title: Heterochromatinization associated with cell differentiation as a model to study DNA double strand break induction and repair in the context of higher-order chromatin structure.
abstract: Cell differentiation is associated with extensive gene silencing, heterochromatinization and potentially decreasing need for repairing DNA double-strand breaks (DSBs). Differentiation stages of blood cells thus represent an excellent model to study DSB induction, repair and misrepair in the context of changing higher-order chromatin structure. We show that immature granulocytes form γH2AX and 53BP1 foci, contrary to the mature cells; however, these foci colocalize only rarely and DSB repair is inefficient. Moreover, specific chromatin structure of granulocytes probably influences DSB induction.
authors: Institute of Biophysics Brno, Czech Academy of Sciences, Brno 61265, Czech Republic. Electronic address: mfalk@seznam.cz.
authors: Martin
authors: M
authors: Falk
authors: Emilie
authors: E
authors: Lukášová
authors: Lenka
authors: L
authors: Štefančíková
authors: Elena
authors: E
authors: Baranová
authors: Iva
authors: I
authors: Falková
authors: Lucie
authors: L
authors: Ježková
authors: Marie
authors: M
authors: Davídková
authors: Alena
authors: A
authors: Bačíková
authors: Jana
authors: J
authors: Vachelová
authors: Anna
authors: A
authors: Michaelidesová
authors: Stanislav
authors: S
authors: Kozubek
mesh_terms: D002454:Cell Differentiation; D002478:Cells, Cultured; D002843:Chromatin / Q000737:chemistry*; D004249:DNA Damage; D004260:DNA Repair; D006801:Humans; D017404:In Situ Hybridization, Fluorescence; D011487:Protein Conformation
chemical_list: D002843:Chromatin
keywords: Chromatin sensitivity to DSB induction; DNA double strand break (DSB) repair; Heterochromatin; Higher-order chromatin structure; Immature and terminally differentiated granulocytes; γH2AX/53BP1 repair foci