Captain Mutation and Evolution

[grandpa]

While "luck" is meaningless in discussions of evolutionary biology, "random"
is not.
Some events are random - stochastic if you prefer.

"Random" is accurate in an evolutionary sense, but only because we don't fully understand what's happening. In fact, I doubt it'ss possible to fully understand anything.

"Luck" implies that there is some sort of target or
goal.
Random just means "unpredictable."
Thus, biologists talk about point mutations as being random, although
with a quite limited set of possibilities.
They aren't predictable because they happen for a multitude of
reasons; replication errors, radiation (cosmic, medical, and otherwise).
It is impossible to predict at what locus, in which
individual, on which chromosome, in which gene a mutation will
occur.
Further, it is impossible to predict how any such mutation
will effect the protein encoded in that gene.

So, in many areas it's like a mysterious shroud covers our understanding. There seem to be real factors in how species develop, though. Logically it seems certain critters are small enough to not get caught so easily, but others would be larger either to defend themselves or to hunt down prey. But that's just speculation, and the imperfection of all such types implies just what you say -- the unpredictable aspects of life. It seems to involve how species react to certain types of problems, both biologically and more consciously.

Biology is not my profession by any means, but I've read that it's impossible to prove absence of function for any region of DNA. Then again, those who claim this is impossible are relying on the fact it hasn't been done yet, and the whole "disproving a negative" phenomenon. It's easy to narrow things down. We learn that enzymes are proteins that spur chemical processes, which may include the production of another protein. We know those probably can't do anything they want.

Some form of radiation or replication error causes a mutation.
That mutation causes a change in the form of the
protein that it encoded.
The mutated protein causes a change in form or a
change in function in an organism.
It's still random.

In other words, it's very unpredictable now. Still, we know there is an inertial force in
the process. We know something triggers a mutation, we just don't fully know what it is. "Random" is then just a loose, relative term.

Here's something that seems relevant:
"Inside the cochlea are specialized 'hair' cells that have symmetric
arrays of stereocilia extending out from their surface. The movement of
the fluid inside the cochlea causes the stereocilia to move. This
physical change creates an electrical change and causes ion channels to
open. The opening of these channels is monitored by sensory neurons
surrounding the hair cells, and these neurons then communicate the
electrical signals to neurons in the auditory association cortex of the
brain.

In Usher syndrome and some other 'sensory neuronal' diseases that cause
deafness, the hair cells in the cochlea are unable to maintain the
symmetric arrays of stereocilia.
A few decades ago, a molecular complex called the tip link was
discovered in the stereocilia. These tip links connect the tips of
stereocilia and are also thought to be important for the transmission of
physical force to mechanically gated ion channels. For years, the
molecules that make up the tip link were not known. Now Mueller and his
colleagues have identified one of the key proteins that forms the tip
link -- the protein cadherin 23....

The identification of cadherin 23 is a great example of molecular
sleuthing.
For Mueller, who studies topics at the intersection of neuroscience and
genetics, tip links appeared to be the key to understanding and
addressing Usher syndrome, and the way forward was to identify the
proteins in the tip links.
Mueller and his colleagues reasoned that one of the molecules in tip
links would be the type of molecule that mediates cell-cell interactions
and keep the stereocilia bundled. They also had evidence from studies of
colleagues that these molecules were dependent upon calcium for their
action.
With these facts in mind, they scanned all known proteins in the human
and mouse genome to see which fit the profile, and they were able to
focus in on two gene families -- the cadherins and the integrins.

The scientists then looked at the relative sizes of cadherins and the
integrins. One particular cadherin protein, cadherin 23, appeared to be
the right size. Combined with the fact that mutations in the cadherin 23
gene are associated with deafness and deaf-blindness, it became the
prime suspect in their search.
In their Nature article, Mueller and his colleagues show that the
protein cadherin 23 is expressed in the right place in the hair cell to
be part of the tip link, that it has the correct biochemistry, and that
it seems to be responsible for opening the ion channels. They also
showed that cadherin 23 protein forms a complex with another protein
called myosin 1c, which helps to close the channel once it is open.
They predict that these two proteins form a complex with the unknown ion
channels, and they are now trying to identify other molecular components
of the tip links.
Interestingly, age-related hearing loss in humans may also be related to
problems in the tip links and defects in mechanotransduction."
http://www.sciencedaily.com/releases...0329075604.htm

If we examine protein encoding genes and their roles, things look a little less random and fairly predictable. Also, it's easier to learn what causes the central nervous system to develop. Even if one knows nothing about it now, one could potentially do a bit of research and find that it doesn't appear as random anymore.

Another, arguably grosser example would be what is producing sperm. The point is, it's pretty easy to chip away at the full meaning of "random," even if it's never totally destroyed.

Grandpa h.