ABSTRACT
Programmed cell death (PCD) plays a key role in plant responses to pathogens, determining the success of infection depending on the pathogen lifestyle and on which participant of the interaction triggers cell death. The hemibiotrophic basidiomycete Moniliophthora perniciosa is the causal agent of witches' broom disease of Theobroma cacao L. (cacao), a serious constraint for production in South America and the Caribbean. It has been hypothesized that M. perniciosa pathogenesis involves PCD, initially as a plant defence mechanism, which is diverted by the fungus to induce necrosis during the dikaryotic phase of the mycelia. Here, we evaluated whether the expression of a cacao anti-apoptotic gene would affect the incidence and severity of M. perniciosa infection using the 'Micro-Tom' (MT) tomato as a model. The cacao Bax-inhibitor-1 (TcBI-1) gene, encoding a putative basal attenuator of PCD, was constitutively expressed in MT to evaluate function. Transformants expressing TcBI-1, when treated with tunicamycin, an inducer of endoplasmic reticulum stress, showed a decrease in cell peroxidation. When the same transformants were inoculated with the necrotrophic fungal pathogens Sclerotinia sclerotiorum, Sclerotium rolfsii and Botrytis cinerea, a significant reduction in infection severity was observed, confirming TcBI-1 function. After inoculation with M. perniciosa, TcBI-1 transformant lines showed a significant reduction in disease incidence compared with MT. The overexpression of TcBI-1 appears to affect the ability of germinating spores to penetrate susceptible tissues, restoring part of the non-host resistance in MT against the S-biotype of M. perniciosa.
