scholarly journals Resistance mechanisms of white jabon seedlings (Anthocephalus cadamba) against Botryodiplodia theobromae causing dieback disease

2018 ◽  
Vol 19 (4) ◽  
pp. 1441-1450 ◽  
Author(s):  
LOLA ADRES YANTI ◽  
ACHMAD ACHMAD ◽  
NURUL KHUMAIDA
Keyword(s):  
Disease Incidence ◽  
Economic Value ◽  
Resistance Mechanism ◽  
Resistance Mechanisms ◽  
Microscopic Appearance ◽  
Stem Infection ◽  
Structural Resistance ◽  
Dieback Disease ◽  
Biochemical Resistance ◽  
Anthocephalus Cadamba

Yanti LA, Achmad, Khumaida N. 2018. Resistance mechanisms of white jabon seedlings (Anthocephalus cadamba) againstBotryodiplodia theobromae causing dieback disease. Biodiversitas 19: 1441-1450. Anthocephalus cadamba (Roxb.) Miq. seedlings arethe most preferred plant for the nursery as they serve a lot of benefits and can be used as shading trees, reforestation, plywood, pulp,paper, and traditional medicines. Further, those benefits can increase the economic value of this plant. The main problem in the nurseryof forestry plants is pest and disease attacks, one of which is dieback disease. The dieback disease is caused by Botryodiplodiatheobromae Pat. that may lead death of the host plant. Every plant has its resistance mechanism toward pathogen attacks. This researchaimed: (1) to study B. theobromae attack through wounded and non-wounded stem infection methods on white jabon seedlings; (2) tostudy the resistance mechanisms of white jabon seedlings both structural and biochemical resistance against B. theobromae. This studyemployed a factorial treatment design laid out in a completely randomized design. The structural resistance was determined by studyingthe microscopic appearance of the white jabon seedlings’ stem by using a scanning electron microscope. Meanwhile, the biochemicalresistance was determined by characterizing the chemical compounds of white jabon seedlings' stem using phytochemistry analysis. Theresult showed that the disease incidence of the control (inoculated without pathogen isolate) and the inoculated (inoculated withpathogen isolate) seedlings were, respectively, 0% and 100% (with wounded stem) and 0% and 30% (non-wounded). The diseaseseverity of control and inoculated seedlings were 0% and 62% (with wounded stem) and 0% and 12% (non-wounded stem),respectively. The incubation period of wounded and non-wounded stems on inoculated seedlings (inoculated with pathogen isolate) wasone day after inoculation with the numeric values (disease scores) of 4 and 2, respectively. White jabon seedlings had necrotic resistanceas structural resistance mechanism against the pathogen attack. White jabon seedlings also contained secondary metabolites such asalkaloids, flavonoid, phenyl hydroquinone, tannin, saponin, and steroids. The biochemical resistance of white jabon seedling afterpathogen attacks was shown by the increase of accumulated phenolic compounds such as flavonoid and tannin.

scholarly journals Potensi Cendawan Endofit pada Tanaman Binahong (Anredera cordifolia (Ten.) Steenis) untuk Mengendalikan Botryodiplodia theobromae Pat. Penyebab Mati Pucuk pada Bibit Jabon (Anthocephalus cadamba (Roxb.) Miq)

2019 ◽  
Vol 10 (2) ◽  
pp. 114-118
Author(s):  
Yunik Istikorini
Keyword(s):  
Medicinal Plant ◽  
Endophytic Fungi ◽  
Disease Incidence ◽  
Colony Growth ◽  
Colony Development ◽  
Botryodiplodia Theobromae ◽  
Antifungal Effect ◽  
Dieback Disease ◽  
Anthocephalus Cadamba

Endophytic fungi provides potential advantages as biocontrol agents in the plant. Binahong (Anredera cordifolia) is a medicinal plant which can potentially overcome many kinds of diseases. The dieback disease is caused by Botryodiplodia theobromae Pat. that may lead the death of the host. The objective of this research was to analyze the potency of endophytic fungi from binahong leaves to control the fungus B. theobromae as causal agent of dieback disease on jabon (Anthocepalus cadamba). The isolates of endophytic fungi from binahong used were bnh1.1, bnh1.2, bnh1.3, bnh4.2, bnh4.5, bnh3.3 and bnh3.4. The antifungal effect of endophytic fungi againts colony growth of virulent B. theobromae were tested in vitro. The results showed that all endophytic fungus (7 isolates) inhibited the colony development of B. theobromae ranging from 28.52%-52.22%. Treatment with endophytic fungi bnh4.5 and bnh4.2 had protected jabon from virulent B. theobromae. It has been expressed by the delay of the incubation period and the decreasing of disease severity (respectively 33.34% and 40.84%. Key words: Anredera cordifolia, Botryodiplodia theobromae, disease incidence, endophytic fungi

scholarly journals KEEFEKTIFAN KITOSAN DALAM MENGENDALIKAN Botryodiplodia theobromae Pat. PENYEBAB MATI PUCUK PADA BIBIT JABON (Anthocephalus cadamba (Roxb.) Miq) Chitosan’s Effectiveness in Controlling Dieback by Botryodiplodia theobromae Pat on Jabon Seeding

2018 ◽  
Vol 8 (3) ◽  
pp. 170-176
Author(s):  
Desi Nurafida ◽  
Achmad . ◽  
Syamsul Falah
Keyword(s):  
Disease Incidence ◽  
Control Plant ◽  
Chitosan Solution ◽  
Pathogen Resistance ◽  
Solution Viscosity ◽  
Rate Parameter ◽  
Botryodiplodia Theobromae ◽  
Dieback Disease ◽  
Severity Of The Disease ◽  
Anthocephalus Cadamba

Dieback disease by the fungus Botryodiplodia theobromae in Jabon seedlings (Anthocephalus cadamba) inhibits the regeneration of Jabon plant. Synthetic fungicides utilization to several problems such as residue on the environment and pathogen resistance. Chitosan is a potential natural compound used as an alternative to control plant disease.This research aims to examine the effectiveness of chitosan to control B. theobromae as causal agent of dieback on Jabon seedlings and to examine the effect of chitosan to control the viscosity of dieback disease on Jabon seedlings. The results showed that the chitosan solution can decrease the severity of disease in Jabon seedlings. However, it was different with the disease incidence rate parameter. Chitosan solution was not significantly affecting the disease because B. theobromae caused dieback symptoms on Jabon seedlings. The most effective treatment was chitosan solution with a concentration of 0.1% before inoculation with the severity of the disease by 25%. Chitosan solution viscosity was responsible in affecting the percentage of dieback disease in Jabon seeds. The higher the viscosity of chitosan, the higher the percentage of dieback disease attacks. The best viscosity to suppress the development of dieback disease on Jabon seedlings was 8.80 with 7.90% attack.Key words: Anthocephalus cadamba , Botryodiplodia theobromae, chitosan, dieback.

scholarly journals Characterization of resistance mechanisms of Enterobacter cloacae Complex co-resistant to carbapenem and colistin

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Shixing Liu ◽  
Renchi Fang ◽  
Ying Zhang ◽  
Lijiang Chen ◽  
Na Huang ◽  
...  
Keyword(s):  
Lipid A ◽  
Efflux Pump ◽  
Resistance Mechanism ◽  
Carbapenem Resistance ◽  
Enterobacter Cloacae ◽  
Resistance Mechanisms ◽  
Colistin Resistance ◽  
Carbapenem Resistant ◽  
Horizontal Spread

Abstract Background The emergence of carbapenem-resistant and colistin-resistant ECC pose a huge challenge to infection control. The purpose of this study was to clarify the mechanism of the carbapenems and colistin co-resistance in Enterobacter cloacae Complex (ECC) strains. Results This study showed that the mechanisms of carbapenem resistance in this study are: 1. Generating carbapenemase (7 of 19); 2. The production of AmpC or ESBLs combined with decreased expression of out membrane protein (12 of 19). hsp60 sequence analysis suggested 10 of 19 the strains belong to colistin hetero-resistant clusters and the mechanism of colistin resistance is increasing expression of acrA in the efflux pump AcrAB-TolC alone (18 of 19) or accompanied by a decrease of affinity between colistin and outer membrane caused by the modification of lipid A (14 of 19). Moreover, an ECC strain co-harboring plasmid-mediated mcr-4.3 and blaNDM-1 has been found. Conclusions This study suggested that there is no overlap between the resistance mechanism of co-resistant ECC strains to carbapenem and colistin. However, the emergence of strain co-harboring plasmid-mediated resistance genes indicated that ECC is a potential carrier for the horizontal spread of carbapenems and colistin resistance.

scholarly journals Black Queen Evolution and Trophic Interactions Determine Plasmid Survival after the Disruption of the Conjugation Network

mSystems ◽  
2018 ◽  
Vol 3 (5) ◽  
Author(s):  
Johannes Cairns ◽  
Katariina Koskinen ◽  
Reetta Penttinen ◽  
Tommi Patinen ◽  
Anna Hartikainen ◽  
...  
Keyword(s):  
Antibiotic Resistance ◽  
Bacterial Communities ◽  
Resistance Mechanism ◽  
Real Life ◽  
Ecological Factors ◽  
Mobile Genetic Elements ◽  
Resistance Mechanisms ◽  
Antibiotics Resistance ◽  
Bacterial Populations ◽  
Genetic Elements

ABSTRACTMobile genetic elements such as conjugative plasmids are responsible for antibiotic resistance phenotypes in many bacterial pathogens. The ability to conjugate, the presence of antibiotics, and ecological interactions all have a notable role in the persistence of plasmids in bacterial populations. Here, we set out to investigate the contribution of these factors when the conjugation network was disturbed by a plasmid-dependent bacteriophage. Phage alone effectively caused the population to lose plasmids, thus rendering them susceptible to antibiotics. Leakiness of the antibiotic resistance mechanism allowing Black Queen evolution (i.e. a “race to the bottom”) was a more significant factor than the antibiotic concentration (lethal vs sublethal) in determining plasmid prevalence. Interestingly, plasmid loss was also prevented by protozoan predation. These results show that outcomes of attempts to resensitize bacterial communities by disrupting the conjugation network are highly dependent on ecological factors and resistance mechanisms.IMPORTANCEBacterial antibiotic resistance is often a part of mobile genetic elements that move from one bacterium to another. By interfering with the horizontal movement and the maintenance of these elements, it is possible to remove the resistance from the population. Here, we show that a so-called plasmid-dependent bacteriophage causes the initially resistant bacterial population to become susceptible to antibiotics. However, this effect is efficiently countered when the system also contains a predator that feeds on bacteria. Moreover, when the environment contains antibiotics, the survival of resistance is dependent on the resistance mechanism. When bacteria can help their contemporaries to degrade antibiotics, resistance is maintained by only a fraction of the community. On the other hand, when bacteria cannot help others, then all bacteria remain resistant. The concentration of the antibiotic played a less notable role than the antibiotic used. This report shows that the survival of antibiotic resistance in bacterial communities represents a complex process where many factors present in real-life systems define whether or not resistance is actually lost.

scholarly journals Playing the Whack-A-Mole Game: ERK5 Activation Emerges Among the Resistance Mechanisms to RAF-MEK1/2-ERK1/2- Targeted Therapy

2021 ◽  
Vol 9 ◽  
Author(s):  
Alessandro Tubita ◽  
Ignazia Tusa ◽  
Elisabetta Rovida
Keyword(s):  
Tyrosine Kinases ◽  
Resistance Mechanism ◽  
Resistance Mechanisms ◽  
Mitogen Activated Protein Kinase ◽  
Cancer Therapies ◽  
New Era ◽  
Mitogen Activated Protein ◽  
The Impact ◽  
The Ideal

Molecularly tailored therapies have opened a new era, chronic myeloid leukemia being the ideal example, in the treatment of cancer. However, available therapeutic options are still unsatisfactory in many types of cancer, and often fail due to the occurrence of resistance mechanisms. With regard to small-molecule compounds targeting the components of the Mitogen-Activated Protein Kinase (MAPK) cascade RAF-MEK1/2-ERK1/2, these drugs may result ineffective as a consequence of the activation of compensatory pro-survival/proliferative signals, including receptor tyrosine kinases, PI3K, as well as other components of the MAPK family such as TPL2/COT. The MAPK ERK5 has been identified as a key signaling molecule in the biology of several types of cancer. In this review, we report pieces of evidence regarding the activation of the MEK5-ERK5 pathway as a resistance mechanism to RAF-MEK1/2-ERK1/2 inhibitors. We also highlight the known and possible mechanisms underlying the cross-talks between the ERK1/2 and the ERK5 pathways, the characterization of which is of great importance to maximize, in the future, the impact of RAF-MEK1/2-ERK1/2 targeting. Finally, we emphasize the need of developing additional therapeutically relevant MEK5-ERK5 inhibitors to be used for combined treatments, thus preventing the onset of resistance to cancer therapies relying on RAF-MEK1/2-ERK1/2 inhibitors.

scholarly journals IDENTIFICATION OF THE kdr MUTATIONS IN VGSC GENE OF THE DENGUE MOSQUITOES AEDES ALBOPICTUS COLLECTED FROM HANOI AND HAIPHONG

2018 ◽  
Vol 16 (2) ◽  
pp. 273-278
Author(s):  
Nguyen Thi Kim Lien ◽  
Nguyen Thu Hien ◽  
Nguyen Huy Hoang ◽  
Nguyen Thi Hong Ngoc ◽  
Nguyen Thi Huong Binh
Keyword(s):  
Sodium Channel ◽  
Aedes Albopictus ◽  
Novel Mutation ◽  
Resistance Mechanism ◽  
Resistance Mechanisms ◽  
Resistance Mutations ◽  
Well Control ◽  
Voltage Gated ◽  
Activity Of Enzymes ◽  
Dengue Epidemic

Vietnam is one of the countries that is affected by dengue fever in Southeast Asia. The dengue epidemic is becoming increasingly more complex so it is necessary to have a well control to vectors in order to limit the spread of the disease. The Aedes albopictus mosquito is determined as one of the two major vectors that transmitted the dengue. Recent research shows that A. albopictus is present in some parts of Hanoi and Haiphong. In order to control the vector as well as the disease, it is necessary to understand the level of resistance and the resistance mechanism of the vector. Two important resistance mechanisms of insect were known as the mutations in the target protein of the insecticides and enhancing the activity of enzymes that participate in the resolution of the insecticides. In this study, the mosquito samples were collected from Hanoi and Haiphong to identify the level of resistance and detect the knock down resistance mutations in voltage gated sodium channel (VGSC) in membrane of nervecell of mosquito. The results of insecticide susceptibility test showed that A. albopictus in Hanoi and Haiphong were still sensitive to organophosphate but resistant to DDT, carbamate and pyrethroid. Ser989Pro, Ile1011Met, Val1016Gly and Phe1534Cys mutations were not deteced in A. albopictus in Hanoi and Haiphong. However, we detected a novel mutation Tyr986His in VGSC protein.

Distribution and validation of genotypic and phenotypic glyphosate and PPO-nhibitor resistance in Palmer amaranth (Amaranthus palmeri) from southwestern Nebraska

2020 ◽  
pp. 1-12 ◽  
Author(s):  
Maxwel C Oliveira ◽  
Darci A Giacomini ◽  
Nikola Arsenijevic ◽  
Gustavo Vieira ◽  
Patrick J Tranel ◽  
...  
Keyword(s):  
Cluster Analysis ◽  
Gene Amplification ◽  
Cropping Systems ◽  
Resistance Mechanism ◽  
Geographic Area ◽  
Glyphosate Resistance ◽  
Resistance Mechanisms ◽  
Palmer Amaranth ◽  
Resistance Evolution ◽  
Inhibitor Resistance

Abstract Failure to control Palmer amaranth with glyphosate and protoporphyrinogen IX oxidase (PPO)-inhibitor herbicides was reported across southwestern Nebraska in 2017. The objectives of this study were to 1) confirm and 2) validate glyphosate and PPO-inhibitor (fomesafen and lactofen) resistance in 51 Palmer amaranth accessions from southwestern Nebraska using genotypic and whole-plant phenotypic assay correlations and cluster analysis, and 3) determine which agronomic practices might be influencing glyphosate resistance in Palmer amaranth accessions in that location. Based on genotypic assay, 88% of 51 accessions contained at least one individual with amplification (>2 copies) of the 5-enolypyruvyl-shikimate-3-phosphate synthase (EPSPS) gene, which confers glyphosate resistance; and/or a mutation in the PPX2 gene, either ΔG210 or R128G, which endows PPO-inhibitor resistance in Palmer amaranth. Cluster analysis and high correlation (0.83) between genotypic and phenotypic assays demonstrated that EPSPS gene amplification is the main glyphosate resistance mechanism in Palmer amaranth accessions from southwestern Nebraska. In contrast, there was poor association between genotypic and phenotypic responses for PPO-inhibitor resistance, which was attributed to segregation for PPO-inhibitor resistance within these accessions and/or the methodology that was adopted herein. Genotypic assays can expedite the process of confirming known glyphosate and PPO-inhibitor resistance mechanisms in Palmer amaranth from southwestern Nebraska and other locations. Phenotypic assays are also a robust method for confirming glyphosate resistance but not necessarily PPO-inhibitor resistance in Palmer amaranth. Moreover, random forest analysis of glyphosate resistance in Palmer amaranth indicated that EPSPS gene amplification, county, and current and previous crops are the main factors influencing glyphosate resistance within that geographic area. Most glyphosate-susceptible Palmer amaranth accessions were found in a few counties in areas with high crop diversity. Results presented here confirm the spread of glyphosate resistance and PPO-inhibitor resistance in Palmer amaranth accessions from southwestern Nebraska and demonstrate that less diverse cropping systems are an important driver of herbicide resistance evolution in Palmer amaranth.

scholarly journals Persistent Bacteremia fromPseudomonas aeruginosawithIn VitroResistance to the Novel Antibiotics Ceftolozane-Tazobactam and Ceftazidime-Avibactam

2016 ◽  
Vol 2016 ◽  
pp. 1-5 ◽  
Author(s):  
Louie Mar Gangcuangco ◽  
Patricia Clark ◽  
Cynthia Stewart ◽  
Goran Miljkovic ◽  
Zane K. Saul
Keyword(s):  
Susceptibility Testing ◽  
Resistance Mechanism ◽  
Multidrug Resistant ◽  
Resistance Mechanisms ◽  
Blood Cultures ◽  
The Novel ◽  
First Case ◽  
Persistent Bacteremia ◽  
Novel Antibiotics

Ceftazidime-avibactam and ceftolozane-tazobactam are new antimicrobials with activity against multidrug-resistantPseudomonas aeruginosa. We present the first case of persistentP.aeruginosabacteremia within vitroresistance to these novel antimicrobials. A 68-year-old man with newly diagnosed follicular lymphoma was admitted to the medical intensive care unit for sepsis and right lower extremity cellulitis. The patient was placed empirically on vancomycin and piperacillin-tazobactam. Blood cultures from Day 1 of hospitalization grewP.aeruginosasusceptible to piperacillin-tazobactam and cefepime identified using VITEK 2 (Biomerieux, Lenexa, KS). Repeat blood cultures from Day 5 grewP.aeruginosaresistant to all cephalosporins, as well as to meropenem by Day 10. Susceptibility testing performed by measuring minimum inhibitory concentration byE-test (Biomerieux, Lenexa, KS) revealed that blood cultures from Day 10 were resistant to ceftazidime-avibactam and ceftolozane-tazobactam. The Verigene Blood Culture-Gram-Negative (BC-GN) microarray-based assay (Nanosphere, Inc., Northbrook, IL) was used to investigate underlying resistance mechanism in theP.aeruginosaisolate but CTX-M, KPC, NDM, VIM, IMP, and OXA gene were not detected. This case report highlights the well-documented phenomenon of antimicrobial resistance development inP.aeruginosaeven during the course of appropriate antibiotic therapy. In the era of increasing multidrug-resistant organisms, routine susceptibility testing ofP. aeruginosato ceftazidime-avibactam and ceftolozane-tazobactam is warranted. Emerging resistance mechanisms to these novel antibiotics need to be further investigated.

scholarly journals Advanced Resistance Studies Identify Two Discrete Mechanisms in Staphylococcus aureus to Overcome Antibacterial Compounds that Target Biotin Protein Ligase

Antibiotics ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 165 ◽  
Author(s):  
Andrew J. Hayes ◽  
Jiulia Satiaputra ◽  
Louise M. Sternicki ◽  
Ashleigh S. Paparella ◽  
Zikai Feng ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Transcriptional Repression ◽  
Molecular Mechanisms ◽  
Resistance Mechanism ◽  
Resistance Mechanisms ◽  
Resistance Rate ◽  
Biotin Protein Ligase ◽  
Essential Enzyme

Biotin protein ligase (BPL) inhibitors are a novel class of antibacterial that target clinically important methicillin-resistant Staphylococcus aureus (S. aureus). In S. aureus, BPL is a bifunctional protein responsible for enzymatic biotinylation of two biotin-dependent enzymes, as well as serving as a transcriptional repressor that controls biotin synthesis and import. In this report, we investigate the mechanisms of action and resistance for a potent anti-BPL, an antibacterial compound, biotinyl-acylsulfamide adenosine (BASA). We show that BASA acts by both inhibiting the enzymatic activity of BPL in vitro, as well as functioning as a transcription co-repressor. A low spontaneous resistance rate was measured for the compound (<10−9) and whole-genome sequencing of strains evolved during serial passaging in the presence of BASA identified two discrete resistance mechanisms. In the first, deletion of the biotin-dependent enzyme pyruvate carboxylase is proposed to prioritize the utilization of bioavailable biotin for the essential enzyme acetyl-CoA carboxylase. In the second, a D200E missense mutation in BPL reduced DNA binding in vitro and transcriptional repression in vivo. We propose that this second resistance mechanism promotes bioavailability of biotin by derepressing its synthesis and import, such that free biotin may outcompete the inhibitor for binding BPL. This study provides new insights into the molecular mechanisms governing antibacterial activity and resistance of BPL inhibitors in S. aureus.

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