Just Not Enough Steppingstones
Sean
D. Pitman, M.D.
©
March 2004
Imagine
yourself beside a very wide river. As you look out across this river you
see various steppingstones. Close to the bank of the river there are lots
of these steppingstones such that the average distance between them is
rather minimal. However, you notice that the number of steppingstones
rapidly decreases as you look out farther and farther from the bank.
The average distance between the stones quickly grows, so that a
simple jump from one to the next becomes impossible without
getting wet.
This is the fundamental problem faced by evolutionists. How do the mindless processes of random mutation and natural selection get from one novel steppingstone function to the next without getting wet at higher and higher levels of functional complexity?
Of course, random mutations (or “letter changes”) to the codes of life do occur quite often in every living thing. These letter changes can result in the evolution of a new type or level of function or in no functional change at all. When no functional change is realized, this is called “neutral evolution.”1 For example, a change from the letter sequence grft to agrft via the addition of the letter a would be a neutral change with respect to meaning in the English language system since both letter sequences are equally meaningless.
The
information systems that code for all the parts of living things often have
such functionally neutral mutations. In fact, the large majority of
all mutational changes are thought to be functionally neutral. What is especially
interesting about these neutral mutations is that nature cannot tell the difference
between them, since nature only recognizes differences in function, not
“spelling.” However, on occasion, a mutation will actually change the
meaning or function of a genetic word or phrase.
For example,
if the spelling of vacation happened to get “mutated” to read vocation
or even vucation, there would be a big change in meaning. Of
course the word vucation has no meaning in the English language, but
a loss of the meaning of the word vacation might be beneficial
in certain circumstances, as would the gain of the meaning of the word
vocation. Such meaningful changes, when they happen in the
genetic codes of living things, can be detected by natural selection as
either beneficial or detrimental. If they are deemed to be beneficial,
they are kept for the next generation to use, but if detrimental, they are
eliminated from the gene pool over the course of time.
Nature plays a brutal game of competition, where the strongest survives to pass on genetic information while the weakest, along with the weaker genetic information, dies out. However brutal this game of survival is, it is a real game and it works very well as a preserving force that keeps the strong and gets rid of the weak. The question is, are there any examples of mindless evolutionary processes actually creating novel functions that were not there before?
The
clear answer to this question is yes ; mindless evolutionary
processes do actually create novel functions in creatures that were never
there before. For example, antibiotic resistance is a famous case of
evolution in action. As it turns out, all bacteria seem to be able to
rapidly evolve de novo resistance to just about any antibiotic that
comes their way. But how, exactly, do such novel functions evolve?
In
the case of de novo antibiotic resistance, such rapid evolution is made
possible because there are so many beneficial “steppingstones” so
close together, right beside what the bacterial colony already has. Success
is only one or two mutational steps away in many different directions since a
multitude of different single mutations will result in a beneficial
increase in resistance. How is this possible?
In
short, this is made possible because of the way in which antibiotics
work. All antibiotics attack rather specific target sequences inside
certain bacteria. Many times all the colony under attack has to do is alter
the target sequence in just one bacterium by one or two genetic
“characters” and resistance will be gained since the offspring of this
resistant bacterium, being more fit than their peers, will take over
the colony in short order. A simple “spelling change” made the target
less recognizable to the antibiotic, and so the antibiotic became less
effective. In other words, the pre-established antibiotic- target
interaction was damaged or destroyed by one or two monkey-wrench mutations. As
with Humpty Dumpty and all the king’s men, it is far easier to destroy or
interfere with a pre-established function or interaction than it is to
create a new one, since there are so many more ways to destroy than there
are to create.
So, do all functions within living things evolve as easily as the antibiotic resistance function? As it turns out, those independent functions that are not based on the destruction of or interference with other pre-established functions are much more difficult to evolve. For example, single protein enzymes catalyze many biochemical events within living things. They help to build and break down other molecules via their own independent abilities, which are not based on the gain or loss of any other system, function, or interaction.
Consider
that several forms of antibiotic resistance are based on the
production and activity of various enzymes.
The
information required to produce an enzyme which is specific enough to chop up
penicillin is far greater than the information required to block the
antibiotic-target interaction, since there are far fewer ways to make
such a specific enzymatic function compared to the number of ways to block a
specific antibiotic function. Creating a block to a previous function is
like breaking Humpty Dumpty, while creating the function of an independent
enzyme is like putting Humpty Dumpty back together again.
As
it turns out, the required code needed for producing the penicillinase
enzyme has never been observed to evolve in any bacterial colony de novo.
Either a penicillinase-producing colony already had this code before it was
exposed to penicillin, or it gained this code by genetic transfer from some
other bacterial population that already had the code.2
Simply put, the penicillinase enzyme does not evolve, or at least
not often enough to have been observed in real time, while other forms
of antibiotic resistance that are based on interference with or destruction
of pre-established functions or interactions evolve all the time.
But
what about other enzymes? Have any novel enzymatic functions ever been
shown to evolve in real time? Interestingly enough, several enzymes
with entirely new and beneficial functions have been shown to evolve in
real time. For example, Kenneth Miller, in his book, Finding Darwin’s
God, references a very interesting research study published by Barry Hall,
an evolutionary biologist from the University of Rochester.3
In
this study, Hall deleted the lactase genes in certain E. coli bacteria. These
genes produced and regulated the production of a lactase enzyme called b-galactosidase. What
this enzyme does is break apart a type of sugar molecule called
lactose into two smaller sugar molecules called glucose and galactose — both
of which E. coli can use for energy production. Obviously then,
without the genes needed to make this lactase enzyme, the mutant E.
coli were no longer able to use lactose for energy despite being placed
in a lactose enriched environment, unless of course they evolved a new
enzyme to replace the one that they lost. And sure enough, they did just
that. In just one or two generations these E. coli successfully
evolved a brand new gene that produced a new lactase enzyme. Aha! Evolution in
action yet again!
Although
most descriptions of Hall’s experiments stop right here, including the one
found in Miller’s book, what Hall did next is most interesting. He
deleted the newly evolved gene as well, to see if any other gene would
evolve the lactase function . . . and nothing happened! Despite tens of thousands
of generations with large population numbers and high mutation rates, no new
lactase enzyme evolved. Hall himself noted in his paper that these double
mutant bacteria seemed to have “limited evolutionary potential.”
Other
unfortunate bacteria seem to be just as limited in their evolutionary
potential. Even though they would significantly benefit, many types of
bacteria, after more than a million generations, have not been observed to
evolve a relatively simple lactase enzyme. This is fewer generations than
it supposedly took humans to evolve from ape-like creatures. One
should also note that these same bacteria, unable to evolve a lactase
enzyme, are all able to evolve, in relatively short order, resistance to
any antibiotic that comes their way. So what is it, exactly, that
“limits” the evolutionary potential of living things, like bacteria,
in their ability to evolve some functions but not others?
I
propose that the answer can be found in the number and density of
beneficial “stepping-stones” available (in the form of genetic
sequences). For forms of antibiotic resistance that are gained by
blocking the antibiotic-target function, there are lots of beneficial
steppingstones very close together, but not so for the enzymatic
functions of lactase or penicillinase. Relatively speaking, there are
very few such enzymes, compared to the total number of possible
sequences.
For
example, there are 676 potential two-letter words in the English language. Of
these, 96 are defined as meaningful, creating a ratio of meaningful to
meaning- less of 1 in 7. Now, there are 296 more meaningful
three-letter words, totaling 972, but the total number of potential words increases
26 fold to 17,576. Since the number of meaningful words only increased by
a fraction of this amount, the ratio of meaningful to meaningless dropped
to 1 in 18.
Still,
such ratios are relatively high, and random walk can get from any one-,
two-, or three-letter words to any other via a path of meaningful
words, as in the steppingstone sequence of cat – hat – bat – bad – bid
– did – dig – dog. “Evolution” (changing meaning or
“function”) at this level is rather simple because the stepping-stones
are so close together. But, with each additional minimum letter
requirement, the growth of the meaningless sequences quickly outpaces the
growth of the total number of meaningful sequences, and the ratio of
meaningful to meaningless gets smaller and smaller at an exponential
rate.
For
example, there are around 30,000 meaningful seven-letter words and
combinations of smaller words totaling seven letters, but there are
8,031,810,176 potential seven-letter sequences. This produces a
situation in which an average meaningful seven-letter sequence is
surrounded by over 250,000 meaningless sequences. Obviously then,
compared to three-letter steppingstones, it is much harder to “evolve”
between meaningful seven-letter steppingstones without having to cross through a little
ocean of meaningless sequences.
The
same thing happens with the genetic codes in living things. The more genetic
letters that are required to achieve a particular function, and the higher
the level of the specificity of their arrangement, the more junk there
is compared to the relatively few beneficial sequences at such a level of complexity.
For
example, a simple BLAST 4 database
search of known proteins will show that the shortest working lactase enzyme found
in a living organism seems to require well over 400 amino acids at minimum
with at least a fair degree of specificity. Some estimates suggest
that the total number of beneficial sequences at the 400-amino-acid level
of specified complexity totals less than 10100 sequences.5,6 Now,
considering that the total number of atoms in the entire known universe is around
1080,
this 10100 number
seems absolutely huge! 7
Huge, that is, until one considers that there are over 10520
possible sequences at this level of complexity, which creates a ratio
of beneficial to non-beneficial sequences of 1 in 10400
(which is like finding a single atom in zillions of universes).
Of
course, since nature cannot tell the difference between two meaningless genetic sequences,
it cannot select between them, making natural selection blind to such
neutral changes. Since there are no recognizable “steppingstones” close
by, all that nature has left, to find new beneficial sequences, is a
blind random walk through enormous piles of junk sequences. Of course, this random,
curvy walk takes a lot longer than a direct walk would take, and the time involved
increases exponentially with each increase in the minimum sequence and
specificity requirements for a particular function. This prediction is
reflected in real life by an exponential decline in the ability of mindless
evolutionary processes to evolve anything beyond the lowest levels of
functional complexity.
Many simple
functions, such as de novo antibiotic resistance, are easy to evolve
for any bacterial colony in short order. Moving up a level of complexity,
there are far fewer examples of single protein enzymes evolving where a few
hundred amino acids at minimum are required to work together at the same
time (and many types of bacteria cannot evolve even at this level). However,
there are absolutely no examples in the scientific literature of any function
requiring more than a thousand or so amino acids working at the same time (as
in the simplest bacterial motility system) ever evolving — period. The
beneficial “stepping-stones” are just too far apart due to all the
junk that separates the few beneficial islands of function from every other island
in the vast universe of junk sequences at such levels of informational
complexity. The average time needed to randomly sort through enough
junk sequences to find any other beneficial function at such a level of complexity
quickly works its way into trillions upon trillions of years — even for an enormous
population of bacteria with a high mutation rate.
At
this point the mindless processes of evolution simply become untenable as
any sort of viable explanation for the high levels of diverse
complexity that we see within all living things. The only process left that
is known to give rise to functional systems at comparable levels of
complexity involves human intelligence or beyond. No lesser intelligence,
and certainly no other known mindless processes, have ever come close to
producing something like the informational complexity found in the simplest bacterial
motility system.8
“For
the invisible things of him from the creation of the world are clearly seen,
being understood
by
the things that are made, even his eternal power and Godhead.” (Romans
1:20)
Kimura,
M. 1983. Neutral Theory of Molecular Evolution. Cambridge University
Press.
Pitman,
S.D. 2003. Antibiotic resistance. ( http://naturalselection.0catch.com/Files/antibioticresistance.html
)
Hall,
B.G. 1982. Evolution on a petri dish — the evolved b_-galactosidase system
as a model for studying acquisitive evolution in the laboratory. Evolutionary
Biology 15:85-150.
BLAST
Search: http://www.ncbi.nlm.nih.gov/BLAST
Yockey,
H.P. 1992. Information Theory and Molecular Biology. Cambridge
University Press, pp. 255, 257.
Yockey,
H.P., On the information content of cytochrome C, Journal of Theoretical
Biology , 67 (1977), p. 345-376.
Anonymous. n.d. The Universe. National Solar Observatory, Sacramento Peak. http://www.nso.edu/sunspot/pr/answerbook/universe.html/
[ Ed. note: The number of atoms according to this reference is
estimated to be 10 79
.]
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