At what point did "life" start?  What was the spark, so to speak?  What
caused a compound in a "primordial soup" to "feed", to grow and to start
replicating?  (Compound being some aggregate of chemicals, I guess.)

At what point does an evolving organism become "self-aware," or develop a
form of consciousness?  What causes this to occur?  Will a computer
spontaneously become self-aware once it reaches a high enough complexity?
(What is "high enough" complexity?)

If in understand the theory of evolution correctly, there should be no
mechanism in evolution that cannot be explained and shown to have evolved
from something less complex.  There should be no miracle, no "poof, we have
xyz," so to speak.  Everything, down to the molecular level, must be
explainable and shown to have evolved from an "earlier" form.  There must
also be no "direction" or intelligence in the evolution, simply external
forces.

This last bit is very important, and it is one of the places where Dawkin's
otherwise-excellent book asks me to "trust me." In one example, he recounts
the tale of the bombardier beetle.  This lovely insect is able to mix two
chemicals (hydroquinone and hydrogen peroxide) into a storage area inside
its body.  Then by using certain muscles, it moves the mixture into yet
another area aptly named the explosion chamber.  Finally, the beetle is adds
a catalyst in the form of enzymes to the mixture in this explosion chamber
and at that point a boiling and toxic jet is emitted from the butt of the
beetle into the face of the attacker.

Now for this system to work, all three compounds must be present.  Dawkins
simply explains that the chemicals happened to be there, used for other
things and "the beetle's ancestors simply pressed into service chemicals
that happened to be around..." He then explains that evolution helped meter
the right chemicals at the right time and in the right order at the right
place.

It would seem to me that mixing these chemicals incorrectly or at the wrong
time would simply blow the beetle up. I fail to see how evolution goes from
having extra chemicals around to creating another chamber with the proper
enzymes to spark these extra chemicals out the beetle's butt.  So, Wirt if
you could please explain that one, I would really appreciate it.  Dawkins
failed miserably, I trust you can do better.

Let's talk about organs.  This is another area where Dawkins has difficulty
explaining how evolution worked.  Again, I go back to my understanding of
the theory of evolution, taken from Charles Darwin himself:  "If it could be
demonstrated that any complex organ existed, which could not possibly have
been formed by numerous, successive, slight modifications, my theory would
absolutely break down" (Origin of Species, p. 149).

Take the eye.  We all know how the eye works, with cornea, retina, rods and
cones, etc.  The eye focuses light (just like in a camera) onto the retina
and the image is passed on to the brain where it is interpreted.

That's the easy part.  The hard part is explaining the mechanism that makes
vision work.  Forget the lens and all that, how does an organ (retina) sense
light and send that to the brain?

So, I went looking for the mechanism.  This is what I found:

"When light strikes the retina a photon is absorbed by an organic molecule
called 11-cis-retinal, causing it to rearrange within picoseconds to
trans-retinal. The change in shape of retinal forces a corresponding change
in shape of the protein, rhodopsin, to which it is tightly bound. As a
consequence of the protein's metamorphosis, the behavior of the protein
changes in a very specific way. The altered protein can now interact with
another protein called transducin. Before associating with rhodopsin,
transducin is tightly bound to a small organic molecule called GDP, but when
it binds to rhodopsin the GDP dissociates itself from transducin and a
molecule called GTP, which is closely related to, but critically different
from, GDP, binds to transducin.

The exchange of GTP for GDP in the transducinrhodopsin complex alters its
behavior. GTP-transducinrhodopsin binds to a protein called
phosphodiesterase, located in the inner membrane of the cell. When bound by
rhodopsin and its entourage, the phosphodiesterase acquires the ability to
chemically cleave a molecule called cGMP. Initially there are a lot of cGMP
molecules in the cell, but the action of the phosphodiesterase lowers the
concentration of cGMP. Activating the phosphodiesterase can be likened to
pulling the plug in a bathtub, lowering the level of water.

A second membrane protein which binds cGMP, called an ion channel, can be
thought of as a special gateway regulating the number of sodium ions in the
cell. The ion channel normally allows sodium ions to flow into the cell,
while a separate protein actively pumps them out again. The dual action of
the ion channel and pump proteins keeps the level of sodium ions in the cell
within a narrow range. When the concentration of cGMP is reduced from its
normal value through cleavage by the phosphodiesterase, many channels close,
resulting in a reduced cellular concentration of positively charged sodium
ions. This causes an imbalance of charges across the cell membrane which,
finally, causes a current to be transmitted down the optic nerve to the
brain: the result, when interpreted by the brain, is vision.

If the biochemistry of vision were limited to the reactions listed above,
the cell would quickly deplete its supply of 11-cis-retinal and cGMP while
also becoming depleted of sodium ions. Thus a system is required to limit
the signal that is generated and restore the cell to its original state;
there are several mechanisms which do this. Normally, in the dark, the ion
channel, in addition to sodium ions, also allows calcium ions to enter the
cell; calcium is pumped back out by a different protein in order to maintain
a constant intracellular calcium concentration. However, when cGMP levels
fall, shutting down the ion channel and decreasing the sodium ion
concentration, calcium ion concentration is also decreased. The
phosphodiesterase enzyme, which destroys cGMP, is greatly slowed down at
lower calcium concentration. Additionally, a protein called guanylate
cyclase begins to resynthesize cGMP when calcium levels start to fall.
Meanwhile, while all of this is going on, metarhodopsin II is chemically
modified by an enzyme called rhodopsin kinase, which places a phosphate
group on its substrate. The modified rhodopsin is then bound by a protein
dubbed arrestin, which prevents the rhodopsin from further activating
transducin. Thus the cell contains mechanisms to limit the amplified signal
started by a single photon.

Trans-retinal eventually falls off of the rhodopsin molecule and must be
reconverted to 11-cis-retinal and again bound by opsin to regenerate
rhodopsin for another visual cycle. To accomplish this trans-retinal is
first chemically modified by an enzyme to transretinol, a form containing
two more hydrogen atoms. A second enzyme then isomerizes the molecule to
11-cis-retinol. Finally, a third enzyme removes the previously added
hydrogen atoms to form 11-cis-retinal, and the cycle is complete."

This seems to be a rather complex mechanism where all the parts need to work
in order for the organ to do its job.  Could you explain how this evolved as
it seems to me that it cannot be reduced without losing the function in the
first place?

I look forward to your response, probably replete with links.  However just
so you know, what I enjoy the most is your explanation, helping me navigate
these links and tying it all together for me.


Denys

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