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Title:   Author  item
                                            ALI, SHAHIN - Forest Service (FS)item
                                            MELNICK, RACHEL - National Institute Of Food And Agriculture (NIFA)item
                                            Strem, Maryitem
                                            CROZIER, JANE - Catie Tropical Agricultural Researchitem
                                            Shao, Jonathanitem
                                            Sicher  Jr, Richarditem
                                            Zhang, Dapengitem
                                            PHILIPS-MORA, WILBERTH - Catie Tropical Agricultural Researchitem
                                            Meinhardt, Lyndelitem
                                            Bailey, Bryan
  Submitted to: Molecular Plant Pathology
                                    Publication Type: Peer Reviewed Journal
                                    Publication Acceptance Date: 2/15/2014
                                    Publication  Date: 4/14/2014
                                    Citation: Ali, S., Melnick, R., Strem, M.D., Crozier, J., Shao, J.Y., Sicher  Jr, R.C., Zhang, D., Philips-Mora, W., Meinhardt, L.W., Bailey, B.A. 2014. Successful pod infections by Moniliophthora roreri result in differential Theobroma cacao gene expression depending on the clone’s level of tolerance. Molecular Plant Pathology. DOI:10.1111/mpp.12126.Interpretive Summary: Frosty pod rot, caused by the fungus Monilophthora roreri, is a devastating disease on Theobroma cacao (cacao), the source of chocolate. Cacao clones showing tolerance against frosty pod rot are being planted throughout Central America. A significant concern associated with the planting of tolerant clones is that the fungus may mutate and overcome the tolerance making them highly susceptible to frosty pod rot and necessitating the development of new tolerant clones. On relatively rare occasions the fungus succeeds in causing disease on the tolerant clones. We characterized plant gene expression associated with infections of tolerant clones. Tolerant cacao clones express unique defense genes when infected by the fungus. The genes identified likely contribute to the clone’s disease tolerance against frosty pod rot. By knowing the genes specific cacao clones use in resisting infection we can optimize breeding programs, leading to the development of new clones. Chocolate is combined with United States agricultural products providing direct benefit to the American farmer. The development of new clones tolerant against frosty pod rot should help stabilize and increase cacao supplies resulting to increased benefits to the cacao farmer, the cacao industry, and the American farmer.
                                Technical Abstract: As many of the tolerant cacao clones are slowly losing the tolerance against Frosty pod rot (FPR) caused by Moniliophthora roreri, the knowledge of this tolerance at the molecular level can help to generate more stable tolerant clone against FPR. RNA-Seq analysis was carried out to obtain a comparative view of transcript populations from two susceptible and two tolerant clones after successful infections leading to disease. A total of 3009 transcript showed significant differential expression among these clones. KEGG pathways and gene ontology analysis involving the differentially expressed genes indicate a shift in 152 different metabolic pathways between the tolerant and susceptible clones. RT-qPCR analyses of 36 genes verified the differential response of the tolerant and susceptible clones. In the tolerant clones, most of the genes showed induction due to M. roreri infection and an uniform progression in expression in relation to infection level and fungal load, which diverged in the tolerant clones. Many genes showed higher expression at a low level of infection in tolerant clones which was further validated by regression and principle coordinate analysis. Results suggest that defense responses are induced at an earlier stage of infection in the tolerant clones than occurs in the susceptible clones. The elicitor responsive genes were highly active in tolerant clones along with genes associated with the hypersensitive response and other defense mechanisms. Results suggest brassinosteroid (BR) biosynthesis was reduced and catabolic inactivation of both BR and abscisic acids occurs in tolerant clones. The jasmonic acid, ethylene, and salicylic acid mediated defense pathways are enhanced in tolerant clones in response to successful infections by M. roreri.


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