scholarly journals Transcriptional response of Fusarium oxysporum and Neocosmospora solani challenged with amphotericin B or posaconazole

Microbiology ◽  
2020 ◽  
Vol 166 (10) ◽  
pp. 936-946 ◽  
Author(s):  
A. Castillo-Castañeda ◽  
S. J. Cañas-Duarte ◽  
M. Guevara-Suarez ◽  
J. Guarro ◽  
S. Restrepo ◽  
...  
Keyword(s):  
Fusarium Oxysporum ◽  
Amphotericin B ◽  
Molecular Mechanisms ◽  
Transcriptional Response ◽  
Resistance Mechanisms ◽  
Transport Processes ◽  
Major Facilitator Superfamily ◽  
Ergosterol Synthesis ◽  
Transcriptional Changes ◽  
Major Facilitator

Some species of fusaria are well-known pathogens of humans, animals and plants. Fusarium oxysporum and Neocosmospora solani (formerly Fusarium solani) cause human infections that range from onychomycosis or keratitis to severe disseminated infections. In general, these infections are difficult to treat due to poor therapeutic responses in immunocompromised patients. Despite that, little is known about the molecular mechanisms and transcriptional changes responsible for the antifungal resistance in fusaria. To shed light on the transcriptional response to antifungals, we carried out the first reported high-throughput RNA-seq analysis for F. oxysporum and N. solani that had been exposed to amphotericin B (AMB) and posaconazole (PSC). We detected significant differences between the transcriptional profiles of the two species and we found that some oxidation-reduction, metabolic, cellular and transport processes were regulated differentially by both fungi. The same was found with several genes from the ergosterol synthesis, efflux pumps, oxidative stress response and membrane biosynthesis pathways. A significant up-regulation of the C-22 sterol desaturase (ERG5), the sterol 24-C-methyltransferase (ERG6) gene, the glutathione S-transferase (GST) gene and of several members of the major facilitator superfamily (MSF) was demonstrated in this study after treating F. oxysporum with AMB. These results offer a good overview of transcriptional changes after exposure to commonly used antifungals, highlights the genes that are related to resistance mechanisms of these fungi, which will be a valuable tool for identifying causes of failure of treatments.

scholarly journals New Plasmid-Mediated Fluoroquinolone Efflux Pump, QepA, Found in an Escherichia coli Clinical Isolate

2007 ◽  
Vol 51 (9) ◽  
pp. 3354-3360 ◽  
Author(s):  
Kunikazu Yamane ◽  
Jun-ichi Wachino ◽  
Satowa Suzuki ◽  
Kouji Kimura ◽  
Naohiro Shibata ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Molecular Mechanisms ◽  
Efflux Pump ◽  
Resistance Mechanisms ◽  
Major Facilitator Superfamily ◽  
Gene Encoding ◽  
Resistance Level ◽  
E Coli ◽  
Susceptibility Tests ◽  
Major Facilitator

ABSTRACT Plasmid-mediated Qnr and AAC(6′)-Ib-cr have been recognized as new molecular mechanisms affecting fluoroquinolone (FQ) resistance. C316, an Escherichia coli strain demonstrating resistance to various FQs, was isolated in Japan. Resistance to FQs was augmented in an E. coli CSH2 transconjugant, but PCR failed to detect qnr genes, suggesting the presence of novel plasmid-mediated FQ resistance mechanisms. Susceptibility tests, DNA manipulation, and analyses of the gene and its product were performed to characterize the genetic determinant. A novel FQ-resistant gene, qepA, was identified in a plasmid, pHPA, of E. coli C316, and both qepA and rmtB genes were mediated by a probable transposable element flanked by two copies of IS26. Levels of resistance to norfloxacin, ciprofloxacin, and enrofloxacin were significantly elevated in E. coli transformants harboring qepA under AcrB-TolC-deficient conditions. QepA showed considerable similarities to transporters belonging to the 14-transmembrane-segment family of environmental actinomycetes. The effect of carbonyl cyanide m-chlorophenylhydrazone (CCCP) on accumulation of norfloxacin was assayed in a qepA-harboring E. coli transformant. The intracellular accumulation of norfloxacin was decreased in a qepA-expressing E. coli transformant, but this phenomenon was canceled by CCCP. The augmented FQ resistance level acquired by the probable intergeneric transfer of a gene encoding a major facilitator superfamily-type efflux pump from some environmental microbes to E. coli was first identified. Surveillance of the qepA-harboring clinical isolates should be encouraged to minimize further dissemination of the kind of plasmid-dependent FQ resistance determinants among pathogenic microbes.

scholarly journals ‘Candidatus Phytoplasma solani’ interferes with the distribution and uptake of iron in tomato

BMC Genomics ◽  
2019 ◽  
Vol 20 (1) ◽  
Author(s):  
Sara Buoso ◽  
Laura Pagliari ◽  
Rita Musetti ◽  
Marta Martini ◽  
Fabio Marroni ◽  
...  
Keyword(s):  
Plant Pathogens ◽  
Molecular Mechanisms ◽  
Transcriptional Response ◽  
Transcriptome Profiling ◽  
Transport Processes ◽  
Fe Deficiency ◽  
Cultivated Plants ◽  
Chlorophyll Metabolism ◽  
Wide Range ◽  
Phytoplasma Infection

Abstract Background ‘Candidatus Phytoplasma solani’ is endemic in Europe and infects a wide range of weeds and cultivated plants. Phytoplasmas are prokaryotic plant pathogens that colonize the sieve elements of their host plant, causing severe alterations in phloem function and impairment of assimilate translocation. Typical symptoms of infected plants include yellowing of leaves or shoots, leaf curling, and general stunting, but the molecular mechanisms underlying most of the reported changes remain largely enigmatic. To infer a possible involvement of Fe in the host-phytoplasma interaction, we investigated the effects of ‘Candidatus Phytoplasma solani’ infection on tomato plants (Solanum lycopersicum cv. Micro-Tom) grown under different Fe regimes. Results Both phytoplasma infection and Fe starvation led to the development of chlorotic leaves and altered thylakoid organization. In infected plants, Fe accumulated in phloem tissue, altering the local distribution of Fe. In infected plants, Fe starvation had additive effects on chlorophyll content and leaf chlorosis, suggesting that the two conditions affected the phenotypic readout via separate routes. To gain insights into the transcriptional response to phytoplasma infection, or Fe deficiency, transcriptome profiling was performed on midrib-enriched leaves. RNA-seq analysis revealed that both stress conditions altered the expression of a large (> 800) subset of common genes involved in photosynthetic light reactions, porphyrin / chlorophyll metabolism, and in flowering control. In Fe-deficient plants, phytoplasma infection perturbed the Fe deficiency response in roots, possibly by interference with the synthesis or transport of a promotive signal transmitted from the leaves to the roots. Conclusions ‘Candidatus Phytoplasma solani’ infection changes the Fe distribution in tomato leaves, affects the photosynthetic machinery and perturbs the orchestration of root-mediated transport processes by compromising shoot-to-root communication.

scholarly journals Transcriptomic Evidence of Molecular Mechanisms Underlying the Response of Lactobacillus plantarum WCFS1 to Hydroxytyrosol

Antioxidants ◽  
2020 ◽  
Vol 9 (5) ◽  
pp. 442
Author(s):  
Inés Reverón ◽  
Laura Plaza-Vinuesa ◽  
Laura Santamaría ◽  
Juan Carlos Oliveros ◽  
Blanca de las Rivas ◽  
...  
Keyword(s):  
Lactobacillus Plantarum ◽  
Molecular Mechanisms ◽  
Stringent Response ◽  
Antioxidant Response ◽  
Major Facilitator Superfamily ◽  
Subcellular Compartment ◽  
Cell Wall Biogenesis ◽  
Expression Of Genes ◽  
Major Facilitator ◽  
Genome Scale

This study was aimed to gain new insights into the molecular mechanisms used by Lactobacillus plantarum WCFS1 to respond to hydroxytyrosol (HXT), one of the main and health-relevant plant phenolics present in olive oil. To this goal, whole genome transcriptomic profiling was used to better understand the contribution of differential gene expression in the adaptation to HXT by this microorganism. The transcriptomic profile reveals an HXT-triggered antioxidant response involving genes from the ROS (reactive oxygen species) resistome of L. plantarum, genes coding for H2S-producing enzymes and genes involved in the response to thiol-specific oxidative stress. The expression of a set of genes involved in cell wall biogenesis was also upregulated, indicating that this subcellular compartment was a target of HXT. The expression of several MFS (major facilitator superfamily) efflux systems and ABC-transporters was differentially affected by HXT, probably to control its transport across the membrane. L. plantarum transcriptionally reprogrammed nitrogen metabolism and involved the stringent response (SR) to adapt to HXT, as indicated by the reduced expression of genes involved in cell proliferation or related to the metabolism of (p)ppGpp, the molecule that triggers the SR. Our data have identified, at genome scale, the antimicrobial mechanisms of HXT action as well as molecular mechanisms that potentially enable L. plantarum to cope with the effects of this phenolic compound.

scholarly journals Resistance and Adaptation to Quinidine in Saccharomyces cerevisiae: Role of QDR1 (YIL120w), Encoding a Plasma Membrane Transporter of the Major Facilitator Superfamily Required for Multidrug Resistance

2001 ◽  
Vol 45 (5) ◽  
pp. 1528-1534 ◽  
Author(s):  
Patrı́cia A. Nunes ◽  
Sandra Tenreiro ◽  
Isabel Sá-Correia
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Plasma Membrane ◽  
Multidrug Resistance ◽  
Fluorescent Protein ◽  
Resistance Mechanisms ◽  
Major Facilitator Superfamily ◽  
Yeast Cells ◽  
Detectable Effect ◽  
Protein Fusion ◽  
Major Facilitator

ABSTRACT As predicted based on structural considerations, we show results indicating that the member of the major facilitator superfamily encoded by Saccharomyces cerevisiae open reading frameYIL120w is a multidrug resistance determinant. Yil120wp was implicated in yeast resistance to ketoconazole and quinidine, but not to the stereoisomer quinine; the gene was thus named QDR1. Qdr1p was proved to alleviate the deleterious effects of quinidine, revealed by the loss of cell viability following sudden exposure of the unadapted yeast population to the drug, and to allow the earlier eventual resumption of exponential growth under quinidine stress. However, QDR1 gene expression had no detectable effect on the susceptibility of yeast cells previously adapted to quinidine. Fluorescence microscopy observation of the distribution of the Qdr1-green fluorescent protein fusion protein in living yeast cells indicated that Qdr1p is a plasma membrane protein. We also show experimental evidence indicating that yeast adaptation to growth with quinidine involves the induction of active expulsion of the drug from preloaded cells, despite the fact that this antiarrhythmic and antimalarial quinoline ring-containing drug is not present in the yeast natural environment. However, we were not able to prove that Qdr1p is directly implicated in this export. Results clearly suggest that there are other unidentified quinidine resistance mechanisms that can be used in the absence of QDR1.

scholarly journals Proteomic Analysis of Banana Vascular Sap Provides Insight Into Resistance Mechanisms to Fusarium Oxysporum F. Sp. Cubense Tropical Race 4

2021 ◽  
Author(s):  
Lei Zhang ◽  
Lina Liu ◽  
Shu Li ◽  
Alberto Cenci ◽  
Mathieu Rouard ◽  
...  
Keyword(s):  
Fusarium Oxysporum ◽  
Fusarium Wilt ◽  
Proteomic Analysis ◽  
Molecular Mechanisms ◽  
Rna Binding ◽  
Resistance Mechanisms ◽  
Induced Response ◽  
Ubiquitin Ligase E3 ◽  
Protein Response ◽  
Race 4

Abstract Background: Fusarium oxysporum f. sp. cubense tropical race 4 (Foc TR4) is the causal agent of Fusarium wilt, and is the most destructive soil-borne and vascular invasive fungus of banana. The sap circulating in vascular cells transports proteins including those that might be involved in disease-resistance processes. However, there is no research to analyze changes in banana vascular sap protein response to TR4 to date. Results: To gain an integrated understanding of differential protein abundance in banana vascular sap during TR4 infection, we performed a comparative proteomic analysis of vascular sap of the resistant ‘Pahang’ and the susceptible ‘Brazilian’ bananas inoculated with TR4. We identified 129 differential expression proteins (DEPs) between resistant and susceptible tested combinations. Of these DEPs, hypersensitive-induced response protein 1 (HIR1) and E3 ubiquitin ligase (E3) decreased in abundance in Pahang with no change in Brazilian under TR4 infection; chalcone isomerase (CHI) and glycine-rich RNA-binding protein (GRP) increased in abundance in Pahang but no significant changes in Brazilian under TR4 infection; carboxylesterase (CXE) and GDSL lipase (GLIP) were specifically in higher abundance in Pahang response to TR4 compared to that of Brazilian. It suggested that these proteins played important roles in bananas against TR4. Conclusions: Our study identified 129 DEPs in vascular sap between resistant and susceptible tested combinations. Of which, HIR1, E3, CHI, GRP, CXE and GLIP played important roles in bananas response to TR4. To our knowledge, this is first report to analyze changes in banana vascular sap proteins in response to TR4, which help us to explore the molecular mechanisms of banana defense to Fusarium wilt.

scholarly journals Transcriptome analysis reveals major transcriptional changes during regrowth after mowing of red clover (Trifolium pratense)

2020 ◽  
Author(s):  
Denise B Herbert ◽  
Thomas Gross ◽  
Oliver Rupp ◽  
Annette Becker
Keyword(s):  
Nutritional Value ◽  
Molecular Mechanisms ◽  
Trifolium Pratense ◽  
Transcriptional Response ◽  
Red Clover ◽  
Biotic And Abiotic Stress ◽  
Developmental Processes ◽  
Developmental Program ◽  
Transcriptional Changes ◽  
Biomass Loss

Abstract BackgroundRed clover (Trifolium pratense) is globally used as a fodder plant due its high nutritional value and soil improving qualities. In response to mowing, red clover exhibits specific morphological traits to compensate the loss of biomass. The morphological reaction is well described, but the underlying molecular mechanisms and its role for plants grown in the field are unclear. ResultsHere, we characterize the global transcriptional response to mowing of red clover by comparing plants grown under greenhouse conditions with plants growing on agriculturally used fields. Unexpectedly, we found that biotic and abiotic stress related changes of plants grown in the field overlay their regrowth related transcriptional changes and characterized transcription related protein families involved in these processes. Further, we can show that gibberellins, among other phytohormones, also contribute to the developmental processes related to regrowth after biomass-loss. ConclusionsOur findings show that massive biomass loss triggers less transcriptional changes in field grown plants than their struggle with biotic and abiotic stresses and that gibberellins also play a role in the developmental program related to regrowth after mowing in red clover. Our results provide first insights into the physiological and developmental processes of mowing on red clover and may serve as a base for red clover yield improvement.

Molecular mechanisms associated with the resistance of Rhizoctonia solani AG-4 isolates to the succinate dehydrogenase inhibitor, thifluzamide

2021 ◽  
Author(s):  
Can Zhao ◽  
Yuting Li ◽  
Zhijian Liang ◽  
Lihong Gao ◽  
Chenggui Han ◽  
...  
Keyword(s):  
Succinate Dehydrogenase ◽  
Molecular Mechanisms ◽  
Major Facilitator Superfamily ◽  
Cross Resistance ◽  
Active Efflux ◽  
Fitness Evaluation ◽  
Reverse Transcription Pcr ◽  
Major Facilitator ◽  
Median Effective Concentration

Thifluzamide, a succinate dehydrogenase (SDH) inhibitor, possesses high activity against Rhizoctonia. In this study, 144 R. solani AG-4 (4HGI, 4HGII, and 4HGIII) isolates, the predominate pathogen associated with sugar beet seedling damping-off, were demonstrated to be sensitive to thifluzamide with a calculated mean median effective concentration of 0.0682 ± 0.0025 μg/mL. Thifluzamide-resistant isolates were generated using fungicide-amended media, resulting in four AG-4HGI isolates and eight AG-4HGII isolates with stable resistance and almost no loss in fitness. Evaluation of cross-resistance of the twelve thifluzamide-resistant isolates and their corresponding parental-sensitive isolates revealed a moderately positive correlation between thifluzamide resistance and the level of resistance to eight other fungicides from three groups, the exception being fludioxonil. An active efflux of fungicide through ATP-binding cassette and major facilitator superfamily transporters was found to be correlated to the resistance of R. solani AG-4HGII isolates to thifluzamide based on RNA-sequencing and quantitative reverse transcription-PCR analyses. Sequence analysis of sdhA, sdhB, sdhC, and sdhD revealed replacement of isoleucine by phenylalanine at position 61 in SDHC in nine of the twelve generated thifluzamide-resistant isolates. No other mutations were found in any of the other genes. Collectively, the data indicate that the active efflux of fungicide and a point mutation in sdhC may contribute to the resistance of R. solani AG-4HGI and AG-4HGII isolates to thifluzamide in vitro. This is the first characterization of the potential molecular mechanism associated with the resistance of R. solani AG-4 isolates to thifluzamide, and provides practical guidance for the use of this fungicide.

scholarly journals The Role of fnx1, a Fission Yeast Multidrug Resistance Protein, in the Transition of Cells to a Quiescent G0 State

1998 ◽  
Vol 18 (9) ◽  
pp. 5239-5246 ◽  
Author(s):  
Krassen Dimitrov ◽  
Shelley Sazer
Keyword(s):  
Multidrug Resistance ◽  
Molecular Mechanisms ◽  
Morphological Changes ◽  
Sequence Similarity ◽  
Cell Communication ◽  
Major Facilitator Superfamily ◽  
Natural Habitats ◽  
Resistance Protein ◽  
Major Facilitator

ABSTRACT Most microorganisms live in conditions of nutrient limitation in their natural habitats. When exposed to these conditions they respond with physiological and morphological changes that enable them to survive. To obtain insights into the molecular mechanisms of this response a systematic genetic screen was performed to identify genes that when overexpressed can induce a starvation-like response in the yeast species Schizosaccharomyces pombe. One gene that meets these criteria, fnx1 +, induces, transcriptionally correlates with, and is required for the entry into the quiescent G0 state that is normally induced by nitrogen starvation. fnx1 + encodes a protein with sequence similarity to the proton-driven plasma membrane transporters from the multidrug resistance group of the major facilitator superfamily of proteins. We propose that fnx1 +plays a role in the entry into G0, possibly by facilitating the release of a signaling substance into the environment as a means of cell-to-cell communication.

Sign in / Sign up

Export Citation Format

Share Document