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1 s chromosomal fragile sites that can trigger gross chromosomal rearrangements.
2 ogous end-joining, neither of which leads to gross chromosomal rearrangements.
3 as strongly correlated with the formation of gross chromosomal rearrangements.
4 recombinational repair of a DSB and enhances gross chromosomal rearrangements.
5 grity by triggering double-strand breaks and gross chromosomal rearrangements.
6 rate that Smc5-Smc6 is necessary to suppress gross chromosomal rearrangements.
7 d an increase in aneuploidy and had multiple gross chromosomal rearrangements.
8 ctopic recombination promoting site-specific gross chromosomal rearrangements.
9 ic growth defect with sgs1Delta and elevated 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 ed with sgs1Delta and exo1Delta and elevated gross chromosomal rearrangements.
14 ity, ranging from elevated mutation rates to gross chromosomal rearrangements and alterations in chro
16 synthesized B. napus involved aneuploidy and gross chromosomal rearrangements, and that dosage balanc
17 e substitution, tandem gene duplication, and gross chromosomal rearrangement appear to proceed substa
20 t the engineered DRT/DMC chromosomes acquire gross chromosomal rearrangements at an increased rate wh
21 inactivation results in hyper-recombination, gross chromosomal rearrangements, chromosome segregation
22 ck of SGS1 results in a 110-fold increase in gross chromosomal rearrangement frequency during aging o
24 etic screens for mutations causing increased gross chromosomal rearrangement (GCR) rates in Saccharom
26 ments to DNA replication are known to induce gross chromosomal rearrangements (GCRs) and copy-number
30 tutions, small DNA insertions/deletions, and gross chromosomal rearrangements (GCRs) in sch9Delta mut
34 Cancer-causing mutations often arise from gross chromosomal rearrangements (GCRs) such as transloc
35 A damage, telomere shortening, and increased gross chromosomal rearrangements (GCRs) that are frequen
36 sed a S. cerevisiae assay for characterizing gross chromosomal rearrangements (GCRs) to analyze genom
37 r of common processes such as suppression of gross chromosomal rearrangements (GCRs), DNA repair, mod
40 s in SGS1 increased the rate of accumulating gross chromosomal rearrangements (GCRs), including trans
41 ced Cdc28 activity results in suppression of gross chromosomal rearrangements (GCRs), indicating that
42 is often associated with the accumulation of gross chromosomal rearrangements (GCRs), such as translo
47 are known to have a major role in preventing gross chromosomal rearrangements (GCRs); however, relati
50 d semidominant and enhanced the formation of gross chromosomal rearrangements in multiple genetic bac
51 phenotype and the high rate of formation of gross chromosomal rearrangements in pif1Delta mutants, s
52 at harbors a direct repeat, and are prone to gross chromosomal rearrangements in response to replicat
53 ents should be considered as alternatives to gross chromosomal rearrangements in the interpretation o
54 ificantly increased the rate of accumulating gross-chromosomal rearrangements in a dosage-dependent m
55 hese cells exhibit reduced proliferation and gross chromosomal rearrangements including Robertsonian
57 n of cells containing inverted dimers led to gross chromosomal rearrangements, including translocatio
58 ctal cancer epithelial cells did not display gross chromosomal rearrangements nor a change in the rat
60 ng of spontaneous or induced DNA damage into gross chromosomal rearrangements, providing a mechanisti
62 diate ectopic sequence exchange resulting in gross chromosomal rearrangements that could contribute t
63 homologous recombination, but this can cause gross chromosomal rearrangements that subsequently misse
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