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Feedback archiveFeedback 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

Polled Hereford bull

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:

  1. 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
  2. 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.
  3. 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.
  4. 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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