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Sister chromatid exchanges occur in G2-irradiated cells.

Conrad, Sandro ; Künzel, Julia ; Löbrich, Markus (2011)
Sister chromatid exchanges occur in G2-irradiated cells.
In: Cell cycle (Georgetown, Tex.), 10 (2)
Artikel, Bibliographie

Kurzbeschreibung (Abstract)

DNA double-strand breaks (DSBs) are arguably the most important lesions induced by ionizing radiation (IR) since unrepaired or mis-repaired DSBs can lead to chromosomal aberrations and cell death. The two major pathways to repair IR-induced DSBs are non-homologous end-joining (NHEJ) and homologous recombination (HR). Perhaps surprisingly, NHEJ represents the predominant pathway in the G1 and G2 phases of the cell cycle, but HR also contributes and repairs a subset of IR-induced DSBs in G2. Following S-phase-dependent genotoxins, HR events give rise to sister chromatid exchanges (SCEs), which can be detected cytogenetically in mitosis. Here, we describe that HR occurring in G2-irradiated cells also generates SCEs in ~50% of HR events. Since HR of IR-induced DSBs in G2 is a slow process, SCE formation in G2-irradiated cells requires several hours. During this time, irradiated S-phase cells can also reach mitosis, which has contributed to the widely held belief that SCEs form only during S phase. We describe procedures to measure SCEs exclusively in G2-irradiated cells and provide evidence that following IR cells do not need to progress through S phase in order to form SCEs.

Typ des Eintrags: Artikel
Erschienen: 2011
Autor(en): Conrad, Sandro ; Künzel, Julia ; Löbrich, Markus
Art des Eintrags: Bibliographie
Titel: Sister chromatid exchanges occur in G2-irradiated cells.
Sprache: Englisch
Publikationsjahr: 2011
Titel der Zeitschrift, Zeitung oder Schriftenreihe: Cell cycle (Georgetown, Tex.)
Jahrgang/Volume einer Zeitschrift: 10
(Heft-)Nummer: 2
Kurzbeschreibung (Abstract):

DNA double-strand breaks (DSBs) are arguably the most important lesions induced by ionizing radiation (IR) since unrepaired or mis-repaired DSBs can lead to chromosomal aberrations and cell death. The two major pathways to repair IR-induced DSBs are non-homologous end-joining (NHEJ) and homologous recombination (HR). Perhaps surprisingly, NHEJ represents the predominant pathway in the G1 and G2 phases of the cell cycle, but HR also contributes and repairs a subset of IR-induced DSBs in G2. Following S-phase-dependent genotoxins, HR events give rise to sister chromatid exchanges (SCEs), which can be detected cytogenetically in mitosis. Here, we describe that HR occurring in G2-irradiated cells also generates SCEs in ~50% of HR events. Since HR of IR-induced DSBs in G2 is a slow process, SCE formation in G2-irradiated cells requires several hours. During this time, irradiated S-phase cells can also reach mitosis, which has contributed to the widely held belief that SCEs form only during S phase. We describe procedures to measure SCEs exclusively in G2-irradiated cells and provide evidence that following IR cells do not need to progress through S phase in order to form SCEs.

Fachbereich(e)/-gebiet(e): 10 Fachbereich Biologie > Radiation Biology and DNA Repair
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10 Fachbereich Biologie
Hinterlegungsdatum: 14 Mär 2011 15:19
Letzte Änderung: 05 Mär 2013 09:46
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