Mutagenic Events inEscherichia coliand Mammalian Cells Generated in Response to Acetylaminofluorene-Derived DNA Adducts Positioned in theNarI Restriction Enzyme Site†

Biochemistry ◽  
2002 ◽  
Vol 41 (48) ◽  
pp. 14255-14262 ◽  
Author(s):  
Xingzhi Tan ◽  
Naomi Suzuki ◽  
Arthur P. Grollman ◽  
Shinya Shibutani
Keyword(s):  
Dna Adducts ◽  
Restriction Enzyme ◽  
Mammalian Cells ◽  
Restriction Enzyme Site

scholarly journals Mechanisms of Double-Strand-Break Repair During Gene Targeting in Mammalian Cells

Genetics ◽  
1999 ◽  
Vol 151 (3) ◽  
pp. 1127-1141 ◽  
Author(s):  
Philip Ng ◽  
Mark D Baker
Keyword(s):  
Gene Targeting ◽  
Restriction Enzyme ◽  
Mammalian Cells ◽  
Repair Process ◽  
Strand Break ◽  
Double Strand Break ◽  
Patch Repair ◽  
Restriction Enzyme Site ◽  
Dsb Repair ◽  
Vector Borne

AbstractIn the present study, the mechanism of double-strand-break (DSB) repair during gene targeting at the chromosomal immunoglobulin μ-locus in a murine hybridoma was examined. The gene-targeting assay utilized specially designed insertion vectors genetically marked in the region of homology to the chromosomal μ-locus by six diagnostic restriction enzyme site markers. The restriction enzyme markers permitted the contribution of vector-borne and chromosomal μ-sequences in the recombinant product to be determined. The use of the insertion vectors in conjunction with a plating procedure in which individual integrative homologous recombination events were retained for analysis revealed several important features about the mammalian DSB repair process: The presence of the markers within the region of shared homology did not affect the efficiency of gene targeting.In the majority of recombinants, the vector-borne marker proximal to the DSB was absent, being replaced with the corresponding chromosomal restriction enzyme site. This result is consistent with either formation and repair of a vector-borne gap or an “end” bias in mismatch repair of heteroduplex DNA (hDNA) that favored the chromosomal sequence.Formation of hDNA was frequently associated with gene targeting and, in most cases, began ∼645 bp from the DSB and could encompass a distance of at least 1469 bp.The hDNA was efficiently repaired prior to DNA replication.The repair of adjacent mismatches in hDNA occurred predominantly on the same strand, suggesting the involvement of a long-patch repair mechanism.

scholarly journals Spontaneous and restriction enzyme-induced chromosomal recombination in mammalian cells.

1994 ◽  
Vol 91 (26) ◽  
pp. 12554-12558 ◽  
Author(s):  
A. R. Godwin ◽  
R. J. Bollag ◽  
D. M. Christie ◽  
R. M. Liskay
Keyword(s):  
Restriction Enzyme ◽  
Mammalian Cells ◽  
Chromosomal Recombination

Population variation at the polymorphic ApaLI restriction enzyme site in intron 5 of the WT1 gene

2008 ◽  
Vol 50 (6) ◽  
pp. 555-557
Author(s):  
Corinne Besnard-Guérin ◽  
Robert Winqvist ◽  
Irene Newsham ◽  
Webster K. Cavenee
Keyword(s):  
Restriction Enzyme ◽  
Population Variation ◽  
Wt1 Gene ◽  
Restriction Enzyme Site

scholarly journals Alterations of Gene Structure in Ethyl Methane Sulfonate-Induced Mutants of Mammalian Cells

1982 ◽  
Vol 2 (11) ◽  
pp. 1459-1462 ◽  
Author(s):  
Mark Meuth ◽  
Janet E. Arrand
Keyword(s):  
Gene Structure ◽  
Restriction Enzyme ◽  
Mammalian Cells ◽  
Chinese Hamster Ovary Cells ◽  
Alkylating Agents ◽  
Chinese Hamster ◽  
Ovary Cells ◽  
Induced Mutants ◽  
Enzyme Cleavage ◽  
Internal Gene

To determine the types of alterations in gene structure induced by DNA-alkylating agents, we analyzed the restriction enzyme cleavage patterns of adenine phosphoribosyltransferase gene sequences in mutant strains of Chinese hamster ovary cells deficient in this enzyme. Base pair changes as detected by loss of restriction enzyme sites were found, but no major internal gene rearrangements could be detected.

Bacterial artificial chromosome–based physical map of Gibberella zeae (Fusarium graminearum)

Genome ◽  
2007 ◽  
Vol 50 (10) ◽  
pp. 954-962 ◽  
Author(s):  
Yueh-Long Chang ◽  
Seungho Cho ◽  
H. Corby Kistler ◽  
Chun-Sheng Hsieh ◽  
Gary J. Muehlbauer
Keyword(s):  
Bacterial Artificial Chromosome ◽  
Fusarium Graminearum ◽  
Genetic Map ◽  
Genome Sequence ◽  
Restriction Enzyme ◽  
Physical Map ◽  
Artificial Chromosome ◽  
Gibberella Zeae ◽  
Restriction Enzyme Site ◽  
Insert Size

Fusarium graminearum is the primary causal pathogen of Fusarium head blight of wheat and barley. To accelerate genomic analysis of F. graminearum, we developed a bacterial artificial chromosome (BAC)–based physical map and integrated it with the genome sequence and genetic map. One BAC library, developed in the HindIII restriction enzyme site, consists of 4608 clones with an insert size of approximately 107 kb and covers about 13.5 genome equivalents. The other library, developed in the BamHI restriction enzyme site, consists of 3072 clones with an insert size of approximately 95 kb and covers about 8.0 genome equivalents. We fingerprinted 2688 clones from the HindIII library and 1536 clones from the BamHI library and developed a physical map of F. graminearum consisting of 26 contigs covering 39.2 Mb. Comparison of our map with the F. graminearum genome sequence showed that the size of our physical map is equivalent to the 36.1 Mb of the genome sequence. We used 31 sequence-based genetic markers, randomly spaced throughout the genome, to integrate the physical map with the genetic map. We also end-sequenced 17 BamHI BAC clones and identified 4 clones that spanned gaps in the genome sequence. Our new integrated map is highly reliable and useful for a variety of genomics studies.

Mutagenic Specificity of (Acetylamino)fluorene-Derived DNA Adducts in Mammalian Cells†

Biochemistry ◽  
1998 ◽  
Vol 37 (35) ◽  
pp. 12034-12041 ◽  
Author(s):  
Shinya Shibutani ◽  
Naomi Suzuki ◽  
Arthur P. Grollman
Keyword(s):  
Dna Adducts ◽  
Mammalian Cells

scholarly journals The abnormal oocyte phenotype is correlated with the presence of blood transposon in Drosophila melanogaster.

Genetics ◽  
1989 ◽  
Vol 123 (3) ◽  
pp. 485-494
Author(s):  
G Lavorgna ◽  
C Malva ◽  
A Manzi ◽  
S Gigliotti ◽  
F Graziani
Keyword(s):  
Drosophila Melanogaster ◽  
Sequence Analysis ◽  
Restriction Enzyme ◽  
Polymorphism Analysis ◽  
Restriction Map ◽  
Dna Rearrangement ◽  
Restriction Enzyme Site ◽  
Wild Type ◽  
Chromosome Walking ◽  
In The Wild

Abstract The abnormal oocyte mutation (2;44) originates in the wild: it confers no visible phenotype on homozygous abo males or females, but homozygous abo females produce defective eggs and the probability of their developing into adults is much lower than that of heterozygous sister females. We isolated by chromosome walking 200 kb of DNA from region 32. This paper reports that a restriction enzyme site polymorphism analysis in wild type and mutant stocks allowed us to identify a DNA rearrangement present only in stocks carrying the abo mutation. The rearrangement is caused by a DNA insert on the abo chromosome in region 32E which, by restriction map and sequence analysis, was identified as copia-like blood transposon. The transposon, in strains that had remained in abo homozygous conditions for several generations and had lost the abo maternal-effect, was no longer present in region 32E. Certain features of the abo mutation, discussed in the light of this finding, may be ascribed to the nature of the particular allele studied.

Sign in / Sign up

Export Citation Format

Share Document