Submitted to: Plant Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/11/2007
Publication Date: 4/19/2007
Citation: Ceita, G.D., Macedo, J.N., Santos, T.B., Alemanno, L., Gesteira, A.D., Micheli, F., Mariano, A.C., Gramacho, K.P., Silva, D.D., Meinhardt, L.W., Mazzafera, P., Pereira, G.A., Cascardo, J.D. Involvement of calcium oxalate degradation during programmed cell death in Theobroma cacao tissues triggered by the hemibiotrophic fungus Moniliophthora perniciosa. Plant Science. 173 (2007) 106-117 Interpretive Summary: Research into diseases of cacao is important to the USA economy because cacao is the raw material for the production of chocolate and the chocolate industry is one of the main consumers of US grown dairy, nuts, oils and sugar products. Fungal diseases such as Witches’ Broom Disease (WBD) of cacao have devastated cacao production in much of the Western Hemisphere. WBD is caused by the fungus Moniliophthora perniciosa. In the present study we identified microscopic analysis revealed the growth of the fungus between plant cells was associated with the presence of an increasing number of calcium oxalate crystals, an accumulation of hydrogen peroxide and cell death. This information provides insight into how this fungus functions and provides researchers mechanisms to develop new control measures. Plant pathologists, biologists and mycologists will benefit directly from this information.
Technical Abstract: Moniliophthora perniciosa, the causal agent of witches’ broom disease of Theobroma cacao, significantly affected cacao production in South America and Caribbean countries. Host colonization by the pathogen exhibits a concerted succession of symptoms, starting with hypertrophic growth and ‘‘broom’’ formation, followed by tissue degeneration and death. To understand mechanisms of host susceptibility, we investigated fungal development during a compatible interaction with a susceptible genotype. Microscopic analysis revealed the initial fungal biotrophic intercellular growth, followed by intracellular growth associated with the presence of an increasing number of host apoptotic nuclei and calcium oxalate crystals, with subsequent accumulation of hydrogen peroxide and cell death. Active oxalate degradation and its possible source of origin were detected in infected tissues. Together, these processes may increase the availability of nutrients for the fungal mycelia and may contribute to the disease cycle in this plant–fungal hemibiotrophic interaction. Based on the histological and gene expression data, a novel role for calcium oxalate in disease susceptibility is proposed.