Premium
The cellular control of DNA double‐strand breaks
Author(s) -
Scott Shaun P.,
Pandita Tej K.
Publication year - 2006
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.21067
Subject(s) - biology , dna damage , microbiology and biotechnology , effector , dna repair , histone , dna , carcinogenesis , genome , dna replication , computational biology , genetics , gene
DNA double‐strand breaks (DSBs) are the most hazardous lesions arising in the genome of eukaryotic organisms, and yet occur normally during DNA replication, meiosis, and immune system development. The efficient repair of DSBs is crucial in maintaining genomic integrity, cellular viability, and the prevention of tumorigenesis. As a consequence, eukaryotic cells have evolved efficient mechanisms that sense and respond to DSBs and ultimately repair the break. The swiftness of the DNA DSB response has paved to the identification of sensors and transducers which allowed to generate a hierarchical signaling paradigm depicting the transduction of the damage signal to numerous downstream effectors (Fig. 1). The function of such effectors involve posttranslational modifications through phosphorylation, acetylation, and methylation of the substrates. This review will address the control of DSBs in damaged eukaryotic cells, the physiological processes that require the introduction of a DSB into the genome, and the maintenance of DSBs in non‐damaged cells. J. Cell. Biochem. 99: 1463–1475, 2006. © 2006 Wiley‐Liss, Inc.