Telomeres: not all breaks are equal.
ATM, Rad50 and Mre11 have been shown to prevent telomere fusion in Drosophila, thereby extending the protective role of DNA damage checkpoint proteins to non-canonical telomeres formed without telomerase. How do these proteins help chromosomal termini escape fusion through 'repair' while promoting repair of induced DNA breaks?
Molecular, Cellular and Developmental Biology, 347UCB, University of Colorado, Boulder, Colorado, USA. amanda.purdy@colorado.edu
Amanda
A
Purdy
Tin Tin
TT
Su
D017766:Acid Anhydride Hydrolases; D064007:Ataxia Telangiectasia Mutated Proteins; D018797:Cell Cycle Proteins / Q000378:metabolism; D043171:Chromosomal Instability; D004249:DNA Damage / Q000502:physiology; D004260:DNA Repair; D045643:DNA Repair Enzymes / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000378:metabolism; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism; D019098:Telomerase / Q000378:metabolism; D016615:Telomere / Q000378:metabolism*; D034501:Telomere-Binding Proteins / Q000378:metabolism*; D025521:Tumor Suppressor Proteins
D018797:Cell Cycle Proteins; D004268:DNA-Binding Proteins; D034501:Telomere-Binding Proteins; D025521:Tumor Suppressor Proteins; C576324:ATM protein, human; D064007:Ataxia Telangiectasia Mutated Proteins; D017346:Protein Serine-Threonine Kinases; D019098:Telomerase; D017766:Acid Anhydride Hydrolases; C112158:RAD50 protein, human; D045643:DNA Repair Enzymes