THE EFFECTS OF ERYTHROMYCIN AND CHLORAMPHENICOL ON THE ULTRASTRUCTURE OF MITOCHONDRIA IN SENSITIVE AND RESISTANT STRAINS OF PARAMECIUM

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.

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

Plant Disease ◽

10.1094/pdis.1997.81.4.404 ◽

1997 ◽

Vol 81 (4) ◽

pp. 404-409 ◽

Cited By ~ 12

Author(s):

Y. Luo ◽

D. O. TeBeest

Keyword(s):

Fungal Pathogens ◽

Wild Type Strain ◽

Colletotrichum Gloeosporioides ◽

Wild Type ◽

Biological Control Of Weeds ◽

Lesion Number ◽

Mutant Strains ◽

Controlled Environments ◽

Resistant Strains ◽

Type Strains

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.

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Complete Genome Sequences of an Escherichia coli Laboratory Strain and Trimethoprim-Resistant (TMP32XR) Mutant Strains

Genome Announcements ◽

10.1128/genomea.01434-15 ◽

2015 ◽

Vol 3 (6) ◽

Cited By ~ 2

Author(s):

Abhilash Mohan ◽

Amrisha Bhosle ◽

Nagasuma Chandra

Keyword(s):

Escherichia Coli ◽

Type Strain ◽

Laboratory Experiments ◽

Wild Type Strain ◽

Laboratory Strain ◽

Wild Type ◽

Genome Sequences ◽

Mutant Strains ◽

Resistant Strains ◽

Drug Resistant Strains

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.

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Behavior of a Wild-Type and Two Mutant Strains of Colletotrichum gloeosporioides f. sp. aeschynomene on Northern Jointvetch in the Field

Plant Disease ◽

10.1094/pdis.1998.82.4.374 ◽

1998 ◽

Vol 82 (4) ◽

pp. 374-379 ◽

Cited By ~ 4

Author(s):

Y. Luo ◽

D. O. TeBeest

Keyword(s):

Population Density ◽

Wild Type Strain ◽

Colletotrichum Gloeosporioides ◽

Biological Control Agent ◽

Field Tests ◽

The United States ◽

Control Agent ◽

Sampling Time ◽

Wild Type ◽

Mutant Strains

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.

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Sensitivity of normal and mutant strains of Escherichia coli to actinomycin-D

Canadian Journal of Microbiology ◽

10.1139/m72-139 ◽

1972 ◽

Vol 18 (6) ◽

pp. 909-915 ◽

Cited By ~ 4

Author(s):

A. P. Singh ◽

K.-J. Cheng ◽

J. W. Costerton ◽

E. S. Idziak ◽

J. M. Ingram

Keyword(s):

Escherichia Coli ◽

Cell Wall ◽

Wild Type Strain ◽

Actinomycin D ◽

Cytoplasmic Membrane ◽

Cell Envelope ◽

Coli Strain ◽

Wild Type ◽

Mutant Strains ◽

In The Wild

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.

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Cloning, Sequencing, and Characterization of the SdeAB Multidrug Efflux Pump of Serratia marcescens

Antimicrobial Agents and Chemotherapy ◽

10.1128/aac.49.4.1495-1501.2005 ◽

2005 ◽

Vol 49 (4) ◽

pp. 1495-1501 ◽

Cited By ~ 31

Author(s):

Ayush Kumar ◽

Elizabeth A. Worobec

Keyword(s):

Serratia Marcescens ◽

Type Strain ◽

Wild Type Strain ◽

Genomic Library ◽

Efflux Pump ◽

Sodium Dodecyl ◽

Wild Type ◽

Diverse Range ◽

Mutant Strains ◽

Encoding Genes

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.

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Mutagenesis development of actinoplanes sp. KCTC 9161 by N-methyl-N'-nitro-N-nitrosoguanidine (NTG) and screening for acarbose production

Vietnam Journal of Biotechnology ◽

10.15625/1811-4989/14/4/12310 ◽

2018 ◽

Vol 14 (4) ◽

pp. 753-760

Author(s):

Do Thi Tuyen ◽

Nguyen The Duong ◽

Le Thanh Hoang

Keyword(s):

Type Ii Diabetes ◽

Wild Type Strain ◽

Fermentation Medium ◽

Original Strain ◽

Wild Type ◽

Chromatography Method ◽

Mutant Strains ◽

Insulin Dependent ◽

Mutant Lines ◽

Layer Chromatography

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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A mutation in an exbD gene reduces tagetitoxin production by Pseudomonas syringae pv. tagetis

Canadian Journal of Microbiology ◽

10.1139/w06-060 ◽

2006 ◽

Vol 52 (11) ◽

pp. 1027-1035 ◽

Cited By ~ 1

Author(s):

Hyesuk Kong ◽

Cheryl D Patterson ◽

Robin E Mitchell ◽

Jeffrey S Buyer ◽

M Catherine Aime ◽

...

Keyword(s):

Pseudomonas Syringae ◽

Wild Type Strain ◽

Efflux Pump ◽

Wild Type ◽

Chain Reaction ◽

Sequence Identity ◽

Mutant Strains ◽

Tonb System ◽

Polymerase Chain ◽

High Degree

A mutant of Pseudomonas syringae pv. tagetis EB037 with limited ability to produce tagetitoxin was isolated after transposon mutagenesis and the mutation was characterized. The mutation occurred in a gene with a high degree of sequence identity to exbD. exbD is contiguous with tonB and exbB upstream and with a gene for a TonB-dependent receptor downstream. Using reverse transcription – polymerase chain reaction with RNA from the wild-type and exbD mutant strains, we demonstrated that the mutation in exbD did not have a polar affect on the expression of downstream genes. The exbD mutant was able to grow well in conditions where iron is not freely available. Siderophore production by the exbD mutant was similar to that of the wild-type strain. We conclude that the mutation in exbD disrupts tagetitoxin production without compromising iron metabolism. The results indicate that tagetitoxin export by P. syringae pv. tagetis involves an efflux pump that requires a functional TonB system that is not essential for normal iron metabolism.Key words: Pseudomonas syringae pv. tagetis, Pseudomonas putida, tagetitoxin, exbD, exbB, tonB, TonB system, Helianthus annuus L.

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Inactivation of the Crp/Fnr Family of Regulatory Genes in Listeria monocytogenes Strain F2365 Does Not Alter Its Heat Resistance at 60°C†

Journal of Food Protection ◽

10.4315/0362-028x-69.11.2758 ◽

2006 ◽

Vol 69 (11) ◽

pp. 2758-2760 ◽

Cited By ~ 2

Author(s):

DARRELL O. BAYLES ◽

GAYLEN A. UHLICH

Keyword(s):

Listeria Monocytogenes ◽

Heat Resistance ◽

Thermal Tolerance ◽

Type Strain ◽

Transcriptional Control ◽

Wild Type Strain ◽

Gene Cassette ◽

Wild Type ◽

Mutant Strains ◽

Virulence Regulator

A surprising facet of the Listeria monocytogenes genome is the presence of 15 genes that code for regulators in the Crp/Fnr family and include the virulence regulator PrfA. The genes under the transcriptional control of these regulators are currently undetermined, with the exception of some genes controlled by the major virulence regulator PrfA. Using 12 strains of L. monocytogenes, each with an inserted gene cassette that interrupts and renders nonfunctional a different L. monocytogenes strain F2365 Crp/Fnr regulator, we heat challenged each strain at 60°C with an immersed-coil heating apparatus, modeled the survivor data to calculate the underlying mean and mode of the heat resistance distribution for each strain, and compared the thermal tolerance of each mutant to the wild-type strain to determine if any of the Crp/Fnr mutants demonstrated altered heat tolerance. All 12 of the Crp/Fnr mutant strains tested had heat resistance characteristics similar to the wild-type strain (P > 0.05), indicating that mutations in these Crp/Fnr genes neither increased nor decreased the sensitivity of L. monocytogenes strain F2365 to mild heat.

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Role of CpALS4790 and CpALS0660 in Candida parapsilosis Virulence: Evidence from a Murine Model of Vaginal Candidiasis

Journal of Fungi ◽

10.3390/jof6020086 ◽

2020 ◽

Vol 6 (2) ◽

pp. 86

Author(s):

Marina Zoppo ◽

Fabrizio Fiorentini ◽

Cosmeri Rizzato ◽

Mariagrazia Di Luca ◽

Antonella Lupetti ◽

...

Keyword(s):

Cell Wall ◽

Murine Model ◽

Type Strain ◽

Wild Type Strain ◽

Candida Parapsilosis ◽

Vaginal Candidiasis ◽

Phenotypic Characterization ◽

Wild Type ◽

Mutant Strains

The Candida parapsilosis genome encodes for five agglutinin-like sequence (Als) cell-wall glycoproteins involved in adhesion to biotic and abiotic surfaces. The work presented here is aimed at analyzing the role of the two still uncharacterized ALS genes in C. parapsilosis, CpALS4790 and CpALS0660, by the generation and characterization of CpALS4790 and CpALS066 single mutant strains. Phenotypic characterization showed that both mutant strains behaved as the parental wild type strain regarding growth rate in liquid/solid media supplemented with cell-wall perturbing agents, and in the ability to produce pseudohyphae. Interestingly, the ability of the CpALS0660 null mutant to adhere to human buccal epithelial cells (HBECs) was not altered when compared with the wild-type strain, whereas deletion of CpALS4790 led to a significant loss of the adhesion capability. RT-qPCR analysis performed on the mutant strains in co-incubation with HBECs did not highlight significant changes in the expression levels of others ALS genes. In vivo experiments in a murine model of vaginal candidiasis indicated a significant reduction in CFUs recovered from BALB/C mice infected with each mutant strain in comparison to those infected with the wild type strain, confirming the involvement of CpAls4790 and CpAls5600 proteins in C. parapsilosis vaginal candidiasis in mice.

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The RcsCB His-Asp Phosphorelay System Is Essential To Overcome Chlorpromazine-Induced Stress in Escherichia coli

Journal of Bacteriology ◽

10.1128/jb.184.10.2850-2853.2002 ◽

2002 ◽

Vol 184 (10) ◽

pp. 2850-2853 ◽

Cited By ~ 39

Author(s):

Annie Conter ◽

Rachel Sturny ◽

Claude Gutierrez ◽

Kaymeuang Cam

Keyword(s):

Escherichia Coli ◽

Type Strain ◽

Wild Type Strain ◽

Cell Envelope ◽

Wild Type ◽

E Coli ◽

Induced Stress ◽

Mutant Strains ◽

Molecular Nature

ABSTRACT The RcsCB His-Asp phosphorelay system regulates the expression of several genes of Escherichia coli, but the molecular nature of the inducing signal is still unknown. We show here that treatment of an exponentially growing culture of E. coli with the cationic amphipathic compound chlorpromazine (CPZ) stimulates expression of a set of genes positively regulated by the RcsCB system. This induction is abolished in rcsB or rcsC mutant strains. In addition, treatment with CPZ inhibits growth. The wild-type strain is able to recover from this inhibition and resume growth after a period of adaptation. In contrast, strains deficient in the RcsCB His-Asp phosphorelay system are hypersensitive to CPZ. These results suggest that cells must express specific RcsCB-regulated genes in order to cope with the CPZ-induced stress. This is the first report of the essential role of the RcsCB system in a stress situation. These results also strengthen the notion that alterations of the cell envelope induce a signal recognized by the RcsC sensor.

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