Open AccessThe toolbox of T richoderma spp. in the biocontrol of B otrytis cinerea disease
Author(s) -
Vos Christine M. F.,
De Cremer Kaat,
Cammue Bruno P. A.,
De Coninck Barbara
Publication year - 2015
Publication title -
molecular plant pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.945
H-Index - 103
eISSN - 1364-3703
pISSN - 1464-6722
DOI - 10.1111/mpp.12189
Subject(s) - biology , antagonism , fungicide , botrytis cinerea , pathogen , plant disease resistance , systemic acquired resistance , population , biological pest control , microbiology and biotechnology , botany , arabidopsis , mutant , biochemistry , receptor , demography , sociology , gene
Summary B otrytis cinerea is a necrotrophic fungal pathogen causing disease in many plant species, leading to economically important crop losses. So far, fungicides have been widely used to control this pathogen. However, in addition to their detrimental effects on the environment and potential risks for human health, increasing fungicide resistance has been observed in the B . cinerea population. Biological control, that is the application of microbial organisms to reduce disease, has gained importance as an alternative or complementary approach to fungicides. In this respect, the genus T richoderma constitutes a promising pool of organisms with potential for B . cinerea control. In the first part of this article, we review the specific mechanisms involved in the direct interaction between the two fungi, including mycoparasitism, the production of antimicrobial compounds and enzymes (collectively called antagonism), and competition for nutrients and space. In addition, biocontrol has also been observed when T richoderma is physically separated from the pathogen, thus implying an indirect systemic plant defence response. Therefore, in the second part, we describe the consecutive steps leading to induced systemic resistance ( ISR ), starting with the initial T richoderma– plant interaction and followed by the activation of downstream signal transduction pathways and, ultimately, the defence response resulting in ISR ( ISR ‐prime phase). Finally, we discuss the ISR ‐boost phase, representing the effect of ISR priming by T richoderma spp. on plant responses after additional challenge with B . cinerea .