Allow me to predict any potential attempts at 'refutation':
1. It happened in a lab, so it is really evidence for Design!
2. That is not exactly, precisely what I challenged you to present, so it doesn't count.
3. The researchers had evolutionary assumptions, so it is question begging
4. The mice are still mice, so evolution is still a fairy tale.
5. The whole paper likely contains information contraditory to what you see in the abstract, so I cannot comment on this until I get the paper, and I will never try to get the paper.
Did I miss any?
Emphases and comments in italics mine:
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Dev Biol 2002 Sep 1;249(1):96-107
Duplication of the Hoxd11 gene causes alterations in the axial and appendicular skeleton of the mouse.
Boulet AM, Capecchi MR.
Howard Hughes Medical Institute, Department of Human Genetics, University of Utah, School of Medicine, Salt Lake City, Utah 84112-5331, USA.
The Hox genes encode a group of transcription factors essential for proper development of the mouse.
Targeted mutation of the Hoxd11 gene causes reduced male fertility, vertebral transformation, carpal bone fusions, and reductions in digit length. A duplication of the Hoxd11 gene was created with the expectation that the consequences of restricted overexpression in the appropriate cells
would provide further insight into the function of the Hoxd11 gene product.
Genetic assays demonstrated that two tandem copies of Hoxd11 were functionally indistinguishable from the normal two copies of the gene on separate chromosomes with respect to formation of the axial and appendicular skeleton. Extra copies of Hoxd11 caused an increase in the lengths of some bones of the forelimb autopod and a decrease in the number of lumbar vertebrae.
Point 1: 'New information' is NOT required to alter phenotype. One leg knocked out from the YEC information hawks...
Further, analysis of the Hoxd11 duplication demonstrated that the Hoxd11 protein can perform some functions supplied by its paralogue Hoxa11.
For example, the defects in forelimb bones are corrected when extra copies of Hoxd11 are present in the Hoxa11
homozygous mutant background.
Point 2: The presence of a duplicate 'fixes' problems caused bya mutated gene. Beneficial in anyone's book. Both legs gone, YEC information hawk goes tumbling down...
Thus, it appears that Hoxd11 can quantitatively compensate for the absence of Hoxa11 protein, and therefore Hoxa11 and Hoxd11 are functionally equivalent in the zeugopod. However, extra copies of Hoxd11 did not improve male or female fertility in Hoxa11 mutants.
Oops - missed this 'excuse': It isn't all good, so the 'challenge' was not met. Right?
Interestingly, the insertion of an additional Hoxd11 locus into the HoxD complex does not appear to affect the expression patterns of the neighboring Hoxd10, -d12, or -d13 genes.
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Still waiting for lab reports of creation ex nihilo by the deity depicted in the bible, lest YECism is false...