Re: ID and the Difference Between Spheres and Cubes

On 14 May 2006 00:08:46 -0700, "nightlight"
<nightlight@xxxxxxxxxxxxxx> wrote:

The physics can only tell you the probabilities of
various outcomes (mutations), but nothing in the
most precise physical state of the DNA and its
environment determines what the specific outcome
will be in any given instance.

Gibberrish. We can most certainly determine what
the mutations are, after they occur. We do not
need to invoke any quantum effects.

You're arguing completely out of context and consequently talking
nonsense. The point of QM argument is that one cannot claim that
initial state, even if known with maximum precision, fixes the outcome.
It is trivially true that once you examine ("measure" in QM) the
outcome, it is known. Now, the original reason for pointing out that
the outcome is not determined by the initial state is to demonstrate
that there is at least one free (within the probabilistic constraints
of QM) element in a any model which can serve as an interface for
intervention into selection of mutations.

In addition to this free element (the unavoidable QM dice), there are
boundary conditions needed to solve QM equations, and these are values
put in by hand, hence free parameters, to compute QM state (wave
functions) and its transformations. These free parameters would cover
any conventional/classical types of causes which can be activated by an
intelligent agency to produce desired mutation (or make it more likely
than some others or no mutations).

A whole lot of nonsence. Random mutations are what
drives evolution. There are no intelligent agenceys
behind them.

You have flipped here and for much of the rest of your post into a
dictum proclamation mode, sprinkled here and there with simple minded,
out of context bumbling, due to pinhole vision reading, and spouting
trivialities, such as the previous non sequitur comments on QM. I'll
skip the bulk of the nonsense.

As already explained, the LD and similar experiments have
no relation to the RM vs ID criteria (1)-(2). LD only
shows that the adaptive mutations occurred after exposure
to phage, as opposed to adaptation being an infrequent
activation of an existent response mechanism....

You really missed the point of LD. They showed that the
mutations exist prior to exopsure to phage.

The statistics of LD populations is not sensitive to the presence or
existence of the mutation in the initial dish since such mutations are
occurring at some low rate (as a Poissonian process). As soon as one
bacterium acquires the resistance, then the partition of 'mother' dish
into subsequent 'daughter' dishes will automatically bring in the
resistant bacterium into single 'daughter' dish R and no resistant
bacteria into all other 'daughter' dishes S. Then, the next splits of
new 'daughter' dishes will yield more (than the Poissonian rate implied
by the new mutations occurring in all dishes independently from their
'mother' dishes) resistant 'daughter' dishes from the R dish than from
the S dishes. The reason for that excess in the 'descendant' tree of
the R dish is that the reproduction rate of the resistant bacteria was
much larger than the empirical mutation rate of non-resistant bacteria.
The experiment does not compare random vs guided mutation rates but the
rates of reproduction of resistant bacteria vs the rates of mutation of
non-resistant bacteria. Hence, as stated this experiment is irrelevant
for this discussion.

To test between random vs guided mutations, you need an experiment such
as Cairn's lactose enzyme mutation, where indeed it was found that the
rate of specific favorable double mutations was higher when they were
needed than when they were not needed. The interpretations of these
experiments from different quarters are conflicting and not worth
rearguing.

The experiments are not conflicting, and you really need to know the
biology behind the experiments. Let's look at LD. Infection by phage
T1 is rapid, and lethal. Resistance is caused by mutation in the
mutation of the protein in the E. coli cell wall that T1 binds to. So
for a cell to be resistant to T1 infection, it has to have pretty much
no wild-type T1-receptors on it.

So, if you plate a population of cells onto a plate full of phage,
either the cells are resistant prior to plating, or they die. Or a
magic E. coli fairy guards a certain percentage of cells from
infection and then magically tinkers with them to make their offspring
resistant.

You could argue that there is a time window right after plating where
the bacteria could "adapt". The E. coli, sensing danger, mutagenizes
its DNA to make a resistant receptor and lives on. Some slight
problems with that scenario however. Phage binding to a cell at the
concentrations used is literally within seconds. Once bound, game
over for our plucky bacterium. Another problem is that phage
sensitivity is dominant. In other words, if you have a cell that has
both wild-type and mutant Ton (the receptor), the cell is sensitive to
infection by T1.

So, a cell that has a brand spanking new copy of the resistant Ton
gene is still sensitive to T1 infection. You might be asking yourself
"How often to E. coli proteins get replaced?". The answer for cell
wall proteins like Ton, by dilution. Divide enough times and the
progeny will have no wild-type copies of the proteins.

Again, knowing the biology, you get two choices. Mystical phage
slaying fairies, or random pre-existing mutations. Substitute any
desired mechanism for the MPSF as you like as it amounts to the same
thing. A nondeterministic supernatural event.

My description would play better with small children though.

The Cairn's experiments were positive selections. Can you grow on
this media? Yes, E. coli does not starve as gracefully as some other
bugs, and has a fairly steep death curve when you deprive it of usable
carbon sources. You get a lot of lysis. That releases low amounts of
nutrients in the culture, enough to keep a small population of cells
alive long enough. If the same experiments are performed in strains
that are devoid of PolIV, you get a lower frequency of revertants.
This enzyme is one of two of the so-called error prone DNA polymerases
involved in repairing damage that is bad enough to stall the "normal"
polymerases. The kicker is you almost eliminate the Cairns-type
mutations by mutating RpoS. RpoS a transcription factor that E. coli
uses to turn on the so called general stress response.

Oh, and the strains isolated as survivors from a Cairns type
experiment turn out to have a much higher level of mutation in
non-selected genes when compared to their parental strains. The
technology of the time prevented Cairns from looking at neutral
mutations. Science is like that, we get odd results now and then.
This one was a head scratcher when it first came out. It wasn't
ignored even though it appeared to be in direct conflict against
neutral evolution theories. People spent a lot of time on figuring
out what was going on.

And no fairies were harmed at any point in the process.

If you want to get down and dirty at the sequence level, we can do
that. But I think that would really bore people. The Cairns effect
is very interesting in it's own right. And it is real, at least in
enteric bacteria. But it is not directed in the sense that I think
you mean.

Oh, and at no time in in figuring out what was happening with Cairn's
type experiments was QM invoked. At least by any of the folks that
actually figured it out.

B Miller

.

Relevant Pages

  • Re: Supernatural Evolution
    ... Some strains' genetic makeup will give them a slight ... resistant strains may prove harder to kill Over time, ... mutations may only add to their survival ability. ... What a kind and thoughtful god! ...
    (talk.origins)
  • Re: anti-biotic resistance theory false?
    ... First it needs to be understood that the majority or antibiotics ... to say that they stop the bacteria from growning rather than ... Second, mutations certainly occur. ... making a bacterium resistant to an antibiotic. ...
    (talk.origins)
  • Re: ID and the Difference Between Spheres and Cubes
    ... the mutations are, after they occur. ... resistant bacterium into single 'daughter' dish R and no resistant ... colony except for putative new mutation) on a non-selective plate. ... Evidence of selection merely choosing pre-existing ...
    (talk.origins)
  • Re: Increasing information experiment
    ... >> Let's say you took a culture of bacteria that you knew the exact DNA ... the DNA of bacteria that had mutations due to a major upset in DNA relication, ... known as plasmids elsewhere in the cell. ...
    (talk.origins)
  • Re: anti-biotic resistance theory false?
    ... >That is to say there mostly are already resistant strains in the ... all he has to do know is realized these are caused by mutations and ... >This finding would be counter-intuitive to natural selection formulated ... >more likely to reproduce as a non-resistant one. ...
    (talk.origins)
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