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Abstract: Young Theobroma cacao pods, known as cherelles, are commonly lost to physiological thinning known as cherelle wilt. Cherelles are susceptible to frosty pod rot caused by Moniliophthora roreri. We studied the cherelle wilt process and its impact on M. roreri infection using microscopic, metabolite, and gene expression analyses. Wilt was associated with increased levels of tricarboxylic acid cycle intermediaries and decreased levels of major metabolites. Expression changes of cacao ESTs in response to wilt suggest induction of the polyamine, ethylene, and jasmonic acid biosynthetic pathways and regulation of abscisic acid and cytokinin levels. M. roreriinfection caused little alteration of cherelle physiology. M. roreri responded to the late stage of wilt by altering the expression of M. roreri ESTs associated with metabolite detoxification and host tissue degradation. The environment of the wilting cherelles may truncate the disease cycle of frosty pod rot, by limiting M. roreri sporulation and stopping the lifecycle. [Copyright &y& Elsevier]

Abstract: We report the first analysis of polygalacturonase regulation in the basidiomycete Moniliophthora perniciosa. Non-secreted and secreted polygalacturonase activity was obtained from M. perniciosa cultivated on bran-based solid medium or liquid media containing additional carbon sources or cacao extracts (infected or not by the fungus). Polygalacturonase activity assays were carried out under different temperatures and incubation periods. The best secreted polygalacturonase activity was obtained when the enzymatic assay was made at 50 °C for 10 min. Moreover, the polygalacturonase activity was enhanced when the fungus was cultivated on potato dextrose medium, in the presence of additional fermentable carbon sources, in the presence of cacao pulp or non infected cacao extracts. [Copyright &y& Elsevier]

Abstract: Theobroma cacao pods were inoculated with meiospores of Moniliophthora roreri (Mr), a hemibiotrophic basidiomycete causing frosty pod rot. Pods were malformed 30 days after inoculation (DAI) and sporulation was observed 60 DAI. Glucose and asparagine concentrations decreased and mannitol and malonate increased in infected pods 30 DAI. By 60 DAI, most carbohydrates, amino acids, and organic acids were drastically reduced by infection. Mannitol and succinic acid levels increased 60 DAI and likely originated from Mr. RT-qPCR analysis of cacao ESTs indicated a strong response to infection 30 DAI in malformed pod. Evidence indicated that biotrophic hyphae colonized pods and a shift to necrotrophic growth occurred later (during the end stages of infection). Expression of cacao ESTs associated with plant hormone biosynthesis and action was altered. Changes in the expression of Mr ESTs in response to nutrient deficiency in pure culture were small. Changes in Mr gene expression patterns and levels of specific metabolites in necrotic sporulating pods 60 DAI compared to malformed pods 30 DAI indicated that the glyoxylate cycle of Mr was up regulated during the shift from biotrophic to necrotrophic phases of the disease cycle. [Copyright &y& Elsevier]

Abstract: Ustilago maydis, the causal agent of corn smut, has emerged as a basidiomycete model system for signal transduction, dimorphism, and disease development. The well-characterized cAMP/PKA signaling pathway mediates filamentation in response to environmental cues, and in the absence of the cAMP signal, haploid cells grow filamentously. Prior to this report, the G-protein alpha and beta subunits, Gpa3 and Bpp1, respectively, were demonstrated to function upstream of adenylate cyclase, Uac1. In other fungal systems, adenylate cyclase is also positively regulated by the adenylate cyclase-associated protein (CAP). A CAP ortholog, Cap1, was identified by sequence homology in the U. maydis genome. Yeast 2-hybrid analysis indicated that Cap1 bound itself and the C-terminus of Uac1. Deletion of cap1 resulted in abnormal colony formation with filamentous cells that reverted to budding in the presence of exogenous cAMP. The Δcap1 strains had a reduced ability to form mating filaments compared to wild type strains. Pathogenicity was significantly reduced in Δcap1 strains in wild type and solopathogenic genetic backgrounds. These results suggest that Cap1 is an additional component of the cAMP/PKA signaling pathway that coordinates production of cAMP upstream of Uac1. [ABSTRACT FROM AUTHOR]