It’s the same tired junk DNA argument from the ID creationists. But I find this one particularly funny – you’ll see why. Luskin says:
It’s beyond dispute that the false “junk”-DNA mindset was born, bred, and sustained long beyond its reasonable lifetime by the neo-Darwinian paradigm. As one example in Scientific American explained back in 2003, “the introns within genes and the long stretches of intergenic DNA between genes … ‘were immediately assumed to be evolutionary junk.'” But once it was discovered that introns play vital cellular roles regulating gene production within the cell, John S. Mattick, director of the Institute for Molecular Bioscience at the University of Queensland in Brisbane, Australia, was quoted saying the failure to recognize function for introns might have been “one of the biggest mistakes in the history of molecular biology.”
Wow, now that John S. Mattick has said it, it must be true. I’m sure Mattick’s a good guy, but man is he wrong about this one. It’s either that or our “biggest mistake” was really no big deal, because as I pointed out before the use of the junk terminology didn’t stop people from looking for function in non-coding DNA. Further, the assertion that ID figured out something clever is absurd, it’s just prediction of the past from the future and no great feat.
But that doesn’t stop Luskin from putting his foot in his mouth, he’s been a one-trick pony lately with this junk DNA nonsense, but, being a crank, he still can’t figure out why this issue is a loser for ID. Luskin gives his evidence that there was some great harm from the junk DNA theory.
Now it’s turning out that this “mistake” of ignoring function for junk-DNA may have also hindered discovery of the causes of colon cancer. A news article from Science reports: “Three independent groups have hit on the first common genetic variant that appears to raise the risk of colorectal cancer, albeit by a small amount, and which they estimate is found in half the world’s population. Although rare genes have been linked to the disease before, this is the first evidence of common DNA–and also notable because it falls outside a gene, in so-called ‘junk DNA.'” The Washington Post also reported that causes of Type II diabetes may be linked to malfunctions in non-coding “junk” DNA. How much earlier might these non-coding “junk” DNA causes of disease have been recognized had scientists operated under an intelligent design paradigm rather than a Neo-Darwinian one?
Causes of diabetes may be linked to malfunctions in non-coding DNA – what a revolutionary idea! That must be why they were looking at the insulin promoter as early as 1988. That’s a whole 6 years before Forrest Mims wrote an unpublished letter to Science which apparently took the entire scientific world by storm and led us to study non-coding DNA in the past!
And how about studying non-coding DNA to help understand cancer? Now this is the biggest joke of all. For decades we knew that non-coding DNA can be critical to the formation of neoplasms. Just consider the chromosomal rearrangements that happen in cancer. It’s been known for decades that a chromosomal rearrangement that places a proto-oncogene in an activating locus can cause tumors to form, or inactivation of a tumor supressor – either through deletion of the gene or its control region. Take for example this paper on Burkitt’s Lymphoma from 1983. I think the abstract says it all.
The human c-myc oncogene: structural consequences of translocation into the IgH locus in Burkitt lymphoma. J Battey , C Moulding , R Taub , W Murphy , T Stewart , H Potter , G Lenoir , P Leder
We have determined the sequence of the normal human c-myc gene and compared it to portions of a c-myc gene that has been translocated into the immunoglobulin heavy chain locus in a Burkitt lymphoma cell. The normal c-myc gene is encoded in three discrete exons divided by two large intervening sequences. Its mRNA is transcribed from two active promoters located about 150 nucleotides from one another. Each promoter initiates transcription of a long (approximately 550 bp) untranslatable leader sequence encoding the entire first exon. This exon and additional 5′ flanking sequences are tightly conserved between mouse and man. In the Burkitt cell BL22, the rearranged c-myc gene retains both promoters and is unchanged in its amino acid coding domains. Translocation of this gene joins it to the immunoglobulin heavy chain switch region at a point approximately 1000 bp 5′ to the dual c-myc promoters. These genes are joined in opposite transcriptional orientation. The structure of the translocated gene and the nature of its linkage to the immunoglobulin locus and the presence of two c-myc promoters and consequently two long leader sequences raise novel possibilities for the activation of an oncogene.
Wow, a whole 11 years before Forrest Mims didn’t get his letter published, scientists were studying the cytogenetics of cancer with a focus on non-coding DNA and their control of oncogenes.
Another aspect of Luskin’s continual blathering about Junk DNA is that many of the discoveries that we’re enjoying in the last 5 years or so are only possible because of the success of the Human Genome Project. It simply wasn’t possible to do this kind of analysis of genomic DNA 25 years ago. But that doesn’t mean we didn’t think non-coding DNA could be important. After all, the Human Genome Project was started in 1990 and it’s goal was to sequence every single base pair of the genome – not just the coding regions which would have made the job a lot easier. Luskin continually asserts that we were somehow mislead on non-coding DNA and only now we’re seeing the light. This is frankly absurd. We’ve been studying non-coding DNA for decades, before and after the junk DNA idea was even formulated in 1972. The discoveries that are so fantastic today are a benefit of the Human Genome Project – which sought to identify every base of DNA, coding or non-coding, and not some recent revelation that junk DNA is important. Real scientists figured that out long before the Discovery Institute did.