Skip to comments.Junk DNA may not be so junky after all
Posted on 03/29/2006 5:46:20 PM PST by DaveLoneRanger
Researchers develop new tool to find gene control regions
Researchers at the McKusick-Nathans Institute of Genetic Medicine at Johns Hopkins have invented a cost-effective and highly efficient way of analyzing what many have termed "junk" DNA and identified regions critical for controlling gene function. And they have found that these control regions from different species don't have to look alike to work alike.
The study will be published online at Science Express March 23.
The researchers developed a new system that uses zebrafish to test mammalian DNA and identify DNA sequences, known as enhancers, involved in turning on a gene. In studying RET, the major gene implicated in Hirschsprung disease and multiple endocrine neoplasia (MEN2), the team identified DNA sequences that can control RET but had not been identified using standard methods. Hirschsprung disease, also known as congenital megacolon, is a relatively common birth defect marked by bowel obstruction. MEN2 is an inherited predisposition to neuroendocrine cancers.
The notion that mutations in enhancers play a role in human disease progression has been difficult to confirm because usually enhancers are located in the 98 percent of the human genome that does not code for protein, termed non-coding DNA. Unlike DNA sequences that code for protein, non-coding DNA, sometimes referred to as "junk" DNA, follows few rules for organization and sequence patterns and therefore is more difficult to study.
"The difficulty with human genetic approaches to common disease is that we lack the power to precisely localize DNA sequences that are associated with disease, often leaving us immense stretches of DNA to look at," says one of the study's corresponding authors, Andy McCallion, Ph.D., an assistant professor in the McKusick-Nathans Institute. Most often one is limited to looking in the most obvious places, which may not yield the best results. "Until now," he says, "we've only been able to look under the lamplights for the car keys."
Traditionally, DNA sequences are thought to have to look similar to function similarly; this is how scientists identify genes in other species, a strategy best used for studying similar species. From an evolutionary standpoint, the last common ancestor of human and zebrafish lived more than 300 million years ago. Because DNA sequences in each species have changed over time, traditional methods of comparing DNA sequences between humans and zebrafish have failed to identify any potential enhancers around the RET gene because the DNA sequences differ too much.
That drove the Hopkins researchers to seek and develop this new system, by which virtually any DNA sequence can be tested for its ability to turn on a marker gene in zebrafish embryos. The system is a significant advance over current methods in this model species, allowing researchers to study more sequences in a shorter period of time. Using this, they identified several human enhancers able to control expression consistent with the zebrafish ret gene.
Zebrafish have become the ideal system for doing these types of large scale studies. They are small - only about a half inch in length - they grow quickly, and are relatively inexpensive to maintain compared to mice or rats. "Zebrafish are the only vertebrate embryo you can even think about doing this type of work in," says Shannon Fisher, M.D., Ph.D., the study's first author and an assistant professor in cell biology in Johns Hopkins' Institute for Basic Biomedical Sciences.
The researchers' next steps are further study of the RET enhancers they found to identify other mutations that might contribute to Hirschsprung disease and MEN2, and to entice other investigators to collectively build a database of human enhancers. "If there's one thing we've learned here, it's that we are not very good at recognizing enhancers. We just don't know what they look like," says Fisher. "We are anxious for others to use this technology on their favorite genes."
Wikipedia claims junk DNA "is probably an evolutionary artifact that serves no present-day purpose."
Of course, "junk DNA" and "no present-day purpose" really mean "we don't know what function some DNA serves, so we'll call it junk DNA for now."
As science progresses, new functions are being discovered for this "junk" DNA, and evolutionists are having to eat crow.
(( ping ))
Who ever said that tonsils are useless or vestigal? I've never heard that.
"Such large returns of conjecture from such small investment of fact"
If we ever get to the point of being able to accurately manipulate genes, would it be then possible to slip someone like Alec Baldwin a "gene pill" so he grows a penis on his head?
You mean another one?
Alot of doctors used to believe that, its why removing tonsils was so popular for so many years.
I lucked out, my doctor (while being arrogant) was right in his point that if it was useless, then it wouldn't be there, and told my mother the other doctors were just idiots for always removing them.
In studying RET, the major gene implicated in Hirschsprung disease and multiple endocrine neoplasia (MEN2), the team identified DNA sequences that can control RET but had not been identified using standard methods. Hirschsprung disease, also known as congenital megacolon, is a relatively common birth defect marked by bowel obstruction.
Will they claim this is the gay gene now???
Really... I saw someone the other day here on FR (one of the usual suspects) allude to junk DNA as having something to do with homosexual perversions.
Bill Clinton was trying to win the Stanley Cup in tonsil hockey!
The paper was written by members of the scientific community.
If they don't know what they're talking about, then nothing was shown.
Elementary logic is your friend.
Some non-coding DNA clearly does have a purpose. Some equally clearly does not. Finding a purpose for 0.001% of it doesn't really do much to change the picture.
Whether there's a lot or a little noncoding DNA has little effect on whether evolution is true or not. DNA sequences have their utility (coding sequences a GREAT utility, most noncoding sequences not so much), but DNA also exerts a cost. Just what those costs & benefits are will depend on the species, and could fall anywhere along the spectrum from strongly favoring no noncoding DNA to allowing vast amounts of the stuff.
Nature. 2004 Oct 21;431(7011):988-93. Related Articles, Links
Nobrega MA, Zhu Y, Plajzer-Frick I, Afzal V, Rubin EM.
DOE Joint Genome Institute Walnut Creek, California 94598, USA.
The functional importance of the roughly 98% of mammalian genomes not corresponding to protein coding sequences remains largely undetermined. Here we show that some large-scale deletions of the non-coding DNA referred to as gene deserts can be well tolerated by an organism. We deleted two large non-coding intervals, 1,511 kilobases and 845 kilobases in length, from the mouse genome. Viable mice homozygous for the deletions were generated and were indistinguishable from wild-type littermates with regard to morphology, reproductive fitness, growth, longevity and a variety of parameters assaying general homeostasis. Further detailed analysis of the expression of multiple genes bracketing the deletions revealed only minor expression differences in homozygous deletion and wild-type mice. Together, the two deleted segments harbour 1,243 non-coding sequences conserved between humans and rodents (more than 100 base pairs, 70% identity). Some of the deleted sequences might encode for functions unidentified in our screen; nonetheless, these studies further support the existence of potentially 'disposable DNA' in the genomes of mammals.
That's interesting. They removed 2.3 megabases, which sounds impressive, but it's only one tenth of one percent of the mouse genome.
However, on the ID hypothesis, *I'd* think there would be *no* unused DNA.
But until we can get a better description of the hypothetical designer's abilities and aims and so forth, no-one knows what to expect from the ID hypothesis.
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