e. coli
mechanism (as you were here doing), talking in terms of time delay is more
convenient, not more "right."

I'm going to skip over your analysis in terms of elipses for now. (I think
it is incorrect in one respect, but I'll cover that when I return).

One final thought that popped up during an absence from the keyboard.
Long-term survival is not the same thing as maximum short-term reproductive
success (I'm sure this has been said before). As ecological studies
clearly show, a species that reproduces too fast can be as doomed to
extinction as one that reproduces too slowly. The predator can eat up all
the prey and starve to death.

Yes, what counts is the survival of the lineage, not the individual. This
fact is well known.

The rate of reproduction per generation is simply another variable in the
equation for long-term survival of a species. And long-term survival of a
species is not really the ultimate criterion, either.

Correct.

If conditions change,
species evolve so that _life_ continues. It does not matter to living
systems, and particularly not to the basic biochemical processes that I
presume drive evolution, what the physical form of an organism is. The
basic picture is that living systems, by varying their forms and functions
in whatever way is necessary, continue to live. The first declaration is
not "Let there be light." It is "Let there be life."

Is this new to you? I've been taking it as a given. It's at the bottom of
my assertion that evolution is a negative feedback process. Oddly, nobody
has asked me to explain . . .

Regards,

Bruce

[From Bill Powers (970802.0719 MDT)]

Bruce Abbott (970802.0745 EST)--

The process of variation is what is directly affected by the linkage with
error in intrinsic variables: its rate is no longer assumed to be roughly
constant.

Yes, this is the PCT model of evolution.

Natural selection is still natural selection: those organisms
with more of the "right stuff" (given current conditions) contribute a
greater proportion of their genes to the next generation than those with
less of it.

Is that what you meant to say? As I see it, both the relatively fit and the
relatively unfit (after a mutation) contribute exactly the same number of
genes to the next generation: all of them. It's what happens subsequently
that allows fewer of the unfit than the fit to survive to reproduce again.
It's the differential survival-to-reproduce rates that alter the relative
populations of different mutations.

The problem I have with your statement that "natural selection is still
natural selection" is that only the _name_ remains the same. The process is
quite different. You can make any two ideas look the same if you ignore the
differences. Democrats talk about taxes; Libertarians talk about taxes;
therefore Democrats are just like Libertarians.

The E. coli principle shifts the cause of different population sizes from
survival over many generations to internal error signals that create
mutations even among populations that are reproducing quite well. The
effect of differential reproduction rates on population becomes less than
the effect of these internal error signals. The E. coli principle allows
mutation to correct errors in the system long before there would be any
effect on reproduction rate, and indeed independently of reproductive
success. In this way, stress caused by reproduction at too high a rate
could lead to mutations that reduce the rate of reproduction. I don't think
that the standard theory could predict a relative decrease of populations
that reproduce too fast.

In traditional natural selection, if one
lineage encounters an unfavorable mutation, it stops there: it dies out.
That's the only selection mechanism. In the PCT model, an unfavorable
mutation simply shortens the interval (the number of generations that
appear) before the next mutation, so that lineage gets a second, and third,
and so on chance. It dies out only if a whole series of "chances" leads to
worse and worse conditions.

This is an incorrect description of the conventional view. In the
conventional view, even changes that have small effects on reproductive
success will alter the frequency-mix of genes in the next generation. Death
without reproduction is only the severest possible consequence of inheriting
an unfavorable mutation, not the only consequence. Thus, even in the
conventional view, a lineage normally will die out only after a whole series
of "chances" fail to bring about improvement. Reproductive fitness is a
quantitative variable.

All right. But keep in mind that in the conventional view, there is no
linkage between reproductive success and the time of a new mutation. On the
average, a given organism will go on reproducing for the same length of
time before the next mutation whether the first mutation is favorable or
unfavorable. For mildly unfavorable mutations (and I'm happy to put this on
a quantitative basis), the population at the _average_ time of the next
mutation will be considerably less than it is for the mildly favorable
mutations. The fact that many generations may go by (on the average) before
another mutation means that small decrements in fitness are amplified in
their effects.

...

And as a result, the least fit species will mutate sooner than the more
fit, giving it a chance to recover its relative position or head off in
another direction that reduces competition with other species, or both.

See above. What you have described applies to the conventional model.

Yes, putting the discussion on an quantitative basis does make a
difference. However, the conventional model does not take the dependence of
delay to the next mutation on processes in the organism into account. Even
though the existence of this dependence has been known (in microorganisms)
for some time, I don't believe that the closed-loop consequences of this
phenomenon have been realized. And certainly Darwin never heard of it.

Anyway, I don't see how you can say that my description applies to the
conventional model, in which the least fit mutate no sooner than the most fit.
This is inevitable when mutation is seen not as an action by an organism,
but as a passive consequence of external forces.

In the PCT version, the population of a mildly less fit branch at the time
of the next mutation will be (depending on loop gain) about the same as
before the previous mutation, because the next mutation will occur much
sooner. Thus many more of the "unfit" population will be able to mutate
again, before the weeding out has gone very far. For very high loop gains
and large errors, there could be a mutation for every generation. The
weeding-out effects of lethal environmental pressure would become only a
minor factor.

The main issue here, as I see it, is the difference it makes to see
evolution as an active control process versus a passive process of
selection by attrition. In the standard view, the only mechanism for
removing unfit members of a population is for them to succumb before they
reproduce. In the PCT version, failure to reproduce is not a major factor;
far more important is keeping critical variables in the species at their
inherited reference levels. In the PCT model, some individuals under stress
will pass mutated genes on to their offspring, removing their lineages from
the former population but still reproducing successfully as a new
population. This is very different from having the unfit members simply
fail to reproduce at all.

The "quantitative" aspect you bring up is quantitative only in terms of
whole populations. As far as individuals are concerned, the "sieve" still
involves the same criterion: live to reproduce, or die before reproducing.

You have characterized the E. coli method as simply causing a higher
mutation frequency, thus given a apecies "more chances" to find a favorable
mutation. But that isn't quite right. The "decision" as to whether to
mutate again is made continuously during the interval between mutations. If
the result of a mutation is to reduce intrinsic error, the time to the next
mutation is stretched out; if intrinsic error increases, it is shortened.
. . .

I was careful to describe how mutation rate (the inverse of mutation delay)
changes with the size of intrinsic error, so your suggestion that my
description "isn't quite right" isn't quite right. I focused on _rate_
because the conventional view of mutation makes an assumption about
mutational rate, and I wanted to compare the two views in this regard to
show how they differ. For the purpose of describing your proposed e. coli
mechanism (as you were here doing), talking in terms of time delay is more
convenient, not more "right."

It is more right because the processes that affect the delay occur during
_each_ delay, and indeed before a given delay has finished. "Rate" is a
measure that refers to a repetitive measure, and the way you are using it
spans many cycles. In times of stress, mutations occur at a higher rate.
But there is no way to apply the E. coli principle over many cycles; it
must be applied on _each_ cycle independently of all others before or
after. We see the rate as high during times of stress, but as soon as a
mutation results in opposing the effects of the environmental disturbances,
the "rate" instantly becomes lower even though the environment remains the
same.

As ecological studies
clearly show, a species that reproduces too fast can be as doomed to
extinction as one that reproduces too slowly. The predator can eat up all
the prey and starve to death.

Yes, what counts is the survival of the lineage, not the individual. This
fact is well known.

You miss my point. If the predator _lineage_ reproduces too rapidly, it
will die out for lack of prey. I think this is referred to as the
"collapse" of the ecosystem. There are also cases where the populations
oscillate between high and low. This happens when the predator population
increases rapidly, but not too rapidly in comparison with the prey.

The rate of reproduction per generation is simply another variable in the
equation for long-term survival of a species. And long-term survival of a
species is not really the ultimate criterion, either.

Correct.

If conditions change,
species evolve so that _life_ continues. It does not matter to living
systems, and particularly not to the basic biochemical processes that I
presume drive evolution, what the physical form of an organism is. The
basic picture is that living systems, by varying their forms and functions
in whatever way is necessary, continue to live. The first declaration is
not "Let there be light." It is "Let there be life."

Is this new to you? I've been taking it as a given. It's at the bottom of
my assertion that evolution is a negative feedback process. Oddly, nobody
has asked me to explain . . .

No, this is not new to me. I believe that I expressed this same view in my
writings in the 1980s when I first began exploring the E. coli effect and
saw how it might apply to evolution. At that time it was new to me.

[I found the reference, in LCS II: "Learning and Evolution," p. 161, 1983.]

It's interesting that you now claim that the biochemical control-system
basis of variable mutation rates is what you have assumed all along. It
might help communication if you were to say what part of a paragraph
containing several ideas you are referring to with "this."

Standard natural selection is an equilibrium process, not a negative
feedback process. The loop gain in an equilibrium process is always less
than 1. The E. coli principle allows bringing in a (negative) loop gain
considerably higher than 1.

Best,

Bill P.

[From Bruce Abbott (970803.0840 EST)]

Bill Powers (970802.0719 MDT) --

Bruce Abbott (970802.0745 EST)

Natural selection is still natural selection: those organisms
with more of the "right stuff" (given current conditions) contribute a
greater proportion of their genes to the next generation than those with
less of it.

Is that what you meant to say? As I see it, both the relatively fit and the
relatively unfit (after a mutation) contribute exactly the same number of
genes to the next generation: all of them.

You are thinking about an individual organism when you should be thinking
about populations of them. In sexual reproduction, any given offspring only
gets _half_ the genes of a given parent. What counts is the number of
reproducing units (individuals) carrying a particular gene and their rate of
reproduction, relative to the rate of those individuals carrying a different
version of that gene. The collection of the relatively fit contribute more
copies of their genes to the next generation than the collection of the
relatively unfit.

It's what happens subsequently
that allows fewer of the unfit than the fit to survive to reproduce again.
It's the differential survival-to-reproduce rates that alter the relative
populations of different mutations.

That's also part of the picture: if the population is to survive in the long
run, its members must replace themselves, although errors in the direction
of shortfall can occur in the short run so long as the population is large
enough to avoid total collapse.

The problem I have with your statement that "natural selection is still
natural selection" is that only the _name_ remains the same. The process is
quite different. You can make any two ideas look the same if you ignore the
differences. Democrats talk about taxes; Libertarians talk about taxes;
therefore Democrats are just like Libertarians.

This is a false analogy. Natural selection is still natural selection; the
same sieve is being applied. What happens in the rate-control model is that
the supply of variants increases just when new solutions (offspring that
will pass through the sieve) are needed most.

The E. coli principle shifts the cause of different population sizes from
survival over many generations to internal error signals that create
mutations even among populations that are reproducing quite well. The
effect of differential reproduction rates on population becomes less than
the effect of these internal error signals. The E. coli principle allows
mutation to correct errors in the system long before there would be any
effect on reproduction rate, and indeed independently of reproductive
success. In this way, stress caused by reproduction at too high a rate
could lead to mutations that reduce the rate of reproduction. I don't think
that the standard theory could predict a relative decrease of populations
that reproduce too fast.

On the contrary, it makes that prediction. The standard theory is not about
rate of reproduction, but about a balance between reproductive rate and
population loss. Long lived but slow reproducing species (like ourselves)
can be just as "fit" as short lived but rapridly reproducing species (like
house flys). Organisms that reproduce too fast (in relation to their food
supply) have not yet successfully adapted to their situation, but such
adaptations could arise in isolated pockets. The offspring in these pockets
would avoid the collapse of their food supply while the main population was
exterminating itself through overgrazing. The survivors would later radiate
out into the vacant regions left by their starved-to-death compatriots.

All right. But keep in mind that in the conventional view, there is no
linkage between reproductive success and the time of a new mutation. On the
average, a given organism will go on reproducing for the same length of
time before the next mutation whether the first mutation is favorable or
unfavorable. For mildly unfavorable mutations (and I'm happy to put this on
a quantitative basis), the population at the _average_ time of the next
mutation will be considerably less than it is for the mildly favorable
mutations. The fact that many generations may go by (on the average) before
another mutation means that small decrements in fitness are amplified in
their effects.

Yes. I've already noted this difference between the two views.

Yes, putting the discussion on an quantitative basis does make a
difference. However, the conventional model does not take the dependence of
delay to the next mutation on processes in the organism into account. Even
though the existence of this dependence has been known (in microorganisms)
for some time, I don't believe that the closed-loop consequences of this
phenomenon have been realized. And certainly Darwin never heard of it.

No, Darwin did not consider that possibility. But I'll bet that those who
have been looking into the data on variable mutation rate have at least
understood the implication for survival when conditions require a change in
the organism.

Anyway, I don't see how you can say that my description applies to the
conventional model, in which the least fit mutate no sooner than the most fit.
This is inevitable when mutation is seen not as an action by an organism,
but as a passive consequence of external forces.

I didn't say that your description applies to the conventional model. I
said that it builds on the conventional model; it would not be seen as a
total replacement to it but as an elaboration of it.

The main issue here, as I see it, is the difference it makes to see
evolution as an active control process versus a passive process of
selection by attrition. In the standard view, the only mechanism for
removing unfit members of a population is for them to succumb before they
reproduce.

I thought we agreed that this is not the case. Unfit members don't have to
die before reproducing, they only have to reproduce less well than their
more "fit" cousins.

In the PCT version, failure to reproduce is not a major factor;
far more important is keeping critical variables in the species at their
inherited reference levels. In the PCT model, some individuals under stress
will pass mutated genes on to their offspring, removing their lineages from
the former population but still reproducing successfully as a new
population.

This overlooks some important details (like how the mutants remove their
lineages from the former population, i.e., fail to reproduce with nonmutated
survivors).

This is very different from having the unfit members simply
fail to reproduce at all.

True, but as noted, fitness in the standard model is not measured by a
strictly dichotomous criterion of reproduce/fail to reproduce.

The "quantitative" aspect you bring up is quantitative only in terms of
whole populations. As far as individuals are concerned, the "sieve" still
involves the same criterion: live to reproduce, or die before reproducing.

Wrong.

Yes, what counts is the survival of the lineage, not the individual. This
fact is well known.

You miss my point. If the predator _lineage_ reproduces too rapidly, it
will die out for lack of prey. I think this is referred to as the
"collapse" of the ecosystem. There are also cases where the populations
oscillate between high and low. This happens when the predator population
increases rapidly, but not too rapidly in comparison with the prey.

I don't think I missed your point. If the lineage dies out, there is no
more evolution within that lineage. There is nothing left to evolve, and
whatever genes may have appeared through mutation in that lineage, whatever
their advantages for fitness within that environment, are snuffed out.

The unstability of prey/predator population dynamics is a separate issue
(see above).

If conditions change,
species evolve so that _life_ continues. It does not matter to living
systems, and particularly not to the basic biochemical processes that I
presume drive evolution, what the physical form of an organism is. The
basic picture is that living systems, by varying their forms and functions
in whatever way is necessary, continue to live. The first declaration is
not "Let there be light." It is "Let there be life."

Is this new to you? I've been taking it as a given. It's at the bottom of
my assertion that evolution is a negative feedback process. Oddly, nobody
has asked me to explain . . .

No, this is not new to me. I believe that I expressed this same view in my
writings in the 1980s when I first began exploring the E. coli effect and
saw how it might apply to evolution. At that time it was new to me.

I sense that you and I are not talking about the same "this." I'm talking
about what you said in the quoted paragraph, which says nothing about the e.
coli process.

[I found the reference, in LCS II: "Learning and Evolution," p. 161, 1983.]

It's interesting that you now claim that the biochemical control-system
basis of variable mutation rates is what you have assumed all along. It
might help communication if you were to say what part of a paragraph
containing several ideas you are referring to with "this."

No, that is not my claim at all. Allow me to clarify by removing the part
of your paragraph that isn't relevant to my question:

If conditions change,
species evolve so that _life_ continues. It does not matter to living
systems . . .what the physical form of an organism is. The
basic picture is that living systems, by varying their forms and functions
in whatever way is necessary, continue to live. The first declaration is
not "Let there be light." It is "Let there be life."

That is a nice description that applies just as well to the standard theory
as Darwan conveived it as it does to your variation on the same theme.

Standard natural selection is an equilibrium process, not a negative
feedback process. The loop gain in an equilibrium process is always less
than 1. The E. coli principle allows bringing in a (negative) loop gain
considerably higher than 1.

Excuse me, an equilibrium process _is_ a negative feedback process. You
meant to say "not a control process."

Regards,

Bruce

[From Bill Powers (970803.0857 MDT)]

From Bruce Abbott (970803.0840 EST)--

Is that what you meant to say? As I see it, both the relatively fit and the
relatively unfit (after a mutation) contribute exactly the same number of
genes to the next generation: all of them.

You are thinking about an individual organism when you should be thinking
about populations of them. In sexual reproduction, any given offspring only
gets _half_ the genes of a given parent. What counts is the number of
reproducing units (individuals) carrying a particular gene and their rate of
reproduction, relative to the rate of those individuals carrying a different
version of that gene. The collection of the relatively fit contribute more
copies of their genes to the next generation than the collection of the
relatively unfit.

All right, but all parents, whether their offspring are to prove fit or
not, pass half their genes to the next generation. The ensuing "fit" and
"unfit" populations start their lives with the same number of genes. The
sieving occurs between that point and the point where some but not all, of
the "unfit" manage to reproduce themselves. Even the unfit who reproduce
manage to pass half their genes to the next generation, just as the fit do.
There is no "sieve" in the reproduction process.

The problem I have with your statement that "natural selection is still
natural selection" is that only the _name_ remains the same. The process is
quite different. You can make any two ideas look the same if you ignore the
differences. Democrats talk about taxes; Libertarians talk about taxes;
therefore Democrats are just like Libertarians.

This is a false analogy. Natural selection is still natural selection; the
same sieve is being applied. What happens in the rate-control model is that
the supply of variants increases just when new solutions (offspring that
will pass through the sieve) are needed most.

If you're trying to say that the mutations are just as random in the
directed case as they are in the undirected case, I agree. But the _number_
of variants is not increased -- there is still just one mutation at a time
per organism. The number of organisms has not increased, so there are no
more variants than in the uniform-rate model. The only change is in the
TIME dimension; that is, WHEN the variants appear.

The E. coli principle shifts the cause of different population sizes from
survival over many generations to internal error signals that create
mutations even among populations that are reproducing quite well. The
effect of differential reproduction rates on population becomes less than
the effect of these internal error signals. The E. coli principle allows
mutation to correct errors in the system long before there would be any
effect on reproduction rate, and indeed independently of reproductive
success. In this way, stress caused by reproduction at too high a rate
could lead to mutations that reduce the rate of reproduction. I don't think
that the standard theory could predict a relative decrease of populations
that reproduce too fast.

On the contrary, it makes that prediction. The standard theory is not about
rate of reproduction, but about a balance between reproductive rate and
population loss. Long lived but slow reproducing species (like ourselves)
can be just as "fit" as short lived but rapridly reproducing species (like
house flys). Organisms that reproduce too fast (in relation to their food
supply) have not yet successfully adapted to their situation, but such
adaptations could arise in isolated pockets. The offspring in these pockets
would avoid the collapse of their food supply while the main population was
exterminating itself through overgrazing. The survivors would later radiate
out into the vacant regions left by their starved-to-death compatriots.

This is not a prediction of the basic theory; it's an ad-hoc scenario
designed to allow the basic theory to make a "correct prediction" when in
fact it makes the wrong prediction. Where did those "pockets" come from,
except out of your pocket? What is there in the basic theory that predicts
that such pockets of survival would exist? All you're doing is changing the
conditions so the original situation, which would be fatal under the
standard theory, is not allowed to be fatal.

You're describing the _consequences_ that would occur _if_ the basic theory
could bring reproduction into equilibrium with the food supply. But how
does the theory do that, if not given artificial aids? You're working
backward from what you know will really happen, but presenting this as a
deduction from the theory. It isn't a deduction from the theory.

Yes, putting the discussion on an quantitative basis does make a
difference. However, the conventional model does not take the dependence of
delay to the next mutation on processes in the organism into account. Even
though the existence of this dependence has been known (in microorganisms)
for some time, I don't believe that the closed-loop consequences of this
phenomenon have been realized. And certainly Darwin never heard of it.

No, Darwin did not consider that possibility. But I'll bet that those who
have been looking into the data on variable mutation rate have at least
understood the implication for survival when conditions require a change in
the organism.

Bruce, I haven't seen a whisper of this in any of the papers I've seen in
Science or Nature. They're still arguing about whether the mutations
themselves are biased; nobody has even mentioned the E. coli principle,
that I've seen. All you're doing here is revealing your conviction that the
mainstream approach MUST have anticipated this; if you can't find any
evidence to that effect, you simply imagine it.

Look, you consider it very unfair that people accuse you of wanting to
defend traditional science; when you argue like this, your denials look
pretty weak.

Anyway, I don't see how you can say that my description applies to the
conventional model, in which the least fit mutate no sooner than the most

fit.

This is inevitable when mutation is seen not as an action by an organism,
but as a passive consequence of external forces.

I didn't say that your description applies to the conventional model. I
said that it builds on the conventional model; it would not be seen as a
total replacement to it but as an elaboration of it.

What would "total replacement" of the conventional model amount to? You'd
have to deny random variation, evolution, and everything. The basic change
that the PCT model makes is to show evolution as a control process by the
organism rather than a result of external causes. Since that view is
diametrically opposite to the conventional view, it's hard to see how you
can say it is just an "elaboration" on the conventional view. Is PCT just
an "elaboration" on S-R theory, because it accepts that there is a link
from input to output?

The main issue here, as I see it, is the difference it makes to see
evolution as an active control process versus a passive process of
selection by attrition. In the standard view, the only mechanism for
removing unfit members of a population is for them to succumb before they
reproduce.

I thought we agreed that this is not the case. Unfit members don't have to
die before reproducing, they only have to reproduce less well than their
more "fit" cousins.

I guess that's true. But the main issue is still the difference between
passive and active evolution.

In the PCT version, failure to reproduce is not a major factor;
far more important is keeping critical variables in the species at their
inherited reference levels. In the PCT model, some individuals under stress
will pass mutated genes on to their offspring, removing their lineages from
the former population but still reproducing successfully as a new
population.

This overlooks some important details (like how the mutants remove their
lineages from the former population, i.e., fail to reproduce with nonmutated
survivors).

The "new population" would simply be offspring that carry the new gene.

This is very different from having the unfit members simply
fail to reproduce at all.

True, but as noted, fitness in the standard model is not measured by a
strictly dichotomous criterion of reproduce/fail to reproduce.

The "quantitative" aspect you bring up is quantitative only in terms of
whole populations. As far as individuals are concerned, the "sieve" still
involves the same criterion: live to reproduce, or die before reproducing.

Wrong.

OK, wrong. Individuals that normally produce multiple offspring could
simply produce fewer of them. I overlooked that possibility.

Yes, what counts is the survival of the lineage, not the individual. This
fact is well known.

You miss my point. If the predator _lineage_ reproduces too rapidly, it
will die out for lack of prey. I think this is referred to as the
"collapse" of the ecosystem. There are also cases where the populations
oscillate between high and low. This happens when the predator population
increases rapidly, but not too rapidly in comparison with the prey.

I don't think I missed your point. If the lineage dies out, there is no
more evolution within that lineage. There is nothing left to evolve, and
whatever genes may have appeared through mutation in that lineage, whatever
their advantages for fitness within that environment, are snuffed out.

That's my point. This violates the principle that the better an organism
reproduces, the more fit it is. The PCT model, which does not rely on this
principle, can reduce populations when overpopulation creates intrinsic
error, without requiring either "pockets" of survival, or that the
organisms all be snuffed out.

The unstability of prey/predator population dynamics is a separate issue
(see above).

If conditions change,
species evolve so that _life_ continues. It does not matter to living
systems, and particularly not to the basic biochemical processes that I
presume drive evolution, what the physical form of an organism is. The
basic picture is that living systems, by varying their forms and functions
in whatever way is necessary, continue to live. The first declaration is
not "Let there be light." It is "Let there be life."

Is this new to you? I've been taking it as a given. It's at the bottom of
my assertion that evolution is a negative feedback process. Oddly, nobody
has asked me to explain . . .

No, this is not new to me. I believe that I expressed this same view in my
writings in the 1980s when I first began exploring the E. coli effect and
saw how it might apply to evolution. At that time it was new to me.

I sense that you and I are not talking about the same "this." I'm talking
about what you said in the quoted paragraph, which says nothing about the e.
coli process.

[I found the reference, in LCS II: "Learning and Evolution," p. 161, 1983.]

It's interesting that you now claim that the biochemical control-system
basis of variable mutation rates is what you have assumed all along. It
might help communication if you were to say what part of a paragraph
containing several ideas you are referring to with "this."

No, that is not my claim at all. Allow me to clarify by removing the part
of your paragraph that isn't relevant to my question:

If conditions change,
species evolve so that _life_ continues. It does not matter to living
systems . . .what the physical form of an organism is. The
basic picture is that living systems, by varying their forms and functions
in whatever way is necessary, continue to live. The first declaration is
not "Let there be light." It is "Let there be life."

That is a nice description that applies just as well to the standard theory
as Darwan conveived it as it does to your variation on the same theme.

I'm sorry, but you're going to have to explain how natural selection can
reduce populations if that is required for continued life. And without
introducing any convenient aids like "pockets of survival."

Standard natural selection is an equilibrium process, not a negative
feedback process. The loop gain in an equilibrium process is always less
than 1. The E. coli principle allows bringing in a (negative) loop gain
considerably higher than 1.

Excuse me, an equilibrium process _is_ a negative feedback process. You
meant to say "not a control process."

Consider a mass on a spring. Gravity pulls the mass downward with a
particular force; the spring pulls upward with a force proportional to
displacement. The mass will be at equilibrium when the upward force of the
spring is just equal to the weight of the mass.

Let l be the length of the spring, k be the spring constant, w the weight
of the mass, m the mass, and g the gravitational constant. We then have two
equations:

l = kw

w = m*g

Result: l = k*m*g.

As you can see, there is no closed loop, so there is no feedback.

In a more general case,

m*d2l/dt^2 - k1*dl/dt - k2*l = m*g

which is the differential equation for harmonic motion. Again, no feedback.
In order for feedback to be present, the _applied force_ would have to
depend on l through some second _independent_ relationship.

My mistake was not the one you caught: it was in speaking of the "loop
gain" of an equilibrium process. If there is no loop, there is no loop gain.

Best,

Bill P.