Résumé
Moniliophthora Pod Rot (MPR), caused by the fungus Moniliophthora roreri (Cif.) Evans et al is one of the main limiting factors of production in Latin America. Combating MPR is difficult due to the time-consuming and high cost recommended practices. This limitation is due to the current insufficient information on the biology and epidemiology of the pathogen. This research aims to compare MPR development, symptoms onset of the disease and fungal sporulation for three cacao clones in a range of incomplete resistance Pound-7 (highly susceptible), CC-137 (moderately resistant) and CATIE-R4 (highly resistant) and understand the influence of different microclimatic variables on this development. A total of 10,054 pods of 5-10 cm length were labelled during 55 weeks. Pods were observed throughout their lifetime: healthy, diseased with no sporulation, diseased with sporulating lesions, harvested. Incidence curves were built for all of the 55 generations of pods observed. Generations with nonconventional clonal behavior were selected in order to illustrate our hypothesis that environment, especially climate, could affect cacao s incomplete resistance to MPR. Differences in resistance among these clones lie in the number of resistant genes accumulated; however, the resistance of the three may be affected under certain environmental condition. Then, using GLMM, GLM and AIC surfaces we determined the specific period (when and for how long) where each microclimatic variable better explained the disease development. These new variables were combined in a complete GLMM and GLM, where only significant variables were retained. Water-related variables and temperature determine the symptoms expression for the susceptible clones, while, for the resistant clone CATIE-R4, only temperature showed up as explicative variable due to low numbers of CATIE-R4 pods showing symptoms. According to our models, there are two important events where resistance strategies could be developed for the cacao resistance strategy: fungal germination and penetration, where PAMP-triggered immunity (PTI) could be activated; and the symptoms onset, where the effector-triggered immunity (ETI) could occur. Success of these two events responds to the effect of humidity and temperature, respectively. We considered that none of the clones presents PTI as a defense mechanism against spore germination and penetration. Host resistance mechanisms resulting from the ETI are triggered internally and against colonization, where temperatures influence the success of these strategies. CATIE-R4 resistance strategy consists of the interruption of fungal colonization as an ETI strategy. This interruption also avoids fungal reproduction since the fungus has difficulties sporulating over CATIE-R4 pods, causing inoculum suppression. (Résumé d'auteur)