title: Human Xp/Yp telomere analysis by Southern-STELA.
abstract: Telomeres are specialized structures designed to protect the ends of linear chromosomes. They are dynamic structures such that in normal somatic cells they constantly shorten as cell division progresses. There is compelling evidence that telomere shortening leads to cell senescence, a process perceived as the main cause of aging in higher mammals. Therefore, the features of telomere shortening are of great importance in understanding cell senescence and aging in general. By identifying unique subtelomeric regions, large enough to produce strong chemiluminescent signals, we have provided a new tool for Southern blot analysis of individual human Xp/Yp telomeres. We extend these results with quantitative fluorescence in situ hybridization using peptide nucleic acid probe (PNA Q-FISH) analysis of telomeres on the Y chromosome. Our results demonstrates unequal shortening dynamics between the p and q telomeres.
authors.affiliation: Laboratory for Molecular and Cell Biology, Department of Molecular Biology, Ruđer Bošković Institute, Zagreb, Croatia.
authors.forename: Milena
authors.initials: M
authors.lastname: Ivanković
authors.forename: Andrea
authors.initials: A
authors.lastname: Cukušić Kalajžić
authors.forename: Nikolina
authors.initials: N
authors.lastname: Skrobot Vidaček
authors.forename: Ivana
authors.initials: I
authors.lastname: Franić Šimić
authors.forename: Sanja
authors.initials: S
authors.lastname: Davidović Mrsić
authors.forename: Ivica
authors.initials: I
authors.lastname: Rubelj
mesh_terms: D015139:Blotting, Southern / Q000379:methods*; D002478:Cells, Cultured; D041321:Chromosomes, Human, X; D041322:Chromosomes, Human, Y; D005347:Fibroblasts / Q000378:metabolism; D006801:Humans; D017404:In Situ Hybridization, Fluorescence; D008677:Metaphase; D015341:Nucleic Acid Probes; D020135:Peptide Nucleic Acids; D016615:Telomere / Q000378:metabolism*; D059506:Telomere Shortening
chemical_list: D015341:Nucleic Acid Probes; D020135:Peptide Nucleic Acids