PCR analysis of mitochondrial DNA from normal and transgenic glutathione peroxidase mice

1995 ◽  
pp. 179-190
Author(s):  
P. J. Singh ◽  
J. Legault ◽  
A. Tremblay ◽  
P. Julien ◽  
M. R. Ven Murthy ◽  
...  
2004 ◽  
Vol 69 (1-4) ◽  
pp. 449-459 ◽  
Author(s):  
Alla G. Oleinik ◽  
Lubov A. Skurikhina ◽  
Sergei V. Frolov ◽  
Vladimir A. Brykov ◽  
Igor A. Chereshnev

Parasitology ◽  
2019 ◽  
Vol 146 (8) ◽  
pp. 1022-1029 ◽  
Author(s):  
Diana Minardi ◽  
David J. Studholme ◽  
Birgit Oidtmann ◽  
Tobia Pretto ◽  
Mark van der Giezen

AbstractAphanomyces astacicauses crayfish plague, which is a devastating disease of European freshwater crayfish. The likely first introduction ofA. astaciinto Europe was in the mid-19th century in Italy, presumably with the introduction of North American crayfish. These crayfish can carryA. astaciin their cuticle as a benign infection.Aphanomyces astacirapidly spread across Europe causing the decline of the highly susceptible indigenous crayfish species. Random amplified polymorphic DNA-PCR analysis ofA. astacipure cultures characterized five genotype groups (A, B, C, D and E). CurrentA. astacigenotyping techniques (microsatellites and genotype-specific regions, both targeting nuclear DNA) can be applied directly to DNA extracted from infected cuticles but require high infection levels. Therefore, they are not suitable for genotyping benign infections in North American crayfish (carriers). In the present study, we combine bioinformatics and molecular biology techniques to developA. astacigenotyping molecular markers that target the mitochondrial DNA, increasing the sensitivity of the genotyping tools. The assays were validated on DNA extracts ofA. astacipure cultures, crayfish tissue extractions from crayfish plague outbreaks and tissue extractions from North American carriers. We demonstrate the presence ofA. astacigenotype groups A and B in UK waters.


1990 ◽  
Vol 172 (2) ◽  
pp. 483-489 ◽  
Author(s):  
Takayuki Ozawa ◽  
Masashi Tanaka ◽  
Shin-ichiro Ikebe ◽  
Kinji Ohno ◽  
Tomoyoshi Kondo ◽  
...  

Author(s):  
Frederick J. LaRiviere ◽  
Adam G. Newman ◽  
Megan L. Watts ◽  
Sharonda Q. Bradley ◽  
Justin E. Juskewitch ◽  
...  

2011 ◽  
pp. 41-44
Author(s):  
Anikó Szojka ◽  
Mojtaba Asadollahi ◽  
Éva Fekete ◽  
Erzsébet Fekete ◽  
Levente Karaffa ◽  
...  

The genes being in the mitochondrial DNA primarily encode the enzymes of cellular respiration. Fungicides belonging to the family of quinol oxidase inhibitors (QoIs) play on important role in the protection against several plant diseases caused by fungi. These fungicides bind to the cytochrome bc1 complex so they block electron transport between cytochrome b and cytochrome c1. This way these fungicides inhibit the ATP synthesis consequently they inhibit the mitochondrial respiration. The QoI resistance has two mechanisms. One of them is the point mutation of the cytochrome b gene (CYTB), e.g. the substitution of a single glycine by alanine at position 143 results in high-resistance. The other is the cyanide-resistant alternative respiration sustained by the alternative oxidase.In a cell there are several mitochondria. The phenomenon when the genomes of all mitochondria in the cell are identical is called homoplazmy. If in the cell there is wild and mutant mitochondrial DNA this is called heteroplasmy. Whether the mutation in the mitochondria causes fenotypical diversity or does not depend on the dose, i.e. it depends on the percentage of the changed mitochondrials. During our work we investigated Botrytis cinerea single spore isolates which have been collected in 2008-2009 on different host plants. Our goal was to decide whether heteroplasmy influences the level of resistance. We managed to detect the change of the level of heteroplasmy, so the change the level of the resistance due to the treatment with fungicide.


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