University of California-San Francisco's Liz Blackburn got her Nobel Prize for studies that identified the specialized bit of machinery, called telomerase, that maintains the ends of chromosomes, which would otherwise be expected to shrink every time the cell divides. That shrinkage is thought to set a limit on the number of cell divisions that can occur in normal cells, and the Prize recognized that its reactivation appears to be a necessary step in the transformation to cancerous growth. But Blackburn used her talk at the Lindau Nobel Laureates meeting to argue that all sorts of diseases were associated with changes in telomerase activity, and that the chromosome ends provide a readout of a person's life history. And she's got a robot that's busy generating data to back her up.
Bacteria and Archaea have circular chromosomes, which ensures that the DNA has no loose ends in these cells. The complex cells of eukaryotes have linear chromosomes in their nucleus. This creates two problems. The DNA repair abilities of the cells should view the ends, or telomeres, of the chromosomes as a site where a chromosome has broken, and attempt to repair it. In addition, the enzymes that copy DNA are unable to start copying at the end of a piece of DNA. Thus, whenever a cell has to copy the DNA, the copying process will necessarily ignore some of the ends of the chromosome.
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