scholarly journals Microbial and biochemical basis of a Fusarium wilt-suppressive soil

2015 ◽  
Vol 10 (1) ◽  
pp. 119-129 ◽  
Author(s):  
Jae-Yul Cha ◽  
Sangjo Han ◽  
Hee-Jeon Hong ◽  
Hyunji Cho ◽  
Daran Kim ◽  
...  
Keyword(s):  
Fusarium Wilt ◽  
Biochemical Basis ◽  
Suppressive Soil

Microflora that harbor the NRPS gene are responsible for Fusarium wilt disease-suppressive soil

2018 ◽  
Vol 132 ◽  
pp. 83-90 ◽  
Author(s):  
Mengli Zhao ◽  
Jun Yuan ◽  
Ruifu Zhang ◽  
Menghui Dong ◽  
Xuhui Deng ◽  
...  
Keyword(s):  
Fusarium Wilt ◽  
Wilt Disease ◽  
Nrps Gene ◽  
Suppressive Soil ◽  
Fusarium Wilt Disease ◽  
Disease Suppressive Soil

scholarly journals Biochemical basis of improvement of defense in tomato plant against Fusarium wilt by CaCl2

2017 ◽  
Vol 23 (3) ◽  
pp. 581-596 ◽  
Author(s):  
Nilanjan Chakraborty ◽  
Swarnendu Chandra ◽  
Krishnendu Acharya
Keyword(s):  
Fusarium Wilt ◽  
Tomato Plant ◽  
Biochemical Basis

scholarly journals Phenolic Acid-Degrading Consortia Increase Fusarium Wilt Disease Resistance of Chrysanthemum

Agronomy ◽  
2020 ◽  
Vol 10 (3) ◽  
pp. 385
Author(s):  
Cheng Zhou ◽  
Zhongyou Ma ◽  
Xiaoming Lu ◽  
Lin Zhu ◽  
Jianfei Wang
Keyword(s):  
Microbial Community ◽  
Fusarium Wilt ◽  
Wilt Disease ◽  
Disease Suppression ◽  
Suppressive Soil ◽  
Soil Borne Pathogens ◽  
Fusarium Wilt Disease ◽  
Pseudomonas Species ◽  
Conducive Soil

Soil microbial community changes imposed by the cumulative effects of root-secreted phenolic acids (PAs) promote soil-borne pathogen establishment and invasion under monoculture systems, but the disease-suppressive soil often exhibits less soil-borne pathogens compared with the conducive soil. So far, it remains poorly understood whether soil disease suppressiveness is associated with the alleviated negative effects of PAs, involving microbial degradation. Here, the long-term monoculture particularly shaped the rhizosphere microbial community, for example by the enrichment of beneficial Pseudomonas species in the suppressive soil and thus enhanced disease-suppressive capacity, however this was not observed for the conducive soil. In vitro PA-degradation assays revealed that the antagonistic Pseudomonas species, together with the Xanthomonas and Rhizobium species, significantly increased the efficiency of PA degradation compared to single species, at least partially explaining how the suppressive soil accumulated lower PA levels than the conducive soil. Pot experiments further showed that this consortium harboring the antagonistic Pseudomonas species can not only lower PA accumulation in the 15-year conducive soils, but also confer stronger Fusarium wilt disease suppression compared with a single inoculum with the antagonistic bacteria. Our findings demonstrated that understanding microbial community functions, beyond the single direct antagonism, facilitated the construction of active consortia for preventing soil-borne pathogens under intensive monoculture.

scholarly journals Comparative Microbiome Analysis of a Fusarium Wilt Suppressive Soil and a Fusarium Wilt Conducive Soil From the Châteaurenard Region

2018 ◽  
Vol 9 ◽  
Author(s):  
Katarzyna Siegel-Hertz ◽  
Véronique Edel-Hermann ◽  
Emilie Chapelle ◽  
Sébastien Terrat ◽  
Jos M. Raaijmakers ◽  
...  
Keyword(s):  
Fusarium Wilt ◽  
Suppressive Soil ◽  
Microbiome Analysis ◽  
Conducive Soil

Enhancement of Plasminogen Binding to U937 Cells and Fibrin by Complestatin

1997 ◽  
Vol 77 (01) ◽  
pp. 137-142 ◽  
Author(s):  
Kiyoshi Tachikawa ◽  
Keiji Hasurni ◽  
Akira Endo
Keyword(s):  
Binding Site ◽  
Binding Affinity ◽  
Blood Cells ◽  
Aminocaproic Acid ◽  
U937 Cells ◽  
Biochemical Basis ◽  
Equilibrium Binding ◽  
Pharmacological Stimulation ◽  
Endogenous Fibrinolysis ◽  
Stimulation Of

SummaryPlasminogen binds to endothelial and blood cells as well as to fibrin, where the zymogen is efficiently activated and protected from inhibition by α2-antiplasmin. In the present study we have found that complestatin, a peptide-like metabolite of a streptomyces, enhances binding of plasminogen to cells and fibrin. Complestatin, at concentrations ranging from 1 to 5 μM, doubled 125I-plasminogen binding to U937 cells both in the absence and presence of lipoprotein(a), a putative physiological competitor of plasminogen. The binding of 125I-plasminogen in the presence of complestatin was abolished by e-aminocaproic acid, suggesting that the lysine binding site(s) of the plasminogen molecule are involved in the binding. Equilibrium binding analyses indicated that complestatin increased the maximum binding of 125I-plasminogen to U937 cells without affecting the binding affinity. Complestatin was also effective in increasing 125I-plasminogen binding to fibrin, causing 2-fold elevation of the binding at ~1 μM. Along with the potentiation of plasminogen binding, complestatin enhanced plasmin formation, and thereby increased fibrinolysis. These results would provide a biochemical basis for a pharmacological stimulation of endogenous fibrinolysis through a promotion of plasminogen binding to cells and fibrin.

Biochemical basis of selective disease controlling activity of mepanipyrim

2007 ◽  
Vol 32 (2) ◽  
pp. 77-82 ◽  
Author(s):  
Ichiro Miura ◽  
Shinichiro Maeno
Keyword(s):  
Biochemical Basis
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