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Feedback archive → Feedback 2008
Are ‘gain of function’ mutations really downhill and so not supporting
of evolution?
A biologist questions
Published: 20 December 2008(GMT+10)
Photo Commons.wikipedia.org
Mutations are good at getting rid of genetic information; in this case information
for making horns.
Daniel H. of the United Kingdom, who gave permission for the publication of his
name, wrote:
Dear CMI,
I’m a scientific researcher and I came across your site by accident in a google
search, in the form of the article ‘Gain-of-function mutations:
at a loss to explain molecules-to-man evolution’, by Dr Jean Lightner.
I feel the urge to provide you with some feedback on this article. It appears to
me, as written, to demonstrate nothing and to be either misled or misleading. While
the example of TSH receptor gain-of-function mutations producing disease could certainly
be used as part of a wider discussion of gain-of-function mutations in general (which
are also associated with cancer), fundamentally you cannot take one example and
‘prove’ an argument completely based upon it. The author completely
fails to demonstrate how the example of this particular TSH mutation proves some
universal rule about the effects of gain of function mutations.
For instance I work with G protein coupled receptors, a large family of membrane
receptor proteins. The adrenoceptor (for adrenaline) and the nicotinic acid receptor
(for ketone bodies produced in starvation) appear to both result as divergent descendents
of an ‘ancestral’ G protein coupled receptor, through gain/loss of function
mutations over genomic history. Now they both respond to different chemicals; however,
both now also play useful roles, even having grown into vital roles. Would you like
to discuss this possibility as well?
Evolution sometimes means that bad variants of a gene don’t persist—eg
the TSH receptor example—but as any biologist would tell you it also has the
capacity to promote ‘good’ ones.
For the record, I am a Catholic and standing up for Christianity in the field of
biology is a challenging and vitally important thing. I don’t feel this kind
of bad ‘science’ helps at all. It has no credibility. Thanks for the
chance to provide you with this feedback.
Yours sincerely,
Daniel
Here is Daniel’s email repeated with a response from Dr
Jean Lightner, author of the questioned article, interspersed in common
email fashion:
Dear CMI,
I’m a scientific researcher and I came across your site by accident in a google
search, in the form of the article ‘Gain-of-function mutations:
at a loss to explain molecules-to-man evolution’, by Dr Jean Lightner.
I feel the urge to provide you with some feedback on this article. It appears to
me, as written, to demonstrate nothing and to be either misled or misleading. While
the example of TSH receptor gain-of-function mutations producing disease could certainly
be used as part of a wider discussion of gain-of-function mutations in general (which
are also associated with cancer), fundamentally you cannot take one example and
‘prove’ an argument completely based upon it. The author completely
fails to demonstrate how the example of this particular TSH mutation proves some
universal rule about the effects of gain of function mutations.
Dear Daniel,
Thank you for taking the time to write. I wrote the article you mentioned a number
of years ago because the term ‘gain of function’ implies to the lay
person that something like ‘onward, upward evolution’ is occurring.
In the article I was able to give an example of a loss of function mutation and
two types of gain of function mutations. So the intent of the article was to inform
readers about what these terms mean (which is best done, in my opinion, by including
specific examples) and show that they do not inherently support molecules-to-man
evolution.
For instance I work with G protein coupled receptors, a large family of membrane
receptor proteins. The adrenoceptor (for adrenaline) and the nicotinic acid receptor
(for ketone bodies produced in starvation) appear to both result as divergent descendents
of an ‘ancestral’ G protein coupled receptor, through gain/loss of function
mutations over genomic history. Now they both respond to different chemicals; however,
both now also play useful roles, even having grown into vital roles. Would you like
to discuss this possibility as well?
I have been doing some research on seven-transmembrane G-protein coupled receptors
(MCRs and Olfactory receptors). They are fascinating and I have argued that some
were designed to change. In fact, I argue that the Christian worldview gives us
reason to look for directed changes in genes.
One of these articles appears on the web and the other is scheduled to appear
in the next issue of Journal of Creation.
I would love to discuss with you the possibility that the two receptors you mention
may have developed from an ‘ancestral’ G-protein. It would have been
nice to have had a reference which explores this suggestion in more detail, but
we certainly can begin a discussion on the information you provided. First, I would
like to mention a few things that may help you better understand what I am saying.
When doing science we will always have some assumptions, and we should be aware
of what these are.
The word evolution is sometimes defined as ‘change in the genetic makeup of
a population over time.’ I wholeheartedly agree that this occurs (as do the
many other creationists I know) and I discuss it in much of my writing. However,
evolution also refers to the idea that all life on earth has developed from a single
common ancestor by random, chance processes. In college when I asked for evidence
of evolution, I was always given examples of the former and expected to accept that
this implied the latter had occurred.
When doing science we will always have some assumptions and we should be aware of
what these are. One I expect we share is that science is a useful tool for learning
about the world around us. There are a number of assumptions involved in molecules-to-man
evolution that I am unwilling to accept on faith:
- The idea of common ancestry for all life is based on the assumption that
the account in the Bible is false. The historical account in Genesis states that
God created animals according to their kinds and God created mankind separately
from all other creatures. See: Argument: Common design points
to common ancestry
- It ignores the obvious implication that something which is well designed must have
had a designer. I am constantly astounded at the layer upon layer of complexity
we find in living things; there are numerous biological features that ‘wow’
human engineers (hence the rapidly growing field of biomimetics). While
you may believe that somehow ‘God did it,’ by accepting common ancestry
you are still looking at things through an ‘atheistic’ lens which basically
assumes that natural processes can account for this. See:
Design features Q&A.
- It assumes that random errors (which are what evolutionists consider all
mutations to be) can increase the level of complexity of biological systems. Random
errors naturally destroy complexity orders of magnitude faster than they
build it. Natural selection is not effective at eliminating these errors, so there
is no plausible naturalistic way to increase specified complexity. See, for example,
From ape to man via genetic meltdown: a theory in crisis.
- It uses equivocation or bait-and-switch to imply that it is scientifically
plausible. Remember the two definitions of evolution mentioned above? One is expected
to assume they are essentially synonymous. However, observed genetic changes
over time have not been shown to effectively increase biological complexity,
so those who operate in the evolutionary paradigm do so by blind faith and not because
of the evidence. See: Separating the sheep from the goats.
… observed genetic changes over time have not been shown to effectively increase
biological complexity, so those who operate in the evolutionary paradigm do so by
blind faith and not because of the evidence.
Back to the issue of an ‘ancestral’ G protein: I am certain that you
could show that a series of changes from a putative ancestral protein could account
for the two receptors you mention. This is rather weak circumstantial evidence that
something like this may have happened. Would the animal carrying the ‘ancestral’
protein have been viable? Would the intermediates be viable? The ‘circuitry’
these receptors are part of is incredibly complex. How does one propose a series
of possible changes in one protein and have an explanation of how the two actual
proteins are each well integrated into complex circuits where they effectively regulate
important functions?
I’d like to point out that one can always make a ‘phylogenetic tree’
whether things are actually related or not. I can take the silverware and cutlery
in my kitchen, lay them out on the table, and give you a very nice story of how
they all evolved from the spoon over a period of time. Someone else may disagree
and feel they all descended from a butter knife. Either way, a good story does not
necessarily correlate with reality.
Evolution sometimes means that bad variants of a gene don’t persist—eg
the TSH receptor example—but as any biologist would tell you it also has the
capacity to promote ‘good’ ones.
As a veterinarian I know that persistence of bad variants is a widespread problem.
Recessive disorders are common and natural selection is not effective at eliminating
them. In humans, many diseases strike after the childbearing years, and so defective
genes get passed on whether they are recessive or not. As I pointed out in #3 above,
naturalistic processes cannot really account for an increase in complexity even
though we are often told that they can.
For the record, I am a Catholic and standing up for Christianity in the field of
biology is a challenging and vitally important thing. I don’t feel this kind
of bad ‘science’ helps at all. It has no credibility. Thanks for the
chance to provide you with this feedback.
I appreciate that you would want to stand up for Christianity. You have repeated
a common charge that disbelieving evolution is ‘bad ‘science’’,
but not explained why. In my experience, this charge is heavily used by people who
want to ignore the Bible (i.e. they assume it is false without ever seriously
considering it, hardly a scientific mindset). Since Christianity is based on the
Bible, it is important to clearly recognize its claims to effectively take a stand.
Are you aware that Christ explicitly taught the special
creation of man as male and female from the beginning of creation
(Mark 10:6–9. citing Genesis 1:27 and 2:24 as history)? Also, accepting the
evolutionary long history of death prior to man undermines the Gospel connection
to the death brought by Adam’s Fall (1 Corinthians 15:21–22, 26, 45). A ‘God-used-evolution’
approach entails denying these explicit teachings, and much more. See:
Some questions for theistic evolutionists and progressive creationists
Whether or not someone wishes to respect the creationist view as credible is not
necessarily related to whether or not it is true. I was taught that science is a
useful tool for discovering truth, and truth is very important to me as a Christian.
It is the truth that sets people free (John 8:32). I am willing to side with the truth even if
it means I suffer verbal abuse or disrespect. I encourage you to examine in more
detail the scientific arguments creationists use to find out for yourself if you
can identify an example of ‘bad science’. I am sure I could arrange
for you to get a copy of the upcoming Journal of Creation,
which will include an article of mine, if you indicate you would be interested.
Since you are Catholic, you might be interested in knowing about the Kolbe Center, which is
a creationist ministry within the Catholic Church. For most questions regarding
the creation/evolution debate, the CMI website is an excellent searchable
resource.
Yours sincerely,
Daniel
Again, thank you for taking the time to provide your feedback.
Sincerely,
Jean Lightner
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