TY - JOUR
T1 - Early steps of double-strand break repair in Bacillus subtilis
AU - Alonso, Juan C.
AU - Cardenas, Paula P.
AU - Sanchez, Humberto
AU - Hejna, James
AU - Suzuki, Yuki
AU - Takeyasu, Kunio
N1 - Funding Information:
This work was supported by grants BFU2009-07167 and BFU2012-39879-C02-01 from Ministerio de Economia y Competividad-Dirección General de Investigación to JCA; from the Japanese Ministry of Education, Culture, Sports, Science and Technology (Grant-in-Aid for Scientific Research on Priority Areas to KT) and from Japan Society for the Promotion of Science (JSPS) (Grant-in-Aid for Basic Research (A) to KT, Japan-Spain Bilateral Joint Project Award JSPC-CSIC to KT and JCA. YS is a research fellow of the JSPS. HS is a recipient of a Marie Curie Reintegration Grant from the European Commission . We thank Ryosuke L. Ohniwa at Tsukuba University for providing us with the AFM images of B. subtilis nucleoids. We wish to offer our apologies to all researchers whose important work is not cited owing to space limitations.
PY - 2013/3/1
Y1 - 2013/3/1
N2 - All organisms rely on integrated networks to repair DNA double-strand breaks (DSBs) in order to preserve the integrity of the genetic information, to re-establish replication, and to ensure proper chromosomal segregation. Genetic, cytological, biochemical and structural approaches have been used to analyze how Bacillus subtilis senses DNA damage and responds to DSBs. RecN, which is among the first responders to DNA DSBs, promotes the ordered recruitment of repair proteins to the site of a lesion. Cells have evolved different mechanisms for efficient end processing to create a 3'-tailed duplex DNA, the substrate for RecA binding, in the repair of one- and two-ended DSBs. Strand continuity is re-established via homologous recombination (HR), utilizing an intact homologous DNA molecule as a template. In the absence of transient diploidy or of HR, however, two-ended DSBs can be directly re-ligated via error-prone non-homologous end-joining. Here we review recent findings that shed light on the early stages of DSB repair in Firmicutes.
AB - All organisms rely on integrated networks to repair DNA double-strand breaks (DSBs) in order to preserve the integrity of the genetic information, to re-establish replication, and to ensure proper chromosomal segregation. Genetic, cytological, biochemical and structural approaches have been used to analyze how Bacillus subtilis senses DNA damage and responds to DSBs. RecN, which is among the first responders to DNA DSBs, promotes the ordered recruitment of repair proteins to the site of a lesion. Cells have evolved different mechanisms for efficient end processing to create a 3'-tailed duplex DNA, the substrate for RecA binding, in the repair of one- and two-ended DSBs. Strand continuity is re-established via homologous recombination (HR), utilizing an intact homologous DNA molecule as a template. In the absence of transient diploidy or of HR, however, two-ended DSBs can be directly re-ligated via error-prone non-homologous end-joining. Here we review recent findings that shed light on the early stages of DSB repair in Firmicutes.
KW - DNA damage-induced foci
KW - Double-strand break repair
KW - End-resection
KW - Non-homologous end joining
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U2 - 10.1016/j.dnarep.2012.12.005
DO - 10.1016/j.dnarep.2012.12.005
M3 - Review article
C2 - 23380520
AN - SCOPUS:84875364461
SN - 1568-7864
VL - 12
SP - 162
EP - 176
JO - DNA Repair
JF - DNA Repair
IS - 3
ER -