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Chromosome ‘capping’: Study finds differences in human telomeres
  
By
Edward R. Winstead



By disrupting the normal replication of human chromosomes, researchers have found evidence that telomeres, the structures at either end of each chromosome, are different. When a protein involved in manufacturing telomeres was experimentally mutated, only half of the telomeres were affected. This suggests that human cells manufacture two types of telomeres differently at the stage following DNA replication.


Detail of partial metaphases with several telomeric chromatid concatenates (TCCs). View full

Telomeres are essential for the health of genomes. By 'capping' the ends of chromosomes, they prevent DNA from degrading and protect against the inappropriate end-to-end fusion of chromosomes. Fusions can result in severe abnormalities and cancers.

Researchers have long debated whether the two types of telomeres are different. Now, Edwin H. Goodwin, of Los Alamos National Laboratory in New Mexico, and colleagues report that mutations in the TRF2 protein caused inappropriate fusions exclusively in 'leading-strand' telomeres. The two types of telomeres are known by how they are created. One is produced by leading-strand DNA synthesis, the other by lagging-strand DNA synthesis.

Both leading-strand and lagging-strand telomeres replicate from a single parental telomere. "Telomeres face special challenges during replication," the researchers write in Science. "The protective terminal structure of the telomere must not only disassemble in order to replicate, it must also regenerate after replication."

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Bailey, S.M. et al. Strand-specific postreplicative processing of mammalian telomeres. Science 293, 2462-2465 (September 28, 2001).
 

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