Telomeres and DNA damage checkpoints.
In all eukaryotic organisms, interruptions in duplex DNA molecules elicit a DNA damage response, which includes activation of DNA repair machineries and surveillance mechanisms, known as DNA damage checkpoints. Telomeres and double-strand breaks (DSBs) share the common feature of being physical ends of chromosomes. However, unlike DSBs, telomeres do not activate the DNA damage checkpoints and are usually protected from end-to-end fusions and other processing events that normally promote repair of DNA breaks. This indicates that they are shielded from being recognized and processed as DSBs. On the other hand, chromosome ends resemble damaged DNA, as several factors required for DNA repair and checkpoint networks play important roles in telomere length maintenance. Due to the critical role of both DNA damage checkpoints and telomere homeostasis in maintaining genetic stability and in counteracting cancer development, the knowledge of their interconnections is essential for our understanding of these key cellular controls.
Dipartimento di Biotecnologie e Bioscienze, Università di Milano-Bicocca, Piazza della Scienza 2, 20126 Milan, Italy.
Valeria
V
Viscardi
Michela
M
Clerici
Hugo
H
Cartagena-Lirola
Maria Pia
MP
Longhese
D004249:DNA Damage; D004260:DNA Repair; D004261:DNA Replication; D042822:Genomic Instability; D006801:Humans; D019098:Telomerase / Q000378:metabolism*; D016615:Telomere / Q000737:chemistry* / Q000378:metabolism
D019098:Telomerase