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Trichoderma asperellum is effective for biocontrol of Verticillium wilt in olive caused by the defoliating pathotype of Verticillium dahliae

AuthorsCarrero-Carrón, Irene; Trapero Casas, José Luis ; Olivares-García, Concepción; Monte, Enrique; Hermosa, Rosa; Jiménez-Díaz, Rafael M.
Biological control
AntaGrowth promotiongonism
Rhizosphere colonization
Olea europaea
Picual olive
Issue DateOct-2016
CitationCrop Protection 88: 45-52 (2016)
AbstractVerticillium wilt caused by a highly virulent, defoliating (D) pathotype of Verticillium dahliae is threatening olive production in Spain and other Mediterranean countries. This disease must be managed by an integrated strategy, in which biocontrol agents can play an important role. We have investigated the potential of Trichoderma asperellum strains for antagonism against V. dahliae and suppression of Verticillium wilt of olive caused by the D pathotype. First, we tested the antagonistic potential of T. asperellum strains Bt2, Bt3 and T25 against six V. dahliae isolates, four of the D and two of the nondefoliating (ND) pathotypes, in different in vitro assays. All T. asperellum strains overgrew the colonies of all V. dahliae isolates to a similar extent. However, extracellular compounds from strains Bt3 and T25 showed higher anti-V. dahliae activities than those of Bt2 in membrane assays. Also, growth of Bt2 was reduced by ND V. dahliae whereas that of Bt3 and T25 was not affected by V. dahliae-secreted compounds. In planta assays using strains Bt3 and T25, and ’Picual’ olive plants, showed that the two T. asperellum strains significantly reduced the severity of symptoms and the standardized area under the disease progress curve caused by highly virulent D V. dahliae, but not the final disease incidence. Strain T25 significantly increased growth of ‘Picual’ plants and displayed higher ability for colonizing the olive rhizosphere and establishing endophytic infection in olive roots than Bt3.
Publisher version (URL)http://doi.org/10.1016/j.cropro.2016.05.009
Appears in Collections:(IAS) Artículos
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