Researching Creation

June 10, 2009

Biological Change / BSG Conference Registration Now Open


The BSG (Creation Biology Study Group) has officially opened the registration for their conference.  The title of the conference is "Genesis Kinds - Creationism and the Origin of Species".  It will include the set of talks they gave in the UK earlier this year, plus contributed talks by members of the Creation Biology Study Group and the Creation Geology Study Group.

With my new baby (and a lot of stuff going on at work), I can't make it this year, but it sounds like quite an event!

Register Here

April 03, 2009

Biological Change / SNPedia


A new wiki is out, called SNPedia, which documents the effects of DNA variations on phenotypes.  You can also check out the SNPedia blog.

March 06, 2009

Biological Change / Lightner's Most Recent Article on Genetic Change


Jean Lightner just posted a good article up on AiG's website covering Creationary beliefs about biological change.  She notes that Creationists should expect both bad mutations because of sin and death that is in the world, and good mutations because of the care that God put into His creation.  She also made an interesting case for directed mutation in human pigmentation.

Basically, the argument goes like this:

  • MC1R (a gene for human pigmentation) is a highly mutable gene
  • MC1R tends to be regionally adapted
  • 100 Africans were tested, and none of them showed any sequence divergence from other members of the group [UPDATE - Jean pointed out in the comments that this should be "amino acid sequence" - there were some silent DNA mutations]
  • The skin cancers that develop from improper pigmentation don't show up until you are about 57 years of age, and thus will have already finished having children - therefore, natural selection will be unable to effectively remove variants from the population
  • Therefore, it seems reasonable that mutations happen in this gene because of need, rather than accident, and when there is no need, there is little or no mutation.

This is a really cool direction of research.  I also wonder what sort of mechanism would be used to control this.  Is there a feedback loop somewhere which tells the skin that the pigmentation is set at the right level?  Are the mutations prevented by methylation or some other epigenetic mechanism?  Is there something there functioning as a counter to determine how many generations it should search for an optimum versus attempt to establish a constant sequence?

Anyway, another nice thing about this article is it cited my CRSQ paper.  Yay!  Now I just have to find time to finish my BSG paper :)

February 17, 2009

Biological Change / Genetics and Biological Similarity


The recent sequencing efforts of a variety of organisms has been contributing a whole lot to what we know about the genome, and especially the genome's contribution to an organism's form.  One thing Paul Nelson (I think) has brought up before is the fact that the contents of the genome might not be as important as how it is read.  Todd Wood made similar claims in his paper on biological similarity.  Wood made some waves in Creationary camps by suggesting that perhaps chimps and humans originated with the exact same DNA!  Now, I don't think that this was the case, nevertheless it is interesting food for thought - might the same DNA lead to two radically different organisms based on how it is interpretted by the organism?  And might two very different sets of DNA lead to near-identical organisms based on how it is interpretted?

We keep on finding clues to this puzzle that indicate that this might be an affirmative on both cases.

In the case of voles, we find vast genomic differences between species that have nearly-identical morphology.

In the case of sea urchins, we see that they have genomes that are much more similar to humans than fruit flies are.  According to this article:

Sea urchins are closer to human and vertebrates from an evolutionary perspective than other more widely studied animal models, such as fruit fly or worms. The sea urchin, in fact, has 7,000 genes in common with humans [NOTE - this does not mean they are identical, just the same general gene], including genes associated with Parkinson’s, Alzheimer’s and Huntington’s diseases and muscular dystrophy. "Another surprise is that this spiny creature with no eyes, nose or hears has genes involved in vision, hearing and smell in humans,"... [emphases and NOTEs added]

Also striking is the similarity between humans and kangaroos on the genetic level:

"There are a few differences, we have a few more of this, a few less of that, but they are the same genes and a lot of them are in the same order," center Director Jenny Graves told reporters in Melbourne.

Now, for those of you unfamiliar with the evolutionary tree, marsupials and placentals were supposed to have diverged long, long ago, in a small mole- or badger-like creature.  But here we have kangaroos and humans having the same genes (again, not necessarily identical) in the same order, which is supposedly the evidence for our descent from apes (note that I know of no scientist who says that we descended from kangaroos, and yet what we have here is very much the same type of genetic evidence).

In any case, the point is that similarities and differences within genomes may mean something else entirely from what we think it means today.  Are the fundamental components of body morphology even genetic?  Anyway, lots of good questions are lurking around in there.

February 09, 2009

Biological Change / BSG UK Conference Highlights


Todd Wood has been blogging the BSG UK conference, titled Genesis and the Origin of the Species.  This latest post links to all of his daily entries.  The conference is coming soon to the US!  I probably won't get to make it (new child on the way), but it sounds like fun!

January 07, 2009

Biological Change / Contingency Loci and Symbiosis


Caporale's latest work, The Implicit Genome, covers a lot of cool mechanisms for the generation of variability within genomes.  One interesting mechanism is through contingency loci.

A contingency locus is an area of the genome which has a high mutation rate, which is associated with a frequently-changing environment. A typical reason for contingency loci is to get around the immune system.  The contingency loci in many bacteria are for their outer coat proteins, which is what the immune system recognizes.   Bacteria and single-celled eukaryotes can evade the immune system by rapidly mutating their outer coat.

Now, usually the relationship between microbes, hosts, and immune system is discussed in terms of warfare - this fights this, this evades that.  But what if this was instead a mechanism that wasn't nearly as much about warfare as it was about adaptation?

For example, Opa proteins on N. meningitidis are surface proteins that are encoded by contingency loci.  Different versions of these proteins adhere to different types of cells.  So, what I'm wondering is - are mutations in these contingency loci associated with mutations elsewhere, or expression changes elsewhere?  For instance, might certain microbes alter their biochemistry in coordination with their surface proteins so that they assist the right cell type in the correct way?  In other words, instead of "evading the immune system", might it instead be trying to find a biochemistry which is helpful to the organism, and using surface proteins to advertise to the immune system what sort of tissue the organism is best configured for.  The immune system, rather than "combating" the antigen, might be just cleaning up good microbes which are just in the wrong place, or perhaps in the wrong configuration in the wrong place.

Anyway, it's an interesting possibility, but I'm not sure how it might be investigated.  But it might make a good research project for a budding Creation PhD student somewhere.

I'm not quite sure how this question would be investigated, but it's sure worth asking.

November 29, 2008

Biological Change / A Catalogue of Animal and Plant Baramins (Created Kinds)


Todd Wood just release a new monograph containing a whole bunch of data concerning created kinds, called Animal and Plant Baramins.  For those of you new to Creationism, a baramin is the Creationist term for a "created kind".  For those interested in exploring Creation systematics further, I will refer you to Wood and Wise's  A Refined Baramin Concept.

Anyway, this book is significant because it is the first large-scale treatment of what organisms belong with which created kind (again, for those who are new, Creationists believe that Created Kinds are larger than just "species", and usually estimate the Created Kind to be roughly equivalent with the family level of taxonomy).

Now, I have no first-hand information about the book - it just came out so I haven't read any of it yet, but I did talk with Todd about it at this year's BSG.  Based on that conversation, I'm pretty sure that most baramins in the book are defined using statistical baraminic concepts.  I'm not a big fan of statistical baraminology, and prefer hybridization experiments (obviously, however, that data is not available for fossil species).  In any case, this is a great start to our systematics work. 

Another thing that Todd told me is that ark-based animals have much less variability within baramins than non-ark-based animals.  This is quite interesting, since the ark-based animals would have a genetic bottleneck that wouldn't apply to non-ark-based animals.  I believe he also said that the distribution actually follows what would be expected from a Biblical timescale.

Anyway, I plan on purchasing this as soon as I have the funds, and for those into Creation systematics, I would suggest you do, too.

August 29, 2008

Biological Change / The Production of Variability in Spiders


For those interested, I did a follow-up post about the production of variations in spiders over at UncommonDescent.  The original conversation about the production of variability is here.

August 18, 2008

Biological Change / The Production of Variability


Most people don't understand the problems of the production of variability in biology (or actually in any complex system), and especially how it relates to Intelligent Design.  Here are some links to my current work on the subject:

UPDATE - followup blog entry - applying some of these concepts to spiders



August 13, 2008

Biological Change / The Case for and Against Genetic Entropy

NOTE - this has been updated slightly.

At the ICC, the GENE team introduced a new genetics simulation tool which has an astonishing number of input variables - it seems to be really well thought out.  The results of the simulations performed on it show Sanford's "genetic entropy" thesis - that the genetic load that comes with mutation far outweighs any beneficial mutations that may occur.

So the question is, why does evolution go downward?  Sanford's conclusions are:

  • Near-neutral mutations cannot be removed through selection
  • Mutation rate is way too high
  • Nonheritable noise (I think this was random death instead of selective death)
  • Trait linkage and Muller's ratchet (it was unclear how Muller's ratchet was modelled in the software) 
  • Fixation of deleterious mutations (note to non-geneticists - fixation means that the mutation isin every member of the population - it does not mean that the mutation has been fixed from being deleterious).

Sanford said that selection breaks down at the 0.001 fitness reduction level.  At this point, selection is simply unable to remove the trait from the population.  It is also harder to select away recessive genes.

Their software can also simulate a population bottleneck.  It showed that this actually leads to a dramatic loss of fitness because of the rapid fixation of genetic damage.  So, in the fitness graphs, a genetic bottleneck causes a temporary transition from a downhill slope to a downhill cliff.  When the population recovers, it is back on the downhill slope.

Sanford said that this data should cause the following shifts in evolutionary thinking:

  • Switching from Primary Axiom (mutation + selection = increasing fitness over time) to Genetic Entropy concepts
  • Switching from "forward evolution" to "degeneration"
  • Transition from the idea of "creative selection" to focusing almost entirely on "stabilizing selection"
  • Thinking about extinction as a past event to thinking about extinction as a future event

Now, personally, I wonder if some of this relies too much on Darwinian assumptions.  Here are some basic issues:

  • The mutation rate is not really known, it is inferred
  • I have a paper coming out in the Fall CRSQ on "future fitness" explaining some possible reasons nearly-neutral mutations may be occurring for the benefit of the population
  • The rate of beneficial mutations has not been empirically calculated.  One reason evolutionists assume it is so high is that otherwise they have to think about directed mutagenesis
  • Directed mutagenesis throws kinks into most of the areas, and their effects are not modeled by the software

Okay, so I probably need to explain directed mutagenesis a little more and why it impacts their model.

Historically, evolutionary thought has thought of mutations happening essentially haphazardly - that is, without any particular constraint (except perhaps incidental ones) on which DNA bases get modified.  However, what if that assumption is wrong? There are several possibilities:

  • Instead of mutations compounding, many of them are instead cycling.
  • This means that the fixation of a deleterious gene isn't necessarily permanent.  If it is cycling, it may later be replaced again with the original version.
  • If the mutations are cycling, then perhaps they are all beneficial in some circumstance.  Therefore, perhaps at the population bottleneck 50% (just to pull a random number out of the hat) of them switch from deleterious to beneficial. 
This seems, to me, to undermine the concept of Genetic Entropy, or at least greatly reduce its effect.  I don't doubt that some mutations are haphazard, I just wonder if, however, much or most of what we see are instead directed/cyclical mutations.  There certainly is a lot of evidence for this (we've covered this and its mechanisms elsewhere on the blog before - if I get bored I might update this post with links - some examples include SSRs, transposable elements, and Barbara Wright's single-stranded conformation transcriptional mechanism).  Genetic Entropy probably is happening, but probably nowhere near the rate that Sanford's team supposes.

UPDATE: I just looked at my notes again and realized I left off another source of genetic variation which is at odds with Sanford's model - Virus-borne mutations.  These would affect the population in a way which is not birth-dependent.  If viruses are designed to transfer new genes, reconstituted genes, or any other sort of beneficial change, then this could be a source of beneficial mutations which don't rely on the birthing bottleneck.  For those of you who think that viruses are bad, the fact is that we simply don't know what most of them do.  The only ones that we are really sure we know what they do are the disease-causing ones, but they are a minority.

Anyway, it would really be interesting to see the application reworked with some of these concepts in mind.