ライフサイエンスコーパス: DNA break

1 gradation of the 5'-terminated strand of the DNA break.

2 mbination to repair the cleavage of a single DNA break.

3 ain rapidly unfolds when PARP-1 encounters a DNA break.

4 y inducing recombination via a site-specific DNA break.

5 er processing of the initial double-stranded DNA break.

6 signaling and accumulation of protein-linked DNA breaks.

7 ricentromere to suppress crossovers, but not DNA breaks.

8 tions downstream of RAD18 to recruit REV1 to DNA breaks.

9 lications, and generation of double-stranded DNA breaks.

10 le-stranded DNA lesions into double-stranded DNA breaks.

11 -out mice confirms an increase in unrepaired DNA breaks.

12 , is involved in the repair of double-strand DNA breaks.

13 factors organize to repair diverse types of DNA breaks.

14 in normal cells acts to repair double-strand DNA breaks.

15 51 homologous recombination repair factor at DNA breaks.

16 trand, leading to staggered instead of blunt DNA breaks.

17 guided nuclease that creates double-stranded DNA breaks.

18 topology by creating transient double-strand DNA breaks.

19 doses of agents that induce single-stranded DNA breaks.

20 (MRN) complex and other factors at sites of DNA breaks.

21 nce capture during repair of double-stranded DNA breaks.

22 d for the removal of DNA adducts at sites of DNA breaks.

23 e complexes (Top2cc), leading to Top2-linked DNA breaks.

24 nome maintenance by directing a remodeler to DNA breaks.

25 recombination and repair of double-stranded DNA breaks.

26 nucleoplasm and controls its accumulation at DNA breaks.

27 fect p53 function in response to physiologic DNA breaks.

28 A association at both telomeres and internal DNA breaks.

29 -joining (NHEJ) pathway of DNA repair to fix DNA breaks.

30 t functions during recombinational repair of DNA breaks.

31 foci, and can associate with double-stranded DNA breaks.

32 onse mediators, and defects in the repair of DNA breaks.

33 ying the signaling and repair of chromosomal DNA breaks.

34 iruses into nuclease-induced double-stranded DNA breaks.

35 osphorylation of AID at Ser38 was induced by DNA breaks.

36 and prolonged retention of ALC1 at sites of DNA breaks.

37 ith severe DNA lesions such as double strand DNA breaks.

38 recognition and response to double-stranded DNA breaks.

39 RN-generated single strands in the repair of DNA breaks.

40 for NHEJ repair of chromosomal double-strand DNA breaks.

41 function extends beyond timely resolution of DNA breaks.

42 ir abnormalities, accompanied by evidence of DNA breaks.

43 ed cellular network that detects and repairs DNA breaks.

44 meric loci, or non-telomeric double-stranded DNA breaks.

45 to coordinate the repair of double-stranded DNA breaks.

46 erine 569 is required for its recruitment to DNA breaks.

47 required to recruit DNA repair complexes to DNA breaks.

48 A repair factors including 53BP and BRCA1 to DNA breaks.

49 topoisomerases and inducing double-stranded DNA breaks.

50 herefore plays a vital role in processing of DNA breaks.

51 rimentally induced telomeric double-stranded DNA breaks.

52 ction together to recruit PARP-2 to sites of DNA breaks.

53 stress caused by MMS and not to more direct DNA breaks.

54 lymerase Pol IV, overwhelms cells with toxic DNA breaks.

55 or pathway for the repair of double-stranded DNA breaks.

56 as non-self and introduces a double-stranded DNA break [3].

57 enotoxic molecule(s) causing double-stranded DNA breaks(4) and enhanced colorectal cancer development

58 ajor pathway for the repair of double-strand DNA breaks, a highly deleterious form of DNA damage.

59 pendent recruitment of BRCA1 directly to the DNA break and is required for nonhomologous end-joining

60 tein A (RPA) to the RAD51 recombinase during DNA break and replication fork repair by homologous reco

61 events replication fork collapse, a cause of DNA breaks and apoptosis.

62 study, we investigated topoisomerase-induced DNA breaks and chromatin structural alterations in conju

63 the formation of replication stress-induced DNA breaks and chromosomal aberrations in BRCA1/2-defici

64 Quantification of DNA breaks and clonogenic survival assays confirm a role

65 Here we report a significant role for DNA breaks and DDR signalling in the mechanisms of trans

66 DBAN is not mutagenic but causes DNA breaks and elevates sister chromatid exchange in mam

67 e tumors were aneuploid with double-stranded DNA breaks and end-to-end telomere fusions and most were

68 rrow hotspots, observed both at the level of DNA breaks and final crossovers.

69 ncies in unfolding GQ are known to result in DNA breaks and genomic instability, which are prominent

70 participates in the repair of double-strand DNA breaks and in base excision repair of oxidized guani

71 t not normal transcription complexes, induce DNA breaks and orientation-specific DNA damage responses

72 errant proliferation that are independent of DNA breaks and predate evolution of the ARF/Mdm2 axis.

73 is involved in the repair of RAG1/2-mediated DNA breaks and prevents their propagation.

74 s, such as for the repair of double-stranded DNA breaks and protein quality control, are also critica

75 se is involved in repairing damage caused by DNA breaks and stalled replication forks via homologous

76 h acts in both the repair of double-stranded DNA breaks and the degradation of bacteriophage DNA.

77 ality observed between topoisomerase-induced DNA breaks and the RecBCD gene products, suggesting a ne

78 -binding interface to detect and stably bind DNA breaks and to accumulate at sites of chromosome dama

79 ) stage of T-cell development, RAG-dependent DNA breaks and V(D)J recombination occur at three T-cell

80 to replication fork collapse, double-strand DNA breaks, and cell death.

81 g (NHEJ), causes accumulation of spontaneous DNA breaks, and delays recovery from radiation-induced c

82 orks, insufficient repair of double-stranded DNA breaks, and improper segregation of sister chromosom

83 ous recombination, repair of double stranded DNA breaks, and integron recombination.

84 zolid caused S-phase arrest, double-stranded DNA breaks, and p53 stabilization, leading to apoptosis.

85 hways, resulting in mutations, single-strand DNA breaks, and the double-strand breaks required for CS

86 tion of Sp1 inhibits repair of site-specific DNA breaks, and the N-terminal 182-amino-acid peptide, w

87 ase damage and topoisomerase I (Top1)-linked DNA breaks are abundant forms of endogenous DNA breakage

88 study lends further support to a model where DNA breaks are generated by multiple random nicks due to

89 Double-strand DNA breaks are the most cytotoxic form of DNA damage and

90 These DNA breaks are ultimately resolved through the nonhomolo

91 In yeast, DNA breaks are usually repaired by homologous recombinat

92 of rucaparib was associated with persistent DNA breaks, as determined by chi-H2AX, p53BP1, and Rad51

93 NN, like NRG, attenuated the double-stranded DNA breaks associated with DOXO exposure in neonatal rat

94 and provides an environment tolerant of the DNA breaks associated with immunoglobulin gene remodelin

95 The creation of a DNA break at a specific locus by a designer endonuclease

96 ) is more active in creating double-stranded DNA breaks at 37 degrees C than at 22 degrees C, thus in

97 technologies introduce double-stranded (ds) DNA breaks at a target locus as the first step to gene c

98 te nuclease that generates two noncompatible DNA breaks at a target site, effectively deleting the ma

99 ive lymphomagenesis by generating off-target DNA breaks at loci that harbor highly active enhancers a

100 loping lymphocytes by generating "on-target" DNA breaks at matched pairs of bona fide recombination s

101 itive feedback loop for the amplification of DNA breaks at S regions through the phosphorylation- and

102 ily reprogrammed to induce sequence-specific DNA breaks at target loci, resulting in fixed mutations

103 (RAG) 1 and RAG2 protein complex introduces DNA breaks at Tcr and Ig gene segments that are required

104 rangement primarily through stabilization of DNA breaks at TCR loci.

105 in the frequencies of meiotic double-strand DNA breaks at the hotspot near the His4 locus, is found

106 DNA breaks at the Igh switch regions induced by AID lack

107 Upon induction of DNA breaks, ATM activation leads to a cascade of local c

108 s were initially characterized as sensors of DNA breaks but are now known to play key roles not only

109 ding cells accumulate replication-associated DNA breaks but otherwise survive Rev3L deletion, but fun

110 ion and reagents that induce double-stranded DNA breaks, but exhibit normal responses to chemicals th

111 guide RNA (sgRNA) to generate site-specific DNA breaks, but there are few known rules governing on-t

112 ersists until sufficient modification of the DNA break by alternative NHEJ prevents further Cas9 cutt

113 role of BRCA1 in the repair of double-strand DNA breaks by homologous recombination (HR) is its best

114 The repair of DNA breaks by homologous recombination is a high-fidelit

115 inase is recruited to sites of double-strand DNA breaks by the Mre11/Rad50/Nbs1 (MRN) complex, which

116 not required for the repair of double-strand DNA-breaks by homologous recombination.

117 DNA breaks can be repaired with high fidelity by homolog

118 at the expense of genome protection because DNA breaks cannot be repaired in dense heterochromatin.

119 ne marrow cells in response to double-strand DNA breaks caused by ionizing radiation and chemotherape

120 broken DNA strands results in protein-linked DNA breaks, causing neurodegeneration in humans.

121 g RAG DSBs from G1 into S phase, where these DNA breaks could be aberrantly repaired.

122 olism; these lesions include double-stranded DNA breaks, daughter-strand gaps, and DNA cross-links.

123 and ATM-dependent responses to double-strand DNA breaks, demonstrate functional plasticity of introni

124 displayed significantly higher double-strand DNA break (DSB) accumulation and p53 activation than the

125 cell differentiation through double-stranded DNA break (DSB) and ASC-mediated inflammasome assembly i

126 int signalling at a persistent double-strand DNA break (DSB) and at uncapped telomeres.

127 transcriptional regulation and double strand DNA break (DSB) induction.

128 Impairment of double-stranded DNA break (DSB) repair is essential to many cancers.

129 ing infection, but the role of double-strand DNA break (DSB) repair systems is unclear.

130 We focus on regulation of double-strand DNA break (DSB) repair via the non-homologous end joinin

131 h the role of DBHS proteins in double-strand DNA break (DSB) repair, elevated DSBs were observed in c

132 HR) is a crucial pathway for double-stranded DNA break (DSB) repair.

133 anization before and after a double-stranded DNA break (DSB), to estimate the level of chromatin deco

134 lfish elements that catalyze double-stranded DNA breaks (DSB) in a highly specific manner.

135 Recognition and repair of double-stranded DNA breaks (DSB) involves the targeted recruitment of BR

136 ith single-strand DNA (ssDNA), double-strand DNA breaks (DSB), and genomic rearrangements.

137 ctivator of ATM in response to double-strand DNA breaks (DSBs) and as a downstream effector of ATM ac

138 es, which respond primarily to double-strand DNA breaks (DSBs) and replication stress, respectively.

139 nd can induce the formation of double-strand DNA breaks (DSBs) at a site complementary to the guide R

140 ology-directed repair (HDR) of double-strand DNA breaks (DSBs) by initiating DNA resection, a process

141 Repair of double-strand DNA breaks (DSBs) by the homologous recombination (HR) p

142 Double-strand DNA breaks (DSBs) continuously arise and cause mutations

143 inal centers (GCs) and IgH switch (S) region DNA breaks (DSBs) for class-switch recombination (CSR).

144 important process that repairs double strand DNA breaks (DSBs) in eukaryotic cells.

145 w it is enriched at sites of double-stranded DNA breaks (DSBs) in mammalian cells.

146 centric chromosome undergoes double-stranded DNA breaks (DSBs) that can be repaired by mitotic recomb

147 s shown to reduce formation of double-strand DNA breaks (DSBs), as indicated by phosphorylated histon

148 by the programmed induction of double-strand DNA breaks (DSBs), lesions that pose a potential threat

149 pair (BER) enzymes can produce double-strand DNA breaks (DSBs).

150 re BRCA1 facilitates repair of double-strand DNA breaks (DSBs).

151 the subsequent generation of double-stranded DNA breaks (DSBs).

152 for the HMT MMSET in promoting AID-mediated DNA breaks during CSR.

153 xpression in developing lymphocytes prevents DNA breaks during periods of proliferation that could th

154 on compete for the repair of double-stranded DNA breaks during the cell cycle.

155 ion and avoids the creation of double-strand DNA breaks, enabling precise chromosome modifications at

156 zed role of the Dna2 translocase activity in DNA break end resection and in the imposition of the 5'

157 ced DNA damage signaling and accumulation of DNA breaks ex vivo and in vivo.

158 (ADP-ribose) polymerase (PARP) near sites of DNA breaks facilitates recruitment of DNA repair protein

159 cate both proteins as critical for repair of DNA breaks following transposase cleavage in vivo.

160 n both DNA strands to generate double-strand DNA breaks for efficient class switch recombination.

161 cterial cells, processing of double-stranded DNA breaks for repair by homologous recombination is cat

162 cterial cells, processing of double-stranded DNA breaks for repair by homologous recombination is dep

163 fork restart, prevention of double-stranded DNA break formation, and avoidance of replication catast

164 d DNA damage are proportional to the rate of DNA break formation, as measured by replication protein

165 The Ctf19 complex prevents meiotic DNA break formation, the initiating event of recombinati

166 TMPRSS2 gene rearrangements occur at DNA breaks formed during androgen receptor-mediated tran

167 events that are initiated by double-stranded DNA breaks formed prior to replication.

168 cal transformations by providing a transient DNA break, formed by a covalent adduct with the enzyme,

169 end-joining (NHEJ) repair of double-stranded DNA breaks generated by Cas9 are much less amenable to s

170 de that the pattern of mutation hotspots and DNA break generation is influenced by sequence-intrinsic

171 rovement in tumor cell damage (double strand DNA breaks), growth suppression, and overall survival un

172 2 and PARP-3 are preferentially activated by DNA breaks harboring a 5' phosphate (5'P), suggesting se

173 Also, single strand DNA breaking has been observed through comet assay techn

174 cleaved complexes because of the presence of DNA breaks, have been crystallized and found to have the

175 donuclease-1), and repair of double-stranded DNA breaks (homologs of BRCA2, XRCC3, KU80 and WRNexo).

176 In both conditions, Holliday junctions at DNA break hotspots form more frequently between sister c

177 a DNA duplex and pass it through a transient DNA break in a second DNA segment via the sequential ope

178 ng complex/cyclosome (APC/C), accumulates on DNA breaks in a BubR1 KEN box-dependent manner.

179 m and progenitor cells undergo very frequent DNA breaks in a very restricted set of genes involved in

180 DNA breaks in Brca1-deficent cells are aberrantly joined

181 urrence of RAG1/2-dependent and -independent DNA breaks in developing lymphocytes exposed to genotoxi

182 Repair of double-stranded DNA breaks in Escherichia coli is initiated by the RecBC

183 s in B cells and that, when reduced, induces DNA breaks in lymphoma B cell lines in an activation-ind

184 a high efficiency in inducing locus-specific DNA breaks in somatic and germline tissues.

185 stent phosphorylation of H2AX-Y142 along the DNA breaks in stem cells, which promotes apoptosis while

186 can be reprogrammed to create double-strand DNA breaks in the genomes of a variety of organisms, fro

187 rogrammed to create specific double-stranded DNA breaks in the genomes of a variety of organisms, ran

188 loss results in progressive accumulation of DNA breaks in the nervous system, triggering hallmarks o

189 ad50 complex for the repair of double-strand DNA breaks in thermophilic archaea.

190 chromosome copy numbers is seen to increase DNA breaks in U2OS osteosarcoma cells without affecting

191 recruitment without affecting KU dynamics at DNA breaks in vivo.

192 eting the Agouti locus induced site-directed DNA breaks in zygotes within 6 h of injection, an activi

193 that a RecQ helicase, RECQ2, acts to repair DNA breaks, including in the telomeric site of VSG expre

194 induced significant levels of single-strand DNA breaks, indicating a mechanism of action different f

195 absence, chromosomes mostly suffer one-ended DNA breaks, indicating disintegration of replication for

196 uivalent role at chromosomal double-stranded DNA breaks, indicating that tandem duplications form spe

197 sister chromatid exchanges and double strand DNA breaks, indicating the formation of mitotic recombin

198 ination between homologs are double-stranded DNA breaks induced during S or G2 of the cell cycle, in

199 fragments that subsequently reintegrate into DNA breaks induced on a heterologous chromosome.

200 We show here that SSEs can spread via DNA break-induced homologous recombination, a process kn

201 S treatment inhibits repair of AID-initiated DNA breaks, induces apoptosis, and promotes cytotoxicity

202 Here we show that, upon DNA break induction, the budding yeast SUMO ligase Siz2

203 Spontaneous DNA breaks instigate genomic changes that fuel cancer an

204 epair pathways in resolving nuclease-induced DNA breaks into genome editing outcomes, we previously d

205 Here we introduced double-stranded DNA breaks into the nuclear genome of tobacco through in

206 ays following the introduction of a targeted DNA break is essential to further advance the safety and

207 The mechanism by which a double-stranded DNA break is produced following collision of two translo

208 rylation of histone variant H2AX proximal to DNA breaks is an initiating event and a hallmark of euka

209 cted repair and nonhomologous end joining of DNA breaks is impaired in KDM4D-deficient cells.

210 Resection of DNA breaks is impaired when either Sae2 activity is bloc

211 In bacteria, the repair of double-stranded DNA breaks is modulated by Chi sequences.

212 Histone ubiquitination at DNA breaks is required for activation of the DNA damage

213 t recruitment of BRCA1 to chromatin flanking DNA breaks is required for BRCA1 phosphorylation at seri

214 1-dependent, TOP2beta-mediated double-strand DNA breaks is required for efficient GR-stimulated trans

215 on through mitosis following double-stranded DNA breaks leads to the formation of micronuclei, which

216 iation induces more single and double strand DNA breaks, less H2AX phosphorylation, increased Chk2 ph

217 ysed cytidine deamination in the vicinity of DNA breaks, likely through action on single-stranded DNA

218 However, DNA breaks may engage one of several competing repair pa

219 ites can explain how repair of double strand DNA breaks might occur in a mechanism that is independen

220 pairs were designed to induce double-strand DNA break near the starting codon of each gene that eith

221 redominant binding of PARP1 to single-strand DNA breaks, occluding its Erk binding sites, suppressed

222 viability following an induced double-strand DNA break, of a magnitude comparable with the defect mea

223 fragility and suggests potential impacts of DNA breaks on neurodevelopment and neural functions.

224 The complexes failed to induce double-strand DNA breaks or DNA cross-linking but induced significant

225 oes not require formation of double-stranded DNA breaks or provision of a donor DNA template.

226 an be used to simultaneously create multiple DNA breaks or to target multiple transcriptional activat

227 I (TDP1); a key TOP1-mediated protein-linked DNA break (PDB) repair enzyme.

228 on DNA, generating cytotoxic protein-linked DNA breaks (PDBs).

229 uid component controls the rate of repair of DNA breaks per unit volume by repair factors, which are

230 rylation of EXO1 augments its recruitment to DNA breaks possibly via interactions with BRCA1.

231 Following its phosphorylation by ATM at DNA breaks, "primed" PIDD relocates to kinetochores via

232 '-phosphatase activities to modify ends of a DNA break prior to ligation.

233 Here we show that DNA breaks promote dissociation of cohesin loaded during

234 Our results demonstrate that Cas9-induced DNA breaks promote efficient rearrangement between pairs

235 s TIP60-dependent mobilization of 53BP1 from DNA breaks, promoting HR.

236 ng recombinational repair of double-stranded DNA breaks, RAD51 recombinase assembles as a nucleoprote

237 ndicate that this protein damage compromises DNA break rejoining and base and nucleotide excision rep

238 we evaluated the use of a homology-directed DNA break repair (HDR) functional assay as a method for

239 of XRCC5/6 that is not directly involved in DNA break repair (NHEJ).

240 vated levels of Mdmx-inhibited double-strand DNA break repair and induced chromosome and chromatid br

241 n sister chromatid cohesion, double-stranded DNA break repair and regulation of gene expression.

242 However, the interplay between DNA break repair and transcription processivity is uncle

243 gastric cancers have defective double-strand DNA break repair by homologous recombination and may ben

244 was associated with failure of double-strand DNA break repair by homologous recombination based on it

245 Double-stranded DNA break repair by homologous recombination is initiate

246 arrangements, revealing an important role of DNA break repair pathway choice in the preservation of g

247 The major Escherichia coli pathway of DNA break repair requires RecBCD enzyme, a complex prote

248 DNA break repair via homology-based mechanisms involves

249 r of DNA replication timing, double-stranded DNA break repair, and replication fork restart.

250 ein kinase (DNA-PK) mediates double-stranded DNA break repair, V(D)J recombination and immunoglobulin

251 end-joining (NHEJ) pathway of double-strand DNA break repair.

252 ends to facilitate telomere maintenance and DNA break repair.

253 ication fork repair without interfering with DNA break repair.

254 hese proteins in DNA replication rather than DNA break repair.

255 into nuclear genomes through double-stranded DNA break repair.

256 by the RAD51 recombinase enables error-free DNA break repair.

257 e/nuclease that functions in double-stranded DNA break repair.

258 n machine essential for the major pathway of DNA break-repair and recombination.

259 , is a master regulator of the double strand DNA break-repair pathway after genotoxic stress.

260 g the DSB, whereas BRCA1 binding directly to DNA breaks requires Nijmegen breakage syndrome 1 (NBS1).

261 and hotspot scanning during double-stranded DNA break resection.

262 valyl-tRNA synthetase (ValRS(ED)) activated DNA break-responsive H2AX and p53-responsive downstream

263 th topoisomerase I-generated single-stranded DNA breaks resulted in the generation of persistent doub

264 TALENs or CRISPR-Cas9-mediated double-strand DNA breaks resulted in up to 100% targeting of the colon

265 The double-strand DNA breaks resulting from replication fork collapse were

266 DNA breaks sharply elevate PARP-1 catalytic activity to

267 search on how these proteins function at the DNA break site has advanced rapidly in the recent past.

268 ting with different placements of the future DNA break site in the integrating vector, we established

269 importance for normal retention of RAD51 at DNA break sites and regulation of HR.

270 ny proteins in time and space to assemble at DNA break sites.

271 lesions, such as single- and double-stranded DNA breaks (SSBs and DSBs), and single-stranded gaps can

272 ons differ in the density of double-stranded DNA breaks that are generated.

273 rossovers and an excess of the double-strand DNA breaks that are the initiating events for meiotic re

274 It is suggested that for double-strand DNA breaks that have initially formed a complex with PAR

275 ut the genome and can induce double-stranded DNA breaks that lead to chromosome translocations at the

276 was observed, due to increased single-strand DNA breaks that likely occur due to heterodimers consist

277 amage, whole-chromosome aneuploidies lead to DNA breaks that persist into mitosis.

278 tidine deaminase protein induces genome-wide DNA breaks that, if not repaired through RAD51-mediated

279 h fluoroquinolones stabilize double-stranded DNA breaks, the antibacterial thiophenes stabilize gyras

280 cleases, eventually generating double strand DNA breaks, the obligatory intermediates of CSR.

281 mary mesenchymal stem cells (MSCs) increases DNA breaks throughout the nucleoplasm as assessed by end

282 iquitin-mediated degradation and to minimize DNA breaks, thus providing insights into the SUMO and ub

283 ns of life, the resection of double-stranded DNA breaks to form long 3'-ssDNA overhangs in preparatio

284 elves, and thereby recruit repair factors to DNA breaks to increase repair efficiency.

285 bp) to dimerise and produce a double-strand DNA break using just two strand-cleavage events.

286 of Cas9-induced site-specific double-strand DNA breaks using timed delivery of Cas9-guide RNA ribonu

287 me involved in the repair of TOP1-associated DNA breaks via hydrolysis of 3'-phosphotyrosine bonds.

288 AIRE has been shown to promote DNA breaks via its interaction with topoisomerase 2 (TOP

289 the generation of persistent double-stranded DNA breaks was found to be a primary cause of heat stres

290 Inhibition of DNA repair and accumulation of DNA breaks was functionally confirmed by the presence of

291 sely, in the absence of AID phosphorylation, DNA breaks were not efficiently generated at switch (S)

292 nblock significantly reduced double-stranded DNA breaks when compared with a commercial sunscreen for

293 e per unit volume due to naturally occurring DNA breaks, whereas the volume fraction of the fluid com

294 ing apoptotic cell death via double-stranded DNA breaks while causing a remodeling of the tumor micro

295 3A itself is highly proficient at generating DNA breaks, whose repair can trigger the formation of si

296 pacity for DNA 3' capping and the sealing of DNA breaks with 3'-PO4 and 5'-OH termini, with implicati

297 G9a and GLP1 rapidly localizes to DNA breaks, with GLP1 localization being dependent on G9

298 iting through the catalysis of double-strand DNA breaks within target loci and subsequent repair by t

299 Repairing DNA breaks within the complexity of the cell chromatin i

300 we suggest that formation of double-stranded DNA breaks within the Ytel sequences might be responsibl