scholarly journals Infection Components of Wild-Type and Mutant Strains of Colletotrichum gloeosporioides f. sp. aeschynomene on Northern Jointvetch

Plant Disease ◽  
1997 ◽  
Vol 81 (4) ◽  
pp. 404-409 ◽  
Author(s):  
Y. Luo ◽  
D. O. TeBeest

Colletotrichum gloeosporioides f. sp. aeschynomene causes an anthracnose of northern jointvetch, Aeschynomene virginica. Infection components, including lesion number, latent period, lesion expansion rate, and sporulation, were measured in experiments conducted in controlled environments. Two wild-type strains (3-1-3 and CLA 5A), four benomyl-resistant strains (B13, B15, B18 and B21), and four nitrate nonutilizing mutant strains (Nit A, Nit R, Nit L, and Nit T) of the pathogen were tested. Nitrate nonutilizing strains caused significantly fewer lesions on northern jointvetch than did wild-type and benomyl-resistant strains. Latent periods were significantly shorter for the wild-type strain CLA 5A than for most other strains. Lesion expansion rates of all benomyl-resistant strains were significantly slower than those of the wild- type strains. Large variations in sporulation were observed for most strains, and no differences in sporulation were found between wild-type and mutant strains. The usefulness of infection component analysis for the identification of competitiveness of strains of fungal pathogens for biological control of weeds is discussed.

Plant Disease ◽  
1998 ◽  
Vol 82 (4) ◽  
pp. 374-379 ◽  
Author(s):  
Y. Luo ◽  
D. O. TeBeest

The fungus Colletotrichum gloeosporioides f. sp. aeschynomene causes an anthracnose on Aeschynomene virginica and has been used as a biological control agent to control this weed in the United States. The population dynamics of a wild-type strain (3-1-3) and two mutant strains of 3-1-3 of C. gloeosporioides f. sp. aeschynomene, a benomyl-resistant strain (B21) and nitrate-nonutilizing strain (Nit A), were studied in field tests on northern jointvetch in 1994 and 1995 to determine how the strains interacted on infected plants under field conditions. Plants were co-inoculated with strains 3-1-3 and B21, strains 3-1-3 and Nit A, and strains 3-1-3, B21, and Nit A at equal and unequal initial proportions. Plants were grown and maintained under flooded conditions in small wading pools. In co-inoculation of plants with 3-1-3 and B21 from equal initial proportions, the population of 3-1-3 increased slightly until it reached a proportion of 60 to 70%, whereas the population density of B21 reached 30 to 40% at the end of growing season. From unequal initial proportions, the population density of B21 decreased from 90 to about 50%, whereas the 3-1-3 increased from 10 to 50%. The population density of 3-1-3 increased from an equal initial proportion and was significantly greater than that of Nit A on every sampling time. From unequal initial proportions, the population density of 3-1-3 increased from 10 to 90%, whereas that of Nit A declined. In co-inoculation of plants with the three strains, the population density of 3-1-3 was significantly greater than those of the mutant strains at every sampling time. The proportions of mutant strains within the total population of C. gloeosporioides f. sp. aeschynomene on plants varied according to the test conditions and the number and types of strains co-inoculated.


1972 ◽  
Vol 54 (1) ◽  
pp. 8-19 ◽  
Author(s):  
A. Adoutte ◽  
M. Balmefrézol ◽  
J. Beisson ◽  
J. André

The effects on cell structure of 12 hr to 6 days of exposure to erythromycin or chloramphenicol, two antibiotics known to inhibit specifically the mitochondrial protein synthesizing system, have been studied in the ciliate Paramecium aurelia. A wild type strain (sensitive to both antibiotics) and three mutant strains carrying cytoplasmically inherited mutations conferring resistance to one or the other antibiotic have been used In sensitive cells both antibiotics lead to a progressive and profound alteration of mitochondrial structure evidenced by an elongation of the organelle, a considerable decrease in the number of cristae, and the appearance of some abnormal lamellar cristae and of rigid plates of periodic structure. The modifications of cell structure, then, are mainly restricted to mitochondrial cristae. The three resistant mutants studied, on the contrary, retain normal or nearly normal mitochondrial structure in the presence of the antibiotic to which they are resistant. This fact is in good agreement with the postulated location in the mitochondrial DNA of the resistance mutations studied. The results are discussed in the light of present knowledge concerning the function of the mitochondrial protein-synthesizing system.


2015 ◽  
Vol 3 (6) ◽  
Author(s):  
Abhilash Mohan ◽  
Amrisha Bhosle ◽  
Nagasuma Chandra

We report the whole-genome sequences of an Escherichia coli laboratory wild-type strain and trimethoprim-resistant strains (two biological replicates, TMP32XR1 and TMP32XR2). Compared to the U00096.3 strain, a widely used strain in laboratory experiments, the laboratory wild-type strain and the drug-resistant strains evolved from this (TMP32XR1 and TMP32XR2) are 13, 24, and 37 bp longer, respectively.


Genetics ◽  
1989 ◽  
Vol 122 (2) ◽  
pp. 351-361 ◽  
Author(s):  
J E Hamer ◽  
B Valent ◽  
F G Chumley

Abstract Teflon film surfaces are highly conducive to the formation of infection structures (appressoria) in the plant pathogenic fungus, Magnaporthe grisea. We have utilized Teflon films to screen and select for mutants of M. grisea that are defective in appressorium formation. This approach and several others yielded a group of 14 mutants with a similar phenotype. All the mutant strains make abnormally shaped conidia and appressoria. When two mutant strains are crossed, abnormally shaped asci are formed. Ascus shape is normal when a mutant strain is crossed with a wild-type strain. Despite dramatic alterations in cell shape these strains otherwise grow, form conidia, undergo meiosis, and infect plants normally. This mutant phenotype, which we have termed Smo(-), for abnormal spore morphology, segregates in simple Mendelian fashion in crosses with wild-type strains. Some ascospore lethality is associated with smo mutations. In genetic crosses between mutants, smo mutations fail to recombine and do not demonstrate complementation of the abnormal ascus shape phenotype. We conclude that the smo mutations are alleles of a single genetic locus and are recessive with regard to the the ascus shape defect. Mutations at the SMO locus also permit germinating M. grisea conidia to differentiate appressoria on surfaces that are not normally conducive to infection structure formation. A number of spontaneous smo mutations have been recovered. The frequent occurrence of this mutation suggests that the SMO locus may be highly mutable.


1990 ◽  
Vol 36 (7) ◽  
pp. 484-489 ◽  
Author(s):  
G. C. Papavizas ◽  
D. P. Roberts ◽  
K. K. Kim

Aqueous suspensions of conidia of Gliocladium virens strains Gl-3 and Gl-21 were exposed to both ultraviolet radiation and ethyl methanesulfonate. Two mutants of Gl-3 and three of Gl-21 were selected for tolerance to benomyl at 10 μg∙mL−1, as indicated by growth and conidial germination on benomyl-amended potato dextrose agar. The mutants differed considerably from their respective wild-type strains in appearance, growth habit, sporulation, carbon-source utilization, and enzyme activity profiles. Of 10 carbon sources tested, cellobiose, xylose, and xylan were the best for growth, galactose and glucose were intermediate, and arabinose, ribose, and rhamnose were poor sources of carbon. The wild-type strains and the mutants did not utilize cellulose as the sole carbon source for growth. Two benomyl-tolerant mutants of Gl-3 produced less cellulase (β-1,4-glucosidase, carboxymethylcellulase, filter-paper cellulase) than Gl-3. In contrast, mutants of Gl-21 produced more cellulase than the wild-type strain. Only Gl-3 provided control of blight on snapbean caused by Sclerotium rolfsii. Wild-type strain Gl-21 and all mutants from both strains were ineffective biocontrol agents. Key words: Gliocladium, benomyl tolerance, Sclerotium, rhizosphere competence.


2012 ◽  
Vol 56 (8) ◽  
pp. 4146-4153 ◽  
Author(s):  
Zaid Al-Nakeeb ◽  
Ajay Sudan ◽  
Adam R. Jeans ◽  
Lea Gregson ◽  
Joanne Goodwin ◽  
...  

ABSTRACTItraconazole is used for the prevention and treatment of infections caused byAspergillus fumigatus. An understanding of the pharmacodynamics of itraconazole against wild-type and triazole-resistant strains provides a basis for innovative therapeutic strategies for treatment of infections. Anin vitromodel of the human alveolus was used to define the pharmacodynamics of itraconazole. Galactomannan was used as a biomarker. The effect of systemic and airway administration of itraconazole was assessed, as was a combination of itraconazole administered to the airway and systemically administered 5FC. Systemically administered itraconazole against the wild type induced a concentration-dependent decline in galactomannan in the alveolar and endothelial compartments. No exposure-response relationships were apparent for the L98H, M220T, or G138C mutant. The administration of itraconazole to the airway resulted in comparable exposure-response relationships to those observed with systemic therapy. This was achieved without detectable concentrations of drug within the endothelial compartment. The airway administration of itraconazole resulted in a definite but submaximal effect in the endothelial compartment against the L98H mutant. The administration of 5FC resulted in a concentration-dependent decline in galactomannan in both the alveolar and endothelial compartments. The combination of airway administration of itraconazole and systemically administered 5FC was additive. Systemic administration of itraconazole is ineffective against Cyp51 mutants. The airway administration of itraconazole is effective for the treatment of wild-type strains and appears to have some activity against the L98H mutants. Combination with other agents, such as 5FC, may enable the attainment of near-maximal antifungal activity.


AMB Express ◽  
2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Najme Gord Noshahri ◽  
Jamshid Fooladi ◽  
Ulrike Engel ◽  
Delphine Muller ◽  
Michaela Kugel ◽  
...  

Abstractω-Transaminases’ (ω-TAs) importance for synthesizing chiral amines led to the development of different methods to quickly identify and characterize new sources of these enzymes. Here we describe the optimization of growth and induction of such an enzyme in a wild type strain of Bacillus sp. strain BaH (IBRC-M 11337) isolated from Iranian soil in shaking flasks by the response surface methodology (RSM). Optimum conditions were set in a multiplexed bench-top bioreactor system (Sixfors). ω-TA activity of obtained biomass was checked by an innovative efficient colorimetric assay for localizing ω-TAs in crude extracts on acrylamide gel by using ortho-xylylenediamine (OXD) as amino donor. The application of the established OXD assay is thereby expanded from high-throughput activity screenings and colony-based screenings of heterologously expressed mutants to a direct identification of ω-TAs in wild-type strains: This assay can be used to detect the protein band of the respective enzyme in crude extracts of novel isolates by visual inspection of native PAGEs without any upstream protein purification, thus enabling subsequent further investigations of a newly discovered enzyme directly from the crude extract.


1972 ◽  
Vol 18 (6) ◽  
pp. 909-915 ◽  
Author(s):  
A. P. Singh ◽  
K.-J. Cheng ◽  
J. W. Costerton ◽  
E. S. Idziak ◽  
J. M. Ingram

The site of the cell barrier to actinomycin-D uptake was studied using a wild-type Escherichia coli strain P and its cell envelope-defective filamentous mutants, strains 6γ and 12γ, both of which 'leak' β-galactosidase and alkaline phosphatase into the medium during growth indicating both membrane and cell-wall defects. Actinomycin-D entered the cells of these two mutant strains as evidenced by the inhibition of both 14C-uracil incorporation and synthesis of the induced β-galactosidase system. Under similar conditions, no inhibition occurred in the wild-type strain and its sucrose-lysozyme prepared spheroplasts. Actinomycin-D did, however, inhibit the above-mentioned systems in the wild-type sucrose-lysozyme spheroplasts prepared in the presence of 2 mM EDTA. The experimental data indicate that although the cell wall may act as a primary barrier or sieve to actinomycin-D, the cytoplasmic membrane should be considered the final and determinative barrier to this antibiotic.


2005 ◽  
Vol 49 (4) ◽  
pp. 1495-1501 ◽  
Author(s):  
Ayush Kumar ◽  
Elizabeth A. Worobec

ABSTRACT Serratia marcescens is an important nosocomial agent known for causing various infections in immunocompromised individuals. Resistance of this organism to a broad spectrum of antibiotics makes the treatment of infections very difficult. This study was undertaken to identify multidrug resistance efflux pumps in S. marcescens. Three mutant strains of S. marcescens were isolated in vitro by the serial passaging of a wild-type strain in culture medium supplemented with ciprofloxacin, norfloxacin, or ofloxacin. Fluoroquinolone accumulation assays were performed to detect the presence of a proton gradient-dependent efflux mechanism. Two of the mutant strains were found to be effluxing norfloxacin, ciprofloxacin, and ofloxacin, while the third was found to efflux only ofloxacin. A genomic library of S. marcescens wild-type strain UOC-67 was constructed and screened for RND pump-encoding genes by using DNA probes for two putative RND pump-encoding genes. Two different loci were identified: sdeAB, encoding an MFP and an RND pump, and sdeCDE, encoding an MFP and two different RND pumps. Northern blot analysis revealed overexpression of sdeB in two mutant strains effluxing fluoroquinolones. Analysis of the sdeAB and sdeCDE loci in Escherichia coli strain AG102MB, deficient in the RND pump (AcrB), revealed that gene products of sdeAB are responsible for the efflux of a diverse range of substrates that includes ciprofloxacin, norfloxacin, ofloxacin, chloramphenicol, sodium dodecyl sulfate, ethidium bromide, and n-hexane, while those of sdeCDE did not result in any change in susceptibilities to any of these agents.


2018 ◽  
Vol 14 (4) ◽  
pp. 753-760
Author(s):  
Do Thi Tuyen ◽  
Nguyen The Duong ◽  
Le Thanh Hoang

Acarbose has been widely used in the therapy of type II diabetes (non-insulin dependent) because it controls blood sugar contents of patients after meals. Acarbose, a pseudo-oligosaccharide, acts as a competitive -glucosidase inhibitor. Acarbose is produced by the strains of Bacillus, Streptomyces and Actinoplanes sp. The aim of this study was to develop mutagenesis for an Actinoplanes sp. strain and screening for acarbose production. The spores of Actinoplanes sp. KCTC 9161 strain were subjected to be mutated by N-methyl-N'-nitro-N-nitrosoguanidine (NTG) for screening and finding mutant strains that were capable of production of higher acarbose (an inhibitor of α-glucosidase) higher than wild type strain. Firstly, the original NTG solution was prepared in phosphate buffer 0.05 M, pH 6.9 and the safety concentration of NTG was determined at 5 mg/ml. Then, the spores were incubated with different NTG amounts and duration. The living colonies were transferred to fermentation medium. The results obtained showed that 15 mutant strains were produced higher acarbose than wild type when used thin layer chromatography method for analysis and comparing with standard acarbose (Sigma). Three cell lines among total tested 15 mutant lines of Actinoplanes sp. KCTC 9161 produced acarbose at a higher level or indicated a higher inhibitory activity toward α-glucosidase than the original strain. Enzymatic inhibitory ativity of α-glucosidase of three mutant strains (Actinoplanes sp. KCTC- L4, L11, L14) was increased 1.3 fold higher than wild type and Actinoplanes sp. KCTC spores were very sensitive to NTG toxic, 98% spores could not survive at the treatment condition of 50 µg NTG for 30 minutes. In addition, an applicable protocol for mutating Actinoplanes sp. using NTG was suggested for further research.


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