Corrigendum to “Restriction enzyme site-directed amplification PCR: A tool to identify regions flanking a marker DNA” [Anal. Biochem. 340 (2005) 330–335]

2006 ◽  
Vol 353 (2) ◽  
pp. 302 ◽  
Author(s):  
David González-Ballester ◽  
Amaury de Montaigu ◽  
Aurora Galván ◽  
Emilio Fernández
Keyword(s):  
Restriction Enzyme ◽  
Restriction Enzyme Site

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

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.

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.

Restriction enzyme site-directed amplification PCR: A tool to identify regions flanking a marker DNA

2005 ◽  
Vol 340 (2) ◽  
pp. 330-335 ◽  
Author(s):  
David González-Ballester ◽  
Amaury de Montaigu ◽  
Aurora Galván ◽  
Emilio Fernández
Keyword(s):  
Restriction Enzyme ◽  
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 Characterization of pathogenic and non-pathogenic African swine fever virus isolates from Ornithodoros erraticus inhabiting pig premises in Portugal

2004 ◽  
Vol 85 (8) ◽  
pp. 2177-2187 ◽  
Author(s):  
F. S. Boinas ◽  
G. H. Hutchings ◽  
L. K. Dixon ◽  
P. J. Wilkinson
Keyword(s):  
Restriction Enzyme ◽  
African Swine Fever Virus ◽  
African Swine Fever ◽  
Fever Virus ◽  
Restriction Enzyme Site ◽  
Lower Efficiency ◽  
Terminal Fragment ◽  
Site Mapping ◽  
The Right ◽  
Virus Isolates

Ten African swine fever virus isolates from the soft tick Ornithodoros erraticus collected on three farms in the province of Alentejo in Portugal were characterized by their ability to cause haemadsorption (HAD) of red blood cells to infected pig macrophages, using restriction enzyme site mapping of the virus genomes and by experimental infection of pigs. Six virus isolates induced haemadsorption and four were non-haemadsorbing (non-HAD) in pig macrophage cell cultures. The restriction enzyme site maps of two non-HAD viruses, when compared with a virulent HAD isolate, showed a deletion of 9·6 kbp in the fragment adjacent to the left terminal fragment and of 1·6 kbp in the right terminal fragment and an insertion of 0·2 kbp in the central region. The six HAD viruses isolated were pathogenic and produced typical acute African swine fever in pigs and the four non-HAD isolates were non-pathogenic. Pigs that were infected with non-HAD viruses were fully resistant or had a delay of up to 14 days in the onset of disease, after challenge with pathogenic Portuguese viruses. Non-HAD viruses could be transmitted by contact but with a lower efficiency (42–50 %) compared with HAD viruses (100 %). The clinical differences found between the virus isolates from the ticks could have implications for the long-term persistence of virus in the field because of the cross-protection produced by the non-pathogenic isolates. This may also explain the presence of seropositive pigs in herds in Alentejo where no clinical disease had been reported.

scholarly journals Transfusion-associated AIDS: donor-recipient human immunodeficiency virus exhibits genetic heterogeneity

Blood ◽  
1987 ◽  
Vol 69 (6) ◽  
pp. 1766-1770
Author(s):  
A Srinivasan ◽  
D York ◽  
P Ranganathan ◽  
R Ferguson ◽  
D Jr Butler ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Restriction Enzyme ◽  
Molecular Basis ◽  
Genomic Variation ◽  
Restriction Enzyme Site ◽  
Viral Genomes ◽  
Immunodeficiency Virus ◽  
Restriction Sites ◽  
Enzyme Mapping

The genetic diversity of the human immunodeficiency virus (HIV) isolated from transfusion-associated AIDS patients has been examined. Restriction enzyme mapping studies of integrated proviral DNA of donor and recipient origin demonstrated genomic variation between isolates. Analysis of the molecularly cloned viral genomes of one donor-recipient pair showed that virus from the recipient had restriction enzyme site differences from the donor, noticeably clustered in the env and orf-2 regions, and also had a greater number of restriction sites in common with the donor as well. These results suggest that HIV may undergo genomic variation in vivo. Comparison of donor-recipient viruses may further the understanding of the molecular basis for AIDS pathogenesis.

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