scholarly journals Q-PCR analysis of the resistance of Hungarian Botrytis cinerea isolates toward azoxystrobin

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.

1950 ◽  
Vol 34 (2) ◽  
pp. 211-224 ◽  
Author(s):  
E. S. Guzman Barron ◽  
Maria Isabel Ardao ◽  
Marion Hearon

The rate of the aerobic metabolism of pyruvic acid by bakers' yeast cells is determined mainly by the amount of undissociated acid present. As a consequence, the greatest rate of oxidation was observed at pH 2.8. Oxidation, at a slow rate, started at pH 1.08; at pH 9.4 there was no oxidation at all. The anaerobic metabolism, only a fraction of the aerobic, was observed only in acid solutions. There was none at pH values higher than 3. Pyruvic acid in the presence of oxygen was oxidized directly to acetic acid; in the absence of oxygen it was metabolized mainly by dismutation to lactic and acetic acids, and CO2. Acetic acid formation was demonstrated on oxidation of pyruvic acid at pH 1.91, and on addition of fluoroacetic acid. Succinic acid formation was shown by addition of malonic acid. These metabolic pathways in a cell so rich in carboxylase may be explained by the arrangement of enzymes within the cell, so that carboxylase is at the center, while pyruvic acid oxidase is located at the periphery. Succinic and citric acids were oxidized only in acid solutions up to pH 4. Malic and α-ketoglutaric acids were not oxidized, undoubtedly because of lack of penetration.


2007 ◽  
Vol 1 (3) ◽  
pp. 329-333 ◽  
Author(s):  
Qifa Li ◽  
Yinxia Li ◽  
Xingbo Zhao ◽  
Zhenshan Liu ◽  
Yefen Xu ◽  
...  

1982 ◽  
Vol 2 (1) ◽  
pp. 30-41
Author(s):  
N A Oliver ◽  
D C Wallace

Two mitochondrially synthesized marker polypeptides, MV-1 and MV-2, were found in human HeLa and HT1080 cells. These were assigned to the mitochondrial DNA in HeLa-HT1080 cybrids and hybrids by demonstrating their linkage to cytoplasmic genetic markers. These markers include mitochondrial DNA restriction site polymorphisms and resistance to chloramphenicol, an inhibitor of mitochondrial protein synthesis. In the absence of chloramphenicol, the expression of MV-1 and MV-2 in cybrids and hybrids was found to be directly proportional to the ratio of the parental mitochondrial DNAs. In the presence of chloramphenicol, the marker polypeptide linked to the chloramphenicol-sensitive mitochondrial DNA continued to be expressed. This demonstrated that resistant and sensitive mitochondrial DNAs can cooperate within a cell for gene expression and that the CAP-resistant allele was dominant or codominant to sensitive. Such cooperation suggests that mitochondrial DNAs can be exchanged between mitochondria.


2004 ◽  
Vol 25 (4) ◽  
pp. 861-873 ◽  
Author(s):  
Ming Li ◽  
Fuwen Wei ◽  
Chengming Huang ◽  
Ruliang Pan ◽  
Johannes de Ruiter

1995 ◽  
pp. 179-190
Author(s):  
P. J. Singh ◽  
J. Legault ◽  
A. Tremblay ◽  
P. Julien ◽  
M. R. Ven Murthy ◽  
...  

Life ◽  
2020 ◽  
Vol 10 (9) ◽  
pp. 215
Author(s):  
Qiuju Ding ◽  
Róża Kucharczyk ◽  
Weiwei Zhao ◽  
Alain Dautant ◽  
Shutian Xu ◽  
...  

With the advent of next generation sequencing, the list of mitochondrial DNA (mtDNA) mutations identified in patients rapidly and continuously expands. They are frequently found in a limited number of cases, sometimes a single individual (as with the case herein reported) and in heterogeneous genetic backgrounds (heteroplasmy), which makes it difficult to conclude about their pathogenicity and functional consequences. As an organism amenable to mitochondrial DNA manipulation, able to survive by fermentation to loss-of-function mtDNA mutations, and where heteroplasmy is unstable, Saccharomyces cerevisiae is an excellent model for investigating novel human mtDNA variants, in isolation and in a controlled genetic context. We herein report the identification of a novel variant in mitochondrial ATP6 gene, m.8909T>C. It was found in combination with the well-known pathogenic m.3243A>G mutation in mt-tRNALeu. We show that an equivalent of the m.8909T>C mutation compromises yeast adenosine tri-phosphate (ATP) synthase assembly/stability and reduces the rate of mitochondrial ATP synthesis by 20–30% compared to wild type yeast. Other previously reported ATP6 mutations with a well-established pathogenicity (like m.8993T>C and m.9176T>C) were shown to have similar effects on yeast ATP synthase. It can be inferred that alone the m.8909T>C variant has the potential to compromise human health.


1987 ◽  
Vol 42 (11-12) ◽  
pp. 1280-1284 ◽  
Author(s):  
Siegfried Scherer ◽  
Heike Sadowski ◽  
Peter Böger

A cell-free system exhibiting both photophosphorylation (P/2e= 1) and oxidative phosphoryltion (P/O up to 0.8) is described for the cyanobacterium Anabaena variabilis. NADH ant NADPH were found to be equally effective as electron donors for oxidative phosphorylation. Low concentrations of UHDBT, an inhibitor of the cytochrome b/c complex of mitochondria ant loroplasts, were found to inhibit photosystem-II electron transport reactions, but did not affet the cytochrome b6/f-complex of Anabaena. The inhibition by myxothiazol, antimycin and heptyihydroxyquinoline corroborates the hypothesis that both respiration and photosynthesis share the cytochrome b6/f-complex.


Plant Disease ◽  
2010 ◽  
Vol 94 (8) ◽  
pp. 1065-1065 ◽  
Author(s):  
T. L. B. Tarnowski ◽  
R. C. Ploetz

Postharvest anthracnose of papaya, Carica papaya, is an important disease in most production areas worldwide (2). Colletotrichum gloeosporioides causes two types of anthracnose symptoms on papaya: (i) circular, sunken lesions with pink sporulation; and (ii) sharply defined, reddish brown and sunken lesions, described as ‘chocolate spot’ (2). Colletorichum spp. were isolated from lesions of the first type on papaya fruit from the University of Florida Tropical Research and Education Center, Homestead in December 2007 and from fruit imported from Belize in March 2008 (4). Single-spore isolates were identified using colony morphology and internal transcribed spacer (ITS) and mating type (MAT1-2) sequences. Two taxa were identified in both locations: (i) C. gloeosporioides (MAT1-2; GenBank Nos. GQ925065 and GQ925066) with white-to-gray, fluffy colonies with orange sporulation and straight and cylindrical conidia; and (ii) C. capsici (ITS; GenBank Nos. GU045511 to GU045514) with sparse, fluffy, white colonies with setose acervuli and falcate conidia. In addition, in Florida, a Glomerella sp. (ITS; GenBank Nos. GU045518 and GU045520 to GU045522) was recovered with darkly pigmented colonies that produced fertile perithecia after 7 to 10 days on potato dextrose agar (PDA). In each of three experiments, mature fruit (cv. Caribbean Red) were wounded with a sterile needle and inoculated with a 15-μl drop of 0.3% water agar that contained 105 conidia ml–1 of representative isolates of each taxon. The diameters of developing lesions were measured after 7 days of incubation in the dark at 25°C, and the presence of inoculated isolates was confirmed by their recovery from lesion margins on PDA. In all experiments, C. capsici and C. gloeosporioides produced lesions that were significantly larger than those that were caused by the water control and Glomerella sp. (respectively, approximately 12, 17, 0, and <1 mm in diameter). C. gloeosporioides produced sunken lesions with dark gray centers and pink/gray sporulation, which match those previously described for anthracnose on papaya (2). In contrast, C. capsici produced dark lesions due to copious setae of this pathogen; they resembled C. capsici-induced lesions on papaya that were reported previously from the Yucatan Peninsula (3). C. capsici has also been reported to cause papaya anthracnose in Asia (4), but to our knowledge, this is the first time it has been reported to cause this disease in Florida. Since it was also recovered from fruit that were imported from Belize, it probably causes anthracnose of papaya in that country as well. Another falcate-spored species, C. falcatum, was recovered from rotted papaya fruit in Texas (1). The Glomerella sp. was recovered previously from other hosts as an endophyte and causes anthracnose lesions on passionfruit (4). However, its role as a pathogen on papaya is uncertain since it was not pathogenic in the current work; the isolates that were recovered from papaya lesions may have colonized lesions that were caused by C. capsici and C. gloeosporioides. References: (1) Anonymous. Index of Plant Diseases in the United States. U.S. Dept. of Agric. Handb. No. 165. Washington, D.C., 1960. (2) D. M. Persley and R. C. Ploetz. Page 373 in: Diseases of Tropical Fruit Crops. R. C. Ploetz, ed. CABI Publishing. Wallingford, UK, 2003. (3) R. Tapia-Tussell et al. Mol Biotechnol 40:293, 2008. (4) T. L. Tarnowski. Ph.D. diss. University Florida, Gainesville, 2009.


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