ライフサイエンスコーパス: mitotic recombination

1 spontaneous and double-strand break-induced mitotic recombination.

2 f heterozygosity events presumed to arise by mitotic recombination.

3 bility that these variants were generated by mitotic recombination.

4 reaks (DSBs) and can occur by deletion or by mitotic recombination.

5 WTK1 cells could be attributed, in part, to mitotic recombination.

6 ecombination substrates have been studied in mitotic recombination.

7 n young larvae were rendered null for Khc by mitotic recombination.

8 t, Rad1/Rad10 endonuclease also functions in mitotic recombination.

9 m these mice show elevations in the rates of mitotic recombination.

10 he possibility of heterokaryon formation and mitotic recombination.

11 tive mutants are impaired in Alu-IRs-induced mitotic recombination.

12 The remaining cases exhibited mitotic recombination.

13 of the DAP(r) variants were a consequence of mitotic recombination.

14 RAD52 are required for alternate pathways of mitotic recombination.

15 t telomeres also impose a position effect on mitotic recombination.

16 target site preferences, or increase cDNA or mitotic recombination.

17 rec14 mutations had no detectable effect on mitotic recombination.

18 match repair genes MSH2 and MSH3 function in mitotic recombination.

19 -mediated single-strand annealing pathway of mitotic recombination.

20 double-strand break repair, and meiotic and mitotic recombination.

21 leotide excision repair and they also act in mitotic recombination.

22 ng lox-like sequences can exhibit almost 20% mitotic recombination.

23 sion yeast strains also exhibited defects in mitotic recombination.

24 loss of heterozygosity on chromosome 17q via mitotic recombination.

25 ation and elevated rates of both meiotic and mitotic recombination.

26 llicular lymphoma (FL) and is usually due to mitotic recombination.

27 f Mph1-MHF and exerts a procrossover role in mitotic recombination.

28 is the major strand-transferase required for mitotic recombination.

29 ely minor role in regulating the fidelity of mitotic recombination.

30 ted with cancer susceptibility and increased mitotic recombination.

31 genes have conserved function in suppressing mitotic recombination.

32 combination events at intervals of preferred mitotic recombination.

33 ty in desmoids involved deletion rather than mitotic recombination.

34 o whole-chromosome deletion and regain or to mitotic recombination.

35 WC, reversion of KRT1 mutations occurred via mitotic recombination.

36 of TNR expansion, of TNR contraction, and of mitotic recombination.

37 interstitial LOH on 8p12 may be generated by mitotic recombination.

38 red for efficient gamma-ray damage repair or mitotic recombination.

39 oss of ATRX results in increased centromeric mitotic recombination, a high frequency of sister chroma

40 ingle or double homologous and nonhomologous mitotic recombinations, a translocation, chromosome brea

41 cases, representing about 80% of all events, mitotic recombination accounted for all loss of heterozy

42 We examined the frequency of mitotic recombination across an MRS of average size (app

43 nificant bias in apparent nondisjunction vs. mitotic recombination among male vs. female patients or

44 xhibits a 5-fold higher rate of spontaneous, mitotic recombination and a greater than 10-fold increas

45 Elevated mitotic recombination and cell cycle delays are two of t

46 Frequencies of mitotic recombination and chromosome loss are elevated i

47 ave approximately 80-fold increased rates of mitotic recombination and chromosome loss.

48 of DNA translocases required for meiotic and mitotic recombination and DNA repair.

49 instability phenotypes, including increased mitotic recombination and elongated telomeres.

50 pcr1, spc1, or wis1 and was undetectable in mitotic recombination and in meiotic recombination when

51 y of tumors showing allele loss occurring by mitotic recombination and induced by oxidative damage.

52 BALB/c-Trp53(+/-) mammary tumors occurs via mitotic recombination and is a dominant genetic trait th

53 instability, resulting in increased rates of mitotic recombination and mutagenesis.

54 or rad1 mutant strains that are defective in mitotic recombination and removing unpaired DNA single s

55 Most mitotic recombination and repair genes of Saccharomyces

56 hsk1 cells suffer increased rates of mitotic recombination and require recombination proteins

57 Overall, the distributions of mitotic recombination and whole-chromosome LOH in the MS

58 Thus, chromosomal divergence inhibits mitotic recombination and, consequently, may act as a mo

59 These results indicate that mitotic recombination and, to a much lesser extent, dele

60 h complete LOH; 1-2 terminal regions of LOH (mitotic recombination); and 1 interstitial region of LOH

61 ients, homozygous in a subset as a result of mitotic recombination, and arose in a multipotent progen

62 ed reduction in cell proliferation following mitotic recombination, and generate few viable gene conv

63 e findings indicate that WRN plays a role in mitotic recombination, and that a loss of WRN function m

64 However, the genetic modulators of mitotic recombination are not well understood.

65 ains displayed increased chromosome loss and mitotic recombination, as well as defective DNA damage r

66 dicentrics in Saccharomyces cerevisiae by a mitotic recombination assay.

67 Mitotic recombination assays suggest that these elongati

68 e present study we sequenced the products of mitotic recombination between 94%-identical substrates i

69 monstrate that MMR proteins strongly inhibit mitotic recombination between diverged sequences in Sacc

70 We report that mitotic recombination between homologous chromosomes occ

71 fraction of LOH events appears to arise from mitotic recombination between homologous chromosomes, re

72 e to an elevated rate of crossover following mitotic recombination between homologous chromosomes.

73 genes confers defects in the suppression of mitotic recombination between similar but nonidentical (

74 introduced into the same cell and joined by mitotic recombination between the vector arms and the ho

75 of the effect of the MRS on a similar event, mitotic recombination between two chromosome homologs.

76 se rearrangements was measured by monitoring mitotic recombination between two his3 fragments, his3-D

77 is+ prototrophs that result from homologous, mitotic recombination between two truncated his3 genes,

78 rand DNA breaks, indicating the formation of mitotic recombination break points.

79 ely to structural alterations rather than to mitotic recombination, break-induced replication, or gen

80 Mitotic recombination, but not point mutation, partly ac

81 expression also strongly induces intragenic mitotic recombination, but only in a strain possessing u

82 rad27 mutants showed similar high levels of mitotic recombination, but varied in their growth rate a

83 Here we show that mitotic recombination can be reproducibly induced in mou

84 into four classes: apparent point mutation, mitotic recombination, chromosome loss, and large inters

85 r such regions, which are the consequence of mitotic recombination, contain homozygous mutations in g

86 This suggests that mitotic recombination contributes to the survival and th

87 osome 5 is the first large-scale analysis of mitotic recombination done in C. albicans and indicates

88 y, these phenomena suggest that dysregulated mitotic recombination drives the genomic instability und

89 Very few crossovers occurred in ade6 mitotic recombination, either allelic or ectopic.

90 Increased mitotic recombination enhances the risk for loss of hete

91 Mitotic recombination events between homologous chromoso

92 oduction of EDSBs and of ensuing spontaneous mitotic recombination events can account for a substanti

93 uman chromosome 7 and found evidence of rare mitotic recombination events in human lymphocytes.

94 orders of magnitude higher than observed for mitotic recombination events involving single-copy genes

95 Mitotic recombination events resulting in extended loss

96 Mitotic recombination events were found to occur through

97 gion we have searched for small deletions or mitotic recombination events, neither of which would be

98 Mitotic recombination experiments in the germline show S

99 This analysis of mitotic recombination frequencies across a large portion

100 Our results indicate that mitotic recombination frequencies across the MRS were no

101 ation done in C. albicans and indicates that mitotic recombination frequencies are similar to the rat

102 but their near-diploid karyotypes concealed mitotic recombination frequencies similar to those of MS

103 In contrast to meiotic recombination, the mitotic recombination frequency did not decline near the

104 Loss of the JAK2 mutation by mitotic recombination, gene conversion, or deletion was

105 ible mechanisms may be used in this process, mitotic recombination, gene conversion, or loss of one c

106 Additionally, in some revertant patches, mitotic recombination generated areas with homozygous no

107 Mutations in REC103 do not affect mitotic recombination, growth, or repair.

108 oss-of-heterozygosity (LOH), suggesting that mitotic recombination has a significant impact on geneti

109 ion of segmental uniparental disomy (UPD) by mitotic recombination has been reported in 15% to 20% of

110 me (an inverted repeat of 80 bp) conferred a mitotic recombination hotspot relative to a control nonp

111 We found that an Alu-IR is a mitotic recombination hotspot requiring MRE11/RAD50/XRS2

112 ences and inverted Alu repeats (Alu-IRs) are mitotic recombination hotspots, requiring the repair fun

113 By inducing mitotic recombination in a subclass of eye progenitors,

114 Here we have exploited the high rate of mitotic recombination in Bloom's syndrome protein (Blm)-

115 We exploited mitotic recombination in developing Drosophila imaginal

116 To this end, we performed mitotic recombination in Drosophila melanogaster, RNAi-m

117 In contrast, mitotic recombination in ES cells appeared to be suppres

118 direct evidence for a role of Mus81-Eme1 in mitotic recombination in higher eukaryotes and support t

119 ulation of Mus81 by RNA interference reduces mitotic recombination in human somatic cells.

120 enesis and offer a rare opportunity to study mitotic recombination in nonneoplastic cells.

121 hromosomal homology by backcrossing restores mitotic recombination in offspring.

122 Although DNA breaks stimulate mitotic recombination in plants, their effects on meioti

123 epresses not only Ty1 transcription but also mitotic recombination in RDN1.

124 The prevalence of mitotic recombination in regions proximal to Aprt did no

125 Most previous studies of mitotic recombination in Saccharomyces cerevisiae have f

126 The suppression of mitotic recombination in some F1 hybrids in which meioti

127 Meiotic recombination differs from mitotic recombination in that DSBs are repaired using ho

128 Although interhomolog mitotic recombination in the CUP1 locus is elevated rela

129 ng distance from the centromere, implicating mitotic recombination in the process.

130 loss of heterozygosity (LOH) resulting from mitotic recombination in vivo constitutes the underlying

131 d model for studying somatic mutagenesis and mitotic recombination in vivo.

132 dominant-negative RAD51 protein to suppress mitotic recombination in WRN and control cells: the supp

133 These data suggest that homologous mitotic recombination, induced by O6-MeG in a subpopulat

134 o examine recognition of these mismatches in mitotic recombination intermediates.

135 usion of the yeast-derived FRT/FLP system of mitotic recombination into Drosophila.

136 a recombination reporter, we have shown that mitotic recombination is dependent on the RAD52 gene, bu

137 ation reporter we have previously shown that mitotic recombination is dependent on the RAD52 gene.

138 g positive selection and/or that the rate of mitotic recombination is elevated in individuals with th

139 Here we report that mitotic recombination is suppressed, to various degrees

140 ernal alleles were retained, indicating that mitotic recombination is the most likely mechanism of LO

141 itu hybridization analysis demonstrated that mitotic recombination is the predicted mechanism of LOH

142 frequency of Aprt LOH, mediated primarily by mitotic recombination, is fully consistent with our prev

143 rait has mild SCD resulting from postzygotic mitotic recombination leading to UPD.

144 LOH generally occurred by mitotic recombination, leaving two identical alleles, ea

145 itous recombinase Rad51, suggesting that the mitotic recombination machinery is reactivated following

146 n to be required for spontaneous and induced mitotic recombination, meiotic recombination, and mating

147 endent probe amplification (MLPA) identified mitotic recombination (MR) as the cause of LOH in 14 out

148 Mitotic recombination (MR) between chromosome homologs i

149 Such cases appear to result from mitotic recombination occurring in early embryogenesis a

150 highly suppressed in G1 cells to ensure that mitotic recombination occurs solely between sister chrom

151 Mitotic recombination occurs with high frequency in huma

152 This observation demonstrates that mitotic recombination of chromosome 6 can also give rise

153 e in evolution despite its susceptibility to mitotic recombination on inhibition of DNA replication.

154 ause of the observed tk deletions was either mitotic recombination or chromosomal loss accompanied by

155 polycythemia vera does not commonly involve mitotic recombination or chromosome loss and that micros

156 ome 3q to define the minimal region in which mitotic recombination or deletion results in LOH, which

157 Mitotic recombination org nondysjunction are common mech

158 of the copy number gain events occur by the mitotic recombination pathway.

159 We suggest that meiotic and mitotic recombination pathways coexist within meiotic ce

160 are microsatellite repeat distributions with mitotic recombination patterns available from earlier ge

161 hts into the roles that both outcrossing and mitotic recombination play in shaping the genome archite

162 6 kbp convert efficiently during DSB-induced mitotic recombination, primarily by Msh2p- and Pms1p-dep

163 In a proportion of V617F-positive patients, mitotic recombination produces mutation-homozygous cells

164 from heterozygous to homozygous mutations by mitotic recombination provides a mechanism for relapse.

165 FLP/FRT-induced mitotic recombination provides a powerful method for cre

166 ants is not highly unusual in the sense that mitotic recombination rates are normal, implying that a

167 ved genetic escape mechanism was spontaneous mitotic recombination resulting in loss of heterozygosit

168 expansion of beta cells that have undergone mitotic recombination, resulting in paternal disomy of p

169 e frequency of somatic variants derived from mitotic recombination should be diminished in progeny fr

170 of gamma-ray damage, but exhibits decreased mitotic recombination similar to rad52 null strains, was

171 agents and established another site-specific mitotic recombination system.

172 l-cell communication via Notch (N) receptor, mitotic recombination that removes the N ligand Delta (D

173 cases, suggesting negative interference for mitotic recombination, the opposite of what is usually o

174 oth Sgs1 and Srs2 limit the overall level of mitotic recombination, there are distinct differences in

175 r integration, for deletion and for enhanced mitotic recombination, thereby increasing the repertoire

176 We have used mitotic recombination to generate patches of homozygous

177 t for syntaxin1 expression were generated by mitotic recombination to reduce the maternal contributio

178 levels of RNA polymerase II transcription on mitotic recombination was examined using lys2 recombinat

179 cy of clones with point mutations, such that mitotic recombination was still the primary cause of APR

180 The results demonstrate that while mitotic recombination was the mechanism for homozygosis

181 ng an assay to detect unselected products of mitotic recombination, we found a significant decrease i

182 XpF/Ercc1 endonuclease has a similar role in mitotic recombination, we targeted the APRT locus in Chi

183 for spontaneous and transcription-stimulated mitotic recombination were determined using a recombinat

184 rminal domain, but Rad51 focus formation and mitotic recombination were elevated above wild-type leve

185 vious studies involving hetDNA formed during mitotic recombination were restricted to one locus.

186 This implies that mutation precedes mitotic recombination which acts as a "second hit" respo

187 etween homologous chromatids, in contrast to mitotic recombination, which occurs primarily between si

188 The assembled YAC was further extended by mitotic recombination with a YAC containing a 280-kb reg

189 ed DNA breaks (DSBs) that can be repaired by mitotic recombination with the homolog.

190 from silent chromatin regions and increased mitotic recombination within tandem repeats of rDNA.