Today's Nobel Prize announcement has prompted the usual stupidity from the creationist crowd. They don't get things right very often but when they rush into print their track record is even worse. You'd think they would have learned by now.
Most, but not all, bacteria have circular chromosomes. This is undoubtedly the primitive condition of living cells—at least once life got underway.
The advantage of a circular chromosome is that it doesn't have any free ends. This is important for two reasons: (1) nucleases that chew up nucleic acids like to work on free ends so having a circular chromosome increases the stability of the chromosome, and (2) circular chromosomes avoid the problems with replicating the ends of DNA.
That last reason needs a little explanation. DNA replication is complicated because evolution has only produced one kind of polymerase enzyme—the kind that works exclusively in the 5′→3′ direction.
1 This creates a problem when replicating double-stranded DNA because the strands run in opposite directions.
The DNA replication complex (replisome) has evolved a solution to this problem as illustrated in the diagram. As replication proceeds from right to left, one of the strands is copied directly by a DNA polymerase molecule. This new strand is called the
leading strand. The other strand is copied by a separate DNA polymerase molecule but it has to run backwards. That strand, the
lagging strand, is made in short pieces that have to be stitched together. Every now and then a new lagging strand fragment (Okazaki fragment) is initiated using a special RNA primer.
This is not a very good design but it's the only thing that could evolve given that polymerases can only go in one direction. Most of us could have easily designed an better way of replicating DNA if we were in charge. While we were at it we could have designed nucleases that don't attack genes.
The DNA replication complex may be messy but it works. At least it works with circular DNA. When you have free ends there's a bit of a problem. Look at the diagram. You can see that when the replication fork reaches the end on the left, the leading strand will be complete. However, there will likely be a gap at the very end where the lagging strand didn't initiate a new Okazaki fragment. When the replisome dissociates this gap will persist.
As strands continue to be replicated over and over there will be a progressive shortening of the chromosome because of the inefficiency of the replication process.
There are several ways of handling this problem. Some bacteriophage with linear chromosomes form circles during replication in order to avoid shortening. In bacteria, there are two different mechanisms for dealing with the problem. Either the ends of the two strand are covalently joined, creating a hairpin, or a protein is covalently attached to the end of one strand [see
Bacterial Chromosomes]. Either way is effective in preventing chromosome shortening during replication.
Eukaryotes have evolved a third mechanism. The ends of eukaryotic chromosomes have extensive repeat segments called telomeres. This works because the repeats can be shortened for many generations before the "business part" of the chromosome is affected. The repeats can also be extended from time to time by telomerase. This restores the parts that are lost during replication. The copying is crude, but effective. It uses an RNA template that's part of the telomerase.
The net effect is that telomeres protect the ends of eukaryotic chromosomes. This protection is due to the fact that cells have nucleases that can chew up DNA and because the DNA replication machinery has a built-in flaw that doesn't allow it to copy the very ends of double-stranded DNA. All in all you'd have to say that if this was designed then it must have been Rube Goldberg who built it!
This year's Nobel Prize in Physiology & Medicine was awarded to
Elizabeth Blackburn, Carol Greider and Jack Szostak for their work on telomeres and telomerase.
Within hours, DLH posted an article n
Uncommon Descent [
DNA Preservation discovery wins Nobel prize].
Were one to design the encoded DNA “blueprint” of life, would not one incorporate ways to preserve that “blueprint”? The Nobel prize in medicine has just been awarded for discovery of features that look amazingly like design to preserve chromosomes ....
These telomeres can probably be shown to be essential to survival, and are likely to be irreducibly complex. If so, how can macro evolution explain the origin of this marvelous preservation feature that appears to be an Intelligent Design?
Chromosome ends need "protection" because the designer couldn't figure out how to have safe nucleases in a cell and couldn't figure out how to replicate the ends of double-stranded DNA molecules. Several different mechanisms have evolved for dealing with these problems. Telomeres are one solution.
The telomeric repeats evolved from internal repeat sequences. Telomerase is a reverse transcriptase and it likely evolved from a retrovirus-encoded reverse transcriptase. In Drosophila there are no telomers and there isn't a telomerase, Instead, the chromosome ends are protected by multiple copies of defective transposons.
The IDiots are going to have to look elsewhere for evidence of God.
1. There are good reasons for this. They have to do with the acccuracy of DNA replication and proofreading, but that's a story for another posting.
The molecule is 4-sulfonamide-2',4'-diaminobenzol or "Prontosil," a potent antibiotic. Gerhard Domagk received the Nobel Prize for developing Prontosil as a treatment against bacterial infections.
Name this molecule. The common name will do. Briefly describe what it does.
