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Abstract

Background: Several Trichoderma strains have been reported to be effective in controlling plant diseases, and the action of fungal hydrolytic enzymes has been considered as the main mechanism involved in the antagonistic process. However, although Trichoderma strains were found to impair development of Crinipellis perniciosa, the causal agent of cocoa plant witches' broom disease, no fungal strain is available for effective control of this disease. We have then undertaken a program of construction of hydrolytic enzyme-overproducing Trichoderma strains aiming improvement of the fungal antagonistic capacity. The protease of an indian Trichoderma isolate showing antagonistic activity against C. perniciosa was purified to homogeneity and characterized for its kinetic properties and action on the phytopathogen cell wall.

Trichovariability in rhizosphere soil samples and their biocontrol potential against downy mildew pathogen in pearl millet

“…In general, the mechanism involved in plant disease suppression by Trichoderma is identified as, directly through antagonism or indirectly by elicitation of plant-defense responses 61 , 62 . Disease protection by direct suppression is through mycoparasitism 63 , 64 fabrication of lytic enzymes such as chitinase 65 , β-1, 3 glucanase 66 , 67 , protease 68 , and antimicrobial chemicals (Trichoharzianol, Isoharziandione, 6-pentyl-α-pyrone) 69 – 71 and competing for space and food. Disease protection by ISR has been reported in several plant disease managements by Trichoderma spp.…”

Trichoderma- Foliar Pathogen Interactions

“…chitinase, N-acetylglucosaminidase, -1,3-glucanase, protease, cellulose, endoglucanase, glucosidase, amylase were shown to be increased in presence of substrates [37]. T. harzianum isolate 1051 produced a novel protease which was biologically active against Crinipellis perniciosa, the causal agent of witches' broom [38].…”

A Systems Biology Approach to Understanding the Mechanisms of Action of Chinese Herbs for Treatment of Cardiovascular Disease

“…The inactive decapeptide angiotensin I is subsequently converted to the octapeptid angiotensin II by angiotensin converting enzyme (ACE, P209) in the lungs. ACE is a membrane-bound exopeptidase on the plasma membranes of cells and metabolizes a number of other peptides, including the vasodilator peptides bradykinin and kallidin, to inactive metabolites [ 52 ]. Finally, angiotensin II inhibits neuronal nitric oxide synthase (eNOS, P66) activation through the ERK1/2-RSK signaling pathway [ 47 ], regulating fluid balance and the secretion of aldosterone.…”

“…Angiogenesis is a process that is of critical importance to tumorigenesis and tumor metastasis, as well as to the growth and maintenance of normal vasculature. In the VEGF signaling pathway, VEGF is an angiogenic factor that is very closely associated with the induction and maintenance of neovasculature in human cancers [ 52 ]. The receptors tyrosine kinases KDR/Flk-1 and Flt-1 are the VEGF receptors and play important roles in transducing signals upon VEGF stimulation of the endothelium.…”