Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Efficacy of combined formulations of fungicides with different modes of action in controlling botrytis gray mold disease in chickpea.

ABSTRACT: Botrytis gray mold (BGM) caused by Botrytis cinerea Pers. Ex. Fr. is an extremely devastating disease of chickpea (Cicer arietinum L.) and has a regional as well as an international perspective. Unfortunately, nonchemical methods for its control are weak and ineffective. In order to identify an effective control measure, six fungicides with different modes of action were evaluated on a BGM susceptible chickpea variety BARIchhola-1 at a high BGM incidence location (Madaripur) in Bangladesh for three years (2008, 2009, and 2010). Among the six fungicides tested, one was protectant [Vondozeb 42SC, a.i. mancozeb (0.2%)], two systemic [Bavistin 50 WP, a.i. carbendazim (0.2%), and Protaf 250EC, propiconazole (0.05%)], and three combination formulations [Acrobat MZ690, dimethomorph 9% + mancozeb 60%, (0.2%); Secure 600 WG, phenomadone + mancozeb (0.2%); and Companion, mancozeb 63% + carbendazim 12% (0.2%)]. The results showed superiority of combination formulations involving both protectant and systemic fungicides over the sole application of either fungicide separately. Among the combination fungicides, Companion was most effective, resulting in the lowest disease severity (3.33 score on 1-9 scale) and the highest increase (38%) of grain yield in chickpea. Therefore, this product could be preferred over the sole application of either solo protectant or systemic fungicides to reduce yield losses and avoid fungicide resistance.

SUBMITTER: Rashid MH

PROVIDER: S-EPMC3958676 | biostudies-other | 2014

REPOSITORIES: biostudies-other

ACCESS DATA

Json Xml

Similar Datasets

Metabolic Phenotype Characterization of Botrytis cinerea, the Causal Agent of Gray Mold.

Project description:Botrytis cinerea, which causes gray mold, is an important pathogen in four important economic crops, tomato, tobacco, cucumber and strawberry, in China and worldwide. Metabolic phenomics data on B. cinerea isolates from these four crops were characterized and compared for 950 phenotypes with a BIOLOG Phenotype MicroArray (PM). The results showed that the metabolic fingerprints of the four B. cinerea isolates were similar to each other with minimal differences. B. cinerea isolates all metabolized more than 17% of the tested carbon sources, 63% of the amino acid nitrogen substrates, 80% of the peptide nitrogen substrates, 93% of the phosphorus substrates, and 97% of the sulfur substrates. Carbon substrates of organic acids and carbohydrates, and nitrogen substrates of amino acids and peptides were the significant utilization patterns for B. cinerea. Each B. cinerea isolate contained 94 biosynthetic pathways. These isolates showed a large range of adaptabilities and were still able to metabolize substrates in the presence of the osmolytes, including up to 6% potassium chloride, 10% sodium chloride, 5% sodium sulfate, 6% sodium formate, 20% ethylene glycol, and 3% urea. These isolates all showed active metabolism in environments with pH values from 3.5 to 8.5 and exhibited decarboxylase activities. These characterizations provide a theoretical basis for the study of B. cinerea in biochemistry and metabolic phenomics and provide valuable clues to finding potential new ways to manage gray mold.

| S-EPMC5859374 | biostudies-literature

Biological Control of Tomato Gray Mold Caused by Botrytis Cinerea with the Entomopathogenic Fungus Metarhizium Anisopliae.

Project description:Gray mold disease caused by Botrytis cinerea is a devastating disease that leads to serious financial loss. In this study, the entomopathogenic fungus Metarhizium anisopliae that acts against the gray mold pathogen B. cinerea was evaluated. M. anisopliae produced a significant inhibition zone in front of the B. cinerea colony in the dual culture test. In addition, volatile organic compounds generated by M. anisopliae were shown to have an inhibitory effect on B. cinerea mycelia growth and reduced 41% of gray mold severity of postharvest tomatoes. The 10% concentration of the culture filtrate of M. anisopliae inhibited 88.62% of colony radial growth as well as 63.85% of sclerotia germination and all conidia germination of B. cinerea. Furthermore, the culture filtrate of M. anisopliae retained its inhibitory effect against the radial growth of B. cinerea even after heating for 15 min at 100 °C. Feasible mechanisms of M. anisopliae involved in the control of B. cinerea were explored, and it was demonstrated that the plasma membrane of B. cinerea conidia was damaged by the product of metabolism of M. anisopliae. In addition, after treating with culture filtrate of M. anisopliae, the B. cinerea phenotype was shown to be abnormal, and cell organelles of B. cinerea mycelia were damaged significantly. A significant control efficacy of M. anisopliae against tomato gray mold was detected on both the detached leaf assay (84.24%) as well as the whole plant (72.38%). In addition, a 78% reduction in tomato fruit mold was detected at a 10% treated concentration of M. anisopliae. These findings suggest that M. anisopliae possesses potential as a biocontrol agent against tomato gray mold in the greenhouse and during the postharvest stage.

| S-EPMC7157576 | biostudies-literature

A novel biocontrol agent Bacillus velezensis K01 for management of gray mold caused by Botrytis cinerea.

Project description:Gray mold is a destructive plant disease caused by a fungal pathogen Botrytis cinerea. The use of plant growth promoting rhizobacteria (PGPR) has proven to be a promising method to control this disease. Bacillus velezensis K01 was isolated from the rhizosphere of planting tomatoes. Strain K01 has a range of roles, including the ability to solubilize phytate phosphorus, stimulate resistant response, and produce indoleacetic acid (IAA), protease, cellulase, and antimicrobial substances. Strain K01 was found to inhibit 12 phytopathogenic fungi and 5 phytopathogenic bacteria. Specially, strain K01 demonstrated a biocontrol efficiency of over 78% against gray mold caused by B. cinerea on the leaves and fruits of tomato and pepper. Additionally, K01 was found to promote the growth of maize seedlings. Further genomic analysis revealed that K01 belongs to B. velezensis, which is consistent with phylogenetic analysis, average nucleotide polymorphism (ANI), and digital DNA-DNA hybridization (dDDH). The genome of strain K01 had a size of 3,927,799 bp and deduced 3866 predicted genes, with an average guanine-cytosine (GC) content of 46.5%. Based on the analyses of genomic secondary metabolites, over 18.4% of the genome was annotated to 12 gene clusters related to antimicrobial metabolite synthesis. Additionally, genome annotation and comparative genomics identified several genes associated with plant growth promotion and environmental adaption. These findings suggest that B. velezensis K01 has the potential to serve as a new biocontrol agent for management of gray mold on tomato and pepper.

| S-EPMC10465465 | biostudies-literature

Cyclophilin BcCyp2 Regulates Infection-Related Development to Facilitate Virulence of the Gray Mold Fungus Botrytis cinerea.

Project description:Cyclophilin (Cyp) and Ca2+/calcineurin proteins are cellular components related to fungal morphogenesis and virulence; however, their roles in mediating the pathogenesis of Botrytis cinerea, the causative agent of gray mold on over 1000 plant species, remain largely unexplored. Here, we show that disruption of cyclophilin gene BcCYP2 did not impair the pathogen mycelial growth, osmotic and oxidative stress adaptation as well as cell wall integrity, but delayed conidial germination and germling development, altered conidial and sclerotial morphology, reduced infection cushion (IC) formation, sclerotial production and virulence. Exogenous cyclic adenosine monophosphate (cAMP) rescued the deficiency of IC formation of the ?Bccyp2 mutants, and exogenous cyclosporine A (CsA), an inhibitor targeting cyclophilins, altered hyphal morphology and prevented host-cell penetration in the BcCYP2 harboring strains. Moreover, calcineurin-dependent (CND) genes are differentially expressed in strains losing BcCYP2 in the presence of CsA, suggesting that BcCyp2 functions in the upstream of cAMP- and Ca2+/calcineurin-dependent signaling pathways. Interestingly, during IC formation, expression of BcCYP2 is downregulated in a mutant losing BcJAR1, a gene encoding histone 3 lysine 4 (H3K4) demethylase that regulates fungal development and pathogenesis, in B. cinerea, implying that BcCyp2 functions under the control of BcJar1. Collectively, our findings provide new insights into cyclophilins mediating the pathogenesis of B. cinerea and potential targets for drug intervention for fungal diseases.

| S-EPMC7914984 | biostudies-literature

Exploring mechanisms of resistance to respiratory inhibitors in field strains of Botrytis cinerea, the causal agent of gray mold.

Project description:Respiratory inhibitors are among the fungicides most widely used for disease control on crops. Most are strobilurins and carboxamides, inhibiting the cytochrome b of mitochondrial complex III and the succinate dehydrogenase of mitochondrial complex II, respectively. A few years after the approval of these inhibitors for use on grapevines, field isolates of Botrytis cinerea, the causal agent of gray mold, resistant to one or both of these classes of fungicide were recovered in France and Germany. However, little was known about the mechanisms underlying this resistance in field populations of this fungus. Such knowledge could facilitate resistance risk assessment. The aim of this study was to investigate the mechanisms of resistance occurring in B. cinerea populations. Highly specific resistance to strobilurins was correlated with a single mutation of the cytb target gene. Changes in its intronic structure may also have occurred due to an evolutionary process controlling selection for resistance. Specific resistance to carboxamides was identified for six phenotypes, with various patterns of resistance levels and cross-resistance. Several mutations specific to B. cinerea were identified within the sdhB and sdhD genes encoding the iron-sulfur protein and an anchor protein of the succinate dehydrogenase complex. Another as-yet-uncharacterized mechanism of resistance was also recorded. In addition to target site resistance mechanisms, multidrug resistance, linked to the overexpression of membrane transporters, was identified in strains with low to moderate resistance to several respiratory inhibitors. This diversity of resistance mechanisms makes resistance management difficult and must be taken into account when developing strategies for Botrytis control.

| S-EPMC2950445 | biostudies-literature

Involvement of the Autophagy Protein Atg6 in Development and Virulence in the Gray Mold Fungus Botrytis cinerea.

Project description:Gray mold caused by Botrytis cinerea is a devastating disease that leads to huge economic losses worldwide. Autophagy is an evolutionarily conserved process that maintains intracellular homeostasis through self-eating. In this study, we identified and characterized the biological function of the autophagy-related protein Atg6 in B. cinerea. Targeted deletion of the BcATG6 gene showed block of autophagy and several phenotypic defects in aspects of mycelial growth, conidiation, sclerotial formation and virulence. All of the phenotypic defects were restored by targeted gene complementation. Taken together, these results suggest that BcAtg6 plays important roles in the regulation of various cellular processes in B. cinerea.

| S-EPMC8712751 | biostudies-literature

The VELVET complex in the gray mold fungus Botrytis cinerea: impact of BcLAE1 on differentiation, secondary metabolism and virulence

2015-02-01 | GSE63021 | GEO

The VELVET complex in the gray mold fungus Botrytis cinerea: impact of BcLAE1 on differentiation, secondary metabolism and virulence

Project description:Full transcriptomes of the Botrytis cinerea wild-type strain B0510 and the null-mutants deltaBcVEL1 and deltaBcLAE1, cultured onto solid grape juice medium with cellophane overlays , were compared to identify BcVEL1 or/and BcLAE1-dependent genes. The Botrytis cinerea wild-type strain and the null-mutants deltaBcVEL1 and BcLAE1 were cultured for 48h onto solid grape juice medium with cellophane overlays. 4 replicates were performed. The 12 total-RNA samples (3 strains* 4 replicates) were used for hybridization on NimbleGen 4plex gene expression arrays (20,885 gene models from Botrytis cinerea with three 60-mer probes per gene).

2015-02-01 | E-GEOD-63021 | biostudies-arrayexpress

Potential Applications and Antifungal Activities of Engineered Nanomaterials against Gray Mold Disease Agent Botrytis cinerea on Rose Petals.

Project description:Nanoparticles (NPs) have great potential for use in the fields of biomedicine, building materials, and environmental protection because of their antibacterial properties. However, there are few reports regarding the antifungal activities of NPs on plants. In this study, we evaluated the antifungal roles of NPs against Botrytis cinerea, which is a notorious worldwide fungal pathogen. Three common carbon nanomaterials, multi-walled carbon nanotubes, fullerene, and reduced graphene oxide, and three commercial metal oxidant NPs, copper oxide (CuO) NPs, ferric oxide (Fe2O3) NPs, and titanium oxides (TiO2) NPs, were independently added to water-agar plates at 50 and 200-mg/L concentrations. Detached rose petals were inoculated with spores of B. cinerea and co-cultured with each of the six nanomaterials. The sizes of the lesions on infected rose petals were measured at 72 h after inoculation, and the growth of fungi on the rose petals was observed by scanning electron microscopy. The six NPs inhibited the growth of B. cinerea, but different concentrations had different effects: 50 mg/L of fullerene and CuO NPs showed the strongest antifungal properties among the treatments, while 200 mg/L of CuO and Fe2O3 showed no significant antifungal activities. Thus, NPs may have antifungal activities that prevent B. cinerea infections in plants, and they could be used as antifungal agents during the growth and post-harvesting of roses and other flowers.

| S-EPMC5539092 | biostudies-literature

The Ca2+/calcineurin-dependent signaling pathway in the gray mold Botrytis cinerea: the role of calcipressin in modulating calcineurin activity.

Project description:In the gray mold fungus Botrytis cinerea the Gα subunit Bcg1 of a heterotrimeric G protein is an upstream activator of the Ca(2+)/calmodulin-dependent phosphatase calcineurin. In this study we focused on the functional characterization of the catalytic subunit of calcineurin (BcCnA) and its putative regulator calcipressin (BcRcn1). We deleted the genes encoding both proteins to examine their role concerning growth, differentiation and virulence. The ΔbccnA mutant shows a severe growth defect, does not produce conidia and is avirulent, while the loss of BcRcn1 caused retardation of hyphal growth and delayed infection of host plants, but had no impact on conidiation and sclerotia formation. Expression of several calcineurin-dependent genes and bccnA itself is positively affected by BcRcn1. Complementation of the Δbcrcn1 mutant with a GFP-BcRcn1 fusion construct revealed that BcRcn1 is localized in the cytoplasm and accumulates around the nuclei. Furthermore, we showed that BcCnA physically interacts with BcRcn1 and the regulatory subunit of calcineurin, BcCnB. We investigated the impact of several protein domains characteristic for modulation and activation of BcCnA via BcRcn1, such as the phosphorylation sites and the calcineurin-docking site, by physical interaction studies between BcCnA and wild-type and mutated copies of BcRcn1. Based on the observed phenotypes we conclude that BcRcn1 acts as a positive modulator of BcCnA and the Ca(2+)/calcineurin-mediated signal transduction in B. cinerea, and that both proteins regulate fungal development and virulence.

| S-EPMC3402410 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data