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1 ed with sgs1Delta and exo1Delta and elevated gross chromosomal rearrangements.
2 s chromosomal fragile sites that can trigger gross chromosomal rearrangements.
3 ogous end-joining, neither of which leads to gross chromosomal rearrangements.
4 as strongly correlated with the formation of gross chromosomal rearrangements.
5 recombinational repair of a DSB and enhances gross chromosomal rearrangements.
6 grity by triggering double-strand breaks and gross chromosomal rearrangements.
7 rate that Smc5-Smc6 is necessary to suppress gross chromosomal rearrangements.
8 d an increase in aneuploidy and had multiple gross chromosomal rearrangements.
9 ctopic recombination promoting site-specific gross chromosomal rearrangements.
10 ility, but misrepair generates mutations and gross chromosomal rearrangements.
11 n peroxidase, was found to strongly suppress gross chromosomal rearrangements.
12 lved strains were aneuploid as the result of gross chromosomal rearrangements.
13 mitochondrial function or for suppression of gross chromosomal rearrangements.
14 ic growth defect with sgs1Delta and elevated gross chromosomal rearrangements.
15 ss of heterozygosity, genetic mutations, and gross chromosomal rearrangements, all hallmarks of cance
16 ity, ranging from elevated mutation rates to gross chromosomal rearrangements and alterations in chro
17  of inter-genome chromosome collinearity and gross chromosomal rearrangements and have shown that end
18                      Inappropriate HR causes gross chromosomal rearrangements and tumorigenesis in ma
19 synthesized B. napus involved aneuploidy and gross chromosomal rearrangements, and that dosage balanc
20 e substitution, tandem gene duplication, and gross chromosomal rearrangement appear to proceed substa
21 of certain triplet repeat sequences to cause gross chromosomal rearrangements are discussed.
22 t these G-rich/G4 regions as demonstrated by gross chromosomal rearrangement assays.
23 t the engineered DRT/DMC chromosomes acquire gross chromosomal rearrangements at an increased rate wh
24 inactivation results in hyper-recombination, gross chromosomal rearrangements, chromosome segregation
25  association but leads to elevated levels of gross chromosomal rearrangements during replication rest
26 ck of SGS1 results in a 110-fold increase in gross chromosomal rearrangement frequency during aging o
27                                              Gross chromosomal rearrangement (GCR) is a type of genom
28 etic screens for mutations causing increased gross chromosomal rearrangement (GCR) rates in Saccharom
29 eakage of inverted dicentric dimers leads to gross chromosomal rearrangements (GCR).
30 ments to DNA replication are known to induce gross chromosomal rearrangements (GCRs) and copy-number
31                                              Gross chromosomal rearrangements (GCRs) are frequently o
32                                              Gross chromosomal rearrangements (GCRs) are large scale
33                                              Gross chromosomal rearrangements (GCRs) have been observ
34 tutions, small DNA insertions/deletions, and gross chromosomal rearrangements (GCRs) in sch9Delta mut
35                          The accumulation of gross chromosomal rearrangements (GCRs) is characteristi
36 ces cerevisiae genetic system that generates gross chromosomal rearrangements (GCRs) mediated by fold
37                                              Gross Chromosomal Rearrangements (GCRs) play an importan
38                                              Gross chromosomal rearrangements (GCRs) play an importan
39                             Some spontaneous gross chromosomal rearrangements (GCRs) seem to result f
40    Cancer-causing mutations often arise from gross chromosomal rearrangements (GCRs) such as transloc
41 A damage, telomere shortening, and increased gross chromosomal rearrangements (GCRs) that are frequen
42 sed a S. cerevisiae assay for characterizing gross chromosomal rearrangements (GCRs) to analyze genom
43 r of common processes such as suppression of gross chromosomal rearrangements (GCRs), DNA repair, mod
44                                              Gross chromosomal rearrangements (GCRs), including trans
45                           Different types of gross chromosomal rearrangements (GCRs), including trans
46 s in SGS1 increased the rate of accumulating gross chromosomal rearrangements (GCRs), including trans
47 ced Cdc28 activity results in suppression of gross chromosomal rearrangements (GCRs), indicating that
48 is often associated with the accumulation of gross chromosomal rearrangements (GCRs), such as translo
49 ring DNA replication are one likely cause of gross chromosomal rearrangements (GCRs).
50 omosome V to participate in the formation of gross chromosomal rearrangements (GCRs).
51 hal mutations correlated with an increase in gross chromosomal rearrangements (GCRs).
52  broken and subsequently misrepaired to form gross chromosomal rearrangements (GCRs).
53 quences are unstable and prone to triggering gross chromosomal rearrangements (GCRs).
54 are known to have a major role in preventing gross chromosomal rearrangements (GCRs); however, relati
55       Cells lacking Sgs1 and Rrm3 accumulate gross-chromosomal rearrangements (GCRs) that are suppres
56                         Large-scale changes (gross chromosomal rearrangements [GCRs]) are common in g
57 d semidominant and enhanced the formation of gross chromosomal rearrangements in multiple genetic bac
58  phenotype and the high rate of formation of gross chromosomal rearrangements in pif1Delta mutants, s
59 at harbors a direct repeat, and are prone to gross chromosomal rearrangements in response to replicat
60 ents should be considered as alternatives to gross chromosomal rearrangements in the interpretation o
61 ons predicted to form non-B-form DNA induced gross chromosomal rearrangements in yeast and displayed
62 ificantly increased the rate of accumulating gross-chromosomal rearrangements in a dosage-dependent m
63 hese cells exhibit reduced proliferation and gross chromosomal rearrangements including Robertsonian
64                                              Gross chromosomal rearrangements (including translocatio
65 n of cells containing inverted dimers led to gross chromosomal rearrangements, including translocatio
66 ast expressing these variants have increased gross chromosomal rearrangements, increased telomere len
67 ctal cancer epithelial cells did not display gross chromosomal rearrangements nor a change in the rat
68 30-80-fold increase in the rate at which new gross chromosomal rearrangements occurred.
69 safeguard against the deleterious effects of gross chromosomal rearrangements or mutagenic insults ar
70 ng of spontaneous or induced DNA damage into gross chromosomal rearrangements, providing a mechanisti
71                     Translocations and other gross chromosomal rearrangements that break down synteni
72 diate ectopic sequence exchange resulting in gross chromosomal rearrangements that could contribute t
73 homologous recombination, but this can cause gross chromosomal rearrangements that subsequently misse