Phylogenetic analysis of chloroplast restriction enzyme site mutations in the Saccharinae Griseb. subtribe of the Andropogoneae Dumort. tribe

1994 ◽  
Vol 87 (7) ◽  
pp. 843-853 ◽  
Author(s):  
B. W. S. Sobral ◽  
D. P. V. Braga ◽  
E. S. LaHood ◽  
P. Keim
Keyword(s):  
Phylogenetic Analysis ◽  
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 High genetic diversity of hepatitis delta virus in eastern Turkey

2014 ◽  
Vol 8 (01) ◽  
pp. 074-078 ◽  
Author(s):  
Yasemin Bulut ◽  
Ibrahim Halil Bahcecioglu ◽  
Cem Aygun ◽  
Pinar Demirel Oner ◽  
Ibrahim Ozercan ◽  
...  
Keyword(s):  
Genetic Diversity ◽  
Phylogenetic Analysis ◽  
Restriction Enzyme ◽  
Hepatitis Delta Virus ◽  
Rt Pcr ◽  
Genotype I ◽  
High Genetic Diversity ◽  
Hepatitis Delta ◽  
Hdv Genotype ◽  
Delta Virus

Introduction: Hepatitis delta virus (HDV) is a serious cause of liver-related mortality in patients infected with hepatitis B virus (HBV). Determination of genotypes of HDV and phylogenetic analysis are important for better understanding the pathogenesis of the liver diseases associated with HBV infection. The aim of this study was to determine the genotype or genotypes of HDV among chronically infected patients with HBV in eastern Turkey. Methodology: A group of 113 patients infected with HBV and HDV were included in this study. The samples taken from the patients were analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR) and restriction enzyme cleavage. Results: According to the results of the restriction enzyme analysis, all of the RT-PCR products were determined to be HDV genotype I. Furthermore, for phylogenetic analysis and genotyping, 40 of HDV RT-PCR positive products were sequenced. Phylogenetic analysis of the sequences showed that all of the samples were infected with HDV genotype I. In addition, the results of the alignment analysis showed that the sequences of clinical samples were 82%-95% similar. Conclusion: These results indicate that high genetic diversity of the virus is possible in endemic areas such as Turkey.

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.

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
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