Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:4.6.1.1 (adenylate cyclase)
 19,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fusarium verticillioides is one of the most important fungal pathogens of maize. Mycotoxin, fumonisins produced by this pathogen pose a threat to human and animal health. Because cAMP signaling has been implicated in regulating diverse developmental and infection processes in fungal pathogens, in this study, we aimed to elucidate the function of the cAMP-protein kinase A (PKA) pathway in toxin production and plant infection in F. verticillioides. Targeted deletion mutants were generated for the CPK1 and FAC1 genes that encode a catalytic subunit of PKA and the adenylate cyclase, respectively. Defects in radial growth and macroconidiation were observed in both the cpk1 and fac1 deletion mutants. The fac1 mutant also was significantly reduced in virulence and microconidiation but increased in tolerance to heat and oxidative stresses. These phenotypes were not observed in the cpk1 mutant, indicating that additional catalytic subunit of PKA must exist and function downstream from FAC1. The fac1 mutant formed microconidia mainly in false heads. The expression levels of the hydrophobin genes HYD1 and HYD2, which are known to be associated with change in formation of microconidia, were significantly reduced in the fac1 mutant. Expression of F. verticillioides GSY2 and HSP26 genes, two other putative downstream targets of FAC1, was increased in the fac1 mutant and may be associated with its enhanced stress tolerance. Although fumonisin production was normal, biosynthesis of bikaverin was increased in the fac1 mutant, suggesting that FAC1 and cAMP signaling may have pathway-or metabolite-specific regulatory roles in secondary metabolism. Overall, the pleiotropic defects of the fac1 deletion mutant indicate that the cAMP-PKA pathway is involved in growth, conidiation, bikaverin production, and plant infection in F. verticillioides.
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PMID:The cAMP signaling pathway in Fusarium verticillioides is important for conidiation, plant infection, and stress responses but not fumonisin production. 2019 38

Like many other filamentous ascomycetes, Fusarium graminearum contains two genes named CPK1 and CPK2 that encode the catalytic subunits of cyclic AMP (cAMP)-dependent protein kinase A (PKA). To determine the role of cAMP signaling in pathogenesis and development in F. graminearum, we functionally characterized these two genes. In addition, we generated and characterized the cpk1 cpk2 double and fac1 adenylate cyclase gene deletion mutants. The cpk1 mutant was significantly reduced in vegetative growth, conidiation, and deoxynivalenol production but it had increased tolerance to elevated temperatures. It was defective in the production of penetration branches on plant surfaces, colonization of wheat rachises, and spreading in flowering wheat heads. Deletion of CPK1 had no effect on perithecium development but the cpk1 mutant was defective in ascospore maturation and releasing. In contrast, the cpk2 mutant had no detectable phenotypes, suggesting that CPK2 contributes minimally to PKA activities in F. graminearum. Nevertheless, the cpk1 cpk2 double mutant had more severe defects in vegetative growth and rarely produced morphologically abnormal conidia. The double mutant, unlike the cpk1 or cpk2 mutant, was nonpathogenic and failed to form perithecia on self-mating plates. Therefore, CPK1 and CPK2 must have overlapping functions in vegetative growth, differentiation, and plant infection in F. graminearum. The fac1 mutant was also nonpathogenic and had growth defects similar to those of the cpk1 cpk2 mutant. However, deletion of FAC1 had no effect on conidium morphology. These results indicated that CPK1 is the major PKA catalytic subunit gene and that the cAMP-PKA pathway plays critical roles in hyphal growth, conidiation, ascosporogenesis, and plant infection in F. graminearum.
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PMID:The cAMP-PKA pathway regulates growth, sexual and asexual differentiation, and pathogenesis in Fusarium graminearum. 2445 Jul 72