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Adv Protein Chem Struct Biol. 2019;115:95-134. doi: 10.1016/bs.apcsb.2018.10.004. Epub 2018 Dec 5.

Controlling the balance between chromosome break repair pathways.

Author information

1
Departamento de Genética, Universidad de Sevilla, Sevilla, Spain; Centro Andaluz de Biología Molecular y Medicina Regenerativa-CABIMER, Universidad de Sevilla-CSIC-Universidad Pablo de Olavide, Sevilla, Spain.
2
Departamento de Genética, Universidad de Sevilla, Sevilla, Spain; Centro Andaluz de Biología Molecular y Medicina Regenerativa-CABIMER, Universidad de Sevilla-CSIC-Universidad Pablo de Olavide, Sevilla, Spain. Electronic address: pablo.huertas@cabimer.es.

Abstract

Broken chromosomes are among the most complex and more difficult to repair DNA lesions. The loss of the continuity of the DNA molecule presents a challenge to the cells, thus the repair of DNA double strand breaks might lead to genomic alterations. Indeed, to minimize this threat to genomic integrity, different DNA repair pathways can act on a broken chromosome. The balance between them is tightly controlled, and it heavily depends on global and local cellular cues. In this chapter, we review our current understanding on the repair of DNA double strand breaks and focus in the regulation of the balance between alternative pathways. Most of this modulation takes place at the level of DNA end resection. Here, we focus mostly on the local signals that control the repair pathway choice, as the global cues have been extensively reviewed recently. We described epigenetic marks that either facilitate or inhibit DNA resection and homologous recombination, from histone marks and chromatin remodelers to non-coding RNA and RNA-related factors.

KEYWORDS:

Chromatin: ncRNA; DNA end resection; DSB repair; Epigenetics; Homologous recombination; NHEJ

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