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Telomeres are the ends of linear chromosomes. Telomeric DNA is bound by specialized proteins that prevent it from being targeted by DNA damage repair pathways, and is maintained by the enzyme telomerase.
Aberrations in telomere biology occur in prostate cancer tumorigenesis and progression. Graham and Meeker review the role of shortened telomeres in prostate tumour pathogenesis, including genomic instability and mutations. They describe the clinical utility of assessment of telomere dysfunction and the therapeutic potential of treatments targeting telomerase and telomeres.
Structure determination and functional analyses of budding yeast Rif1 reveal a novel, hooked N-terminal DNA-binding domain required for telomere maintenance and checkpoint control and show that Rif1's role in DNA-repair pathway choice is conserved in yeast and mammalian cells.
Although oxidative stress has long been considered to be a major factor contributing to telomere shortening, recent work has established that oxidative stress and DNA damage are linked to telomere lengthening. Now, Opresko and colleagues resolve this apparent discrepancy by showing that differential modulation of telomerase activity depends on the origin of a common oxidative guanine lesion.
Telomerase is a unique reverse transcriptase in that it repetitively uses a short piece of its RNA component as template to synthesize DNA. A new crystal structure of a part of the Tetrahymena telomerase ribonucleoprotein reveals how reverse transcription is limited to this specific template region.