Of Centromeres and Telomeres 10/05/2001
Two cell biology reports are revealing that “mere” parts of DNA are vital. A news release in Nature announced that a university team in Cleveland, Ohio has sequenced the centromere of the human genome. These are the junction points that join the two strands of chromosomes. They consist of long repetitive sequences of genetic letters. Though no one understands how they work at this point, they parcel out equal shares of chromosomes during cell division. Flaws in the centromeres are implicated in many cancers.
In a second news item, a paper in the journal Cell discusses the role of telomeres in cell death and cancer. Telomeres are the “end caps” on DNA strands that prevent them from unraveling; at each cell division, the length of the telomere is reduced by one unit. Researchers found that the shortest telomere determines when the cell signals itself to die, not the average telomere length. Scientific American comments that cells with short telomeres act as if the DNA strand has broken, and receive a signal to “arrest or die as a protection against chromosome rearrangement and cancer.” When the telomere-repair tool, telomerase, is present, it lengthens the telomere just enough to function. Runaway telomere lengthening appears to be a characteristic of some cancers. A related paper published online in the Proceedings of the National Academy of Sciences demonstrates that “telomere dysfunction triggers extensive DNA fragmentation and evolution of complex chromosome abnormalities in human malignant tumors.”
The human genome is so complex, its wonders continue to baffle scientists. It is also apparent that failures in its complex operations lead to cancer and death. When God told man that he would surely die, and cursed the world because of sin, it subjected the original perfect designs to malfunction and entropy. We see the grand design that points to a Designer, but we feel the malfunctions that take us eventually back to the dust from whence we came. Is it possible that early in the history of mankind, better centromere and telomere operation (with fewer accumulated mutations) could have allowed men to live for centuries, like Methuselah?
Evolutionists, however, continue to attribute these complex systems to chance, and look for ape in our ancestry at every turn. Consider this statement from the centromere story:
The group also compared sequences that bookend the alpha repeats with equivalent sections in primates. One part of an ancestral primate centromere is amplified in humans, they found. The work “gives a clear picture of how [the centromere] might have evolved”, says chromosome researcher William Brown of the University of Nottingham, UK. “It grew relatively recently in human evolution.” Even with the sequence in hand, no one knows how centromeres work . . . .
So nobody knows how they work, but it doesn’t stop this scientist from confidently stating with an air of authority how and when they evolved. In the presence of design perfection, a bit of humility is in order.
Two cell biology reports are revealing that “mere” parts of DNA are vital. A news release in Nature announced that a university team in Cleveland, Ohio has sequenced the centromere of the human genome. These are the junction points that join the two strands of chromosomes. They consist of long repetitive sequences of genetic letters. Though no one understands how they work at this point, they parcel out equal shares of chromosomes during cell division. Flaws in the centromeres are implicated in many cancers.
In a second news item, a paper in the journal Cell discusses the role of telomeres in cell death and cancer. Telomeres are the “end caps” on DNA strands that prevent them from unraveling; at each cell division, the length of the telomere is reduced by one unit. Researchers found that the shortest telomere determines when the cell signals itself to die, not the average telomere length. Scientific American comments that cells with short telomeres act as if the DNA strand has broken, and receive a signal to “arrest or die as a protection against chromosome rearrangement and cancer.” When the telomere-repair tool, telomerase, is present, it lengthens the telomere just enough to function. Runaway telomere lengthening appears to be a characteristic of some cancers. A related paper published online in the Proceedings of the National Academy of Sciences demonstrates that “telomere dysfunction triggers extensive DNA fragmentation and evolution of complex chromosome abnormalities in human malignant tumors.”
The human genome is so complex, its wonders continue to baffle scientists. It is also apparent that failures in its complex operations lead to cancer and death. When God told man that he would surely die, and cursed the world because of sin, it subjected the original perfect designs to malfunction and entropy. We see the grand design that points to a Designer, but we feel the malfunctions that take us eventually back to the dust from whence we came. Is it possible that early in the history of mankind, better centromere and telomere operation (with fewer accumulated mutations) could have allowed men to live for centuries, like Methuselah?
Evolutionists, however, continue to attribute these complex systems to chance, and look for ape in our ancestry at every turn. Consider this statement from the centromere story:
The group also compared sequences that bookend the alpha repeats with equivalent sections in primates. One part of an ancestral primate centromere is amplified in humans, they found. The work “gives a clear picture of how [the centromere] might have evolved”, says chromosome researcher William Brown of the University of Nottingham, UK. “It grew relatively recently in human evolution.” Even with the sequence in hand, no one knows how centromeres work . . . .
So nobody knows how they work, but it doesn’t stop this scientist from confidently stating with an air of authority how and when they evolved. In the presence of design perfection, a bit of humility is in order.
