Leishmania mexicana mexicana: Genetic Heterogeneity of Mexican Isolates using Restriction Lenght Polymorphism Analysis of Kinetoplast DNA

2000 ◽  
Vol 28 (5) ◽  
pp. A245-A245
Author(s):  
I. Becker ◽  
M. Berzunza-Cruz ◽  
R. Perez-Montfort
Keyword(s):  
Genetic Heterogeneity ◽  
Polymorphism Analysis ◽  
Kinetoplast Dna ◽  
Leishmania Mexicana

Identification and diagnosis of Leishmania mexicana complex isolates by polymerase chain reaction

Parasitology ◽  
1994 ◽  
Vol 109 (4) ◽  
pp. 423-433 ◽  
Author(s):  
S. Eresh ◽  
S. M. McCallum ◽  
D. C. Barker
Keyword(s):  
Polymerase Chain Reaction ◽  
Dna Sequences ◽  
The Other ◽  
South American ◽  
Kinetoplast Dna ◽  
Leishmania Mexicana ◽  
Chain Reaction ◽  
Potential Host ◽  
Oligonucleotide Primers ◽  
Polymerase Chain

SUMMARYFollowing cloning of Leishmania (L.) amazonensis kinetoplast DNA two recombinant clones were identified: one specific for L. (L.) amazonensis and the other specific for L. (L.) amazonensis and closely related isolates. DNA sequences from these clones were compared with those of other kinetoplastids and oligonucleotide primers were designed to be used in the polymerase chain reaction. A pair of these primers has been shown not only to be highly specific for L. mexicana complex isolates but can also be used to distinguish between L. (L.) mexicana and L. (L.) amazonensis isolates. These primers have been tested with water-lysed cultures, crude DNA extracts from human patients, potential host reservoirs, sandfly vectors and with cell pellets after isoenzyme characterization. The results of these tests indicate that the primers can be used specifically in the presence of excess host DNA originating from the majority of South American countries.

Polymorphism analysis of the internal transcribed spacer and small subunit of ribosomal RNA genes of Leishmania mexicana

2002 ◽  
Vol 88 (10) ◽  
pp. 918-925 ◽  
Author(s):  
Miriam Berzunza-Cruz ◽  
Nallely Cabrera ◽  
Marco Crippa-Rossi ◽  
Tayde Sosa Cabrera ◽  
Ruy Pérez-Montfort ◽  
...  
Keyword(s):  
Ribosomal Rna ◽  
Internal Transcribed Spacer ◽  
Small Subunit ◽  
Ribosomal Rna Genes ◽  
Polymorphism Analysis ◽  
Leishmania Mexicana ◽  
Rna Genes

Evaluation of the dark field method for large association of spread DNA

1978 ◽  
Vol 36 (2) ◽  
pp. 190-191
Author(s):  
Douglas C. Barker
Keyword(s):  
Electron Microscopy ◽  
Molecular Weight ◽  
Mitochondrial Dna ◽  
Extraction Method ◽  
Field Method ◽  
Dark Field ◽  
Kinetoplast Dna ◽  
Field Electron ◽  
Field Electron Microscopy ◽  
Dark Field Electron

A number of satisfactory methods are available for the electron microscopy of nicleic acids. These methods concentrated on fragments of nuclear, viral and mitochondrial DNA less than 50 megadaltons, on denaturation and heteroduplex mapping (Davies et al 1971) or on the interaction between proteins and DNA (Brack and Delain 1975). Less attention has been paid to the experimental criteria necessary for spreading and visualisation by dark field electron microscopy of large intact issociations of DNA. This communication will report on those criteria in relation to the ultrastructure of the (approx. 1 x 10-14g) DNA component of the kinetoplast from Trypanosomes. An extraction method has been developed to eliminate native endonucleases and nuclear contamination and to isolate the kinetoplast DNA (KDNA) as a compact network of high molecular weight. In collaboration with Dr. Ch. Brack (Basel [nstitute of Immunology), we studied the conditions necessary to prepare this KDNA Tor dark field electron microscopy using the microdrop spreading technique.

Cell Wall Ultrastructure in Three Strains of a Cariogenic Streptococcus

1971 ◽  
Vol 29 ◽  
pp. 338-339
Author(s):  
M. J. Kramer ◽  
Alan L. Coykendall
Keyword(s):  
Cell Wall ◽  
Dental Caries ◽  
Streptococcus Mutans ◽  
Microscopic Study ◽  
Electron Microscopic Study ◽  
Genetic Heterogeneity ◽  
Morphological Characteristics ◽  
Electron Microscopic ◽  
Dna Reassociation ◽  
Wall Ultrastructure

During the almost 50 years since Streptococcus mutans was first suggested as a factor in the etiology of dental caries, a multitude of studies have confirmed the cariogenic potential of this organism. Streptococci have been isolated from human and animal caries on numerous occasions and, with few exceptions, they are not typable by the Lancefield technique but are relatively homogeneous in their biochemical reactions. An analysis of the guanine-cytosine (G-C) composition of the DNA from strains K-1-R, NCTC 10449, and FA-1 by one of us (ALC) revealed significant differences and DNA-DNA reassociation experiments indicated that genetic heterogeneity existed among the three strains. The present electron microscopic study had as its objective the elucidation of any distinguishing morphological characteristics which might further characterize the respective strains.

Ectopic Transcript Analysis Indicates that Allelic Exclusion is an Important Cause of Type I Protein C Deficiency in Patients with Nonsense and Frameshift Mutations in the PROC Gene

1996 ◽  
Vol 75 (06) ◽  
pp. 870-876 ◽  
Author(s):  
José Manuel Soria ◽  
Lutz-Peter Berg ◽  
Jordi Fontcuberta ◽  
Vijay V Kakkar ◽  
Xavier Estivill ◽  
...  
Keyword(s):  
Splice Site ◽  
Protein C ◽  
Stop Codon ◽  
Premature Stop Codon ◽  
Allelic Exclusion ◽  
Polymorphism Analysis ◽  
Type I ◽  
Protein C Deficiency ◽  
Nonsense Mutations ◽  
Stop Codons

SummaryNonsense mutations, deletions and splice site mutations are a common cause of type I protein C deficiency. Either directly or indirectly by altering the reading frame, these' lesions generate or may generate premature stop codons and could therefore be expected to result in premature termination of translation. In this study, the possibility that such mutations could instead exert their pathological effects at an earlier stage in the expression pathway, through “allelic exclusion” at the RNA level, was investigated. Protein C (PROC) mRNA was analysed in seven Spanish type I protein C deficient patients heterozygous for two nonsense mutations, a 7bp deletion, a 2bp insertion and three splice site mutations. Ectopic RNA transcripts from patient and control lymphocytes were analysed by RT-PCR and direct sequencing of amplified PROC cDNA fragments. The nonsense mutations and the deletion were absent from the cDNAs indicating that only mRNA derived from the normal allele had been expressed. Similarly for the splice site mutations, only normal PROC cDNAs were obtained. In one case, exclusion of the mutated allele could be confirmed by polymorphism analysis. In contrast to these six mutations, the 2 bp insertion was not associated with loss of mRNA from the mutated allele. In this case, cDNA analysis revealed the absence of 19 bases from the PROC mRNA consistent with the generation and utilization of a cryptic splice site 3’ to the site of mutation, which would result in a frameshift and a premature stop codon. It is concluded that allelic exclusion is a common causative mechanism in those cases of type I protein C deficiency which result from mutations that introduce premature stop codons

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