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Appl Radiat Isot. 2014 Jan;83 Pt B:177-85. doi: 10.1016/j.apradiso.2013.01.029. Epub 2013 Jan 29.

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.

Author information

1
Institute of Biophysics Brno, Czech Academy of Sciences, Brno 61265, Czech Republic. Electronic address: mfalk@seznam.cz.

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.

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

PMID:
23454236
DOI:
10.1016/j.apradiso.2013.01.029
[Indexed for MEDLINE]

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