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Two phosphodiesterase genes, PDEL and PDEH, regulate development and pathogenicity by modulating intracellular cyclic AMP levels in Magnaporthe oryzae.

Zhang H, Liu K, Zhang X, Tang W, Wang J, Guo M, Zhao Q, Zheng X, Wang P, Zhang Z - PLoS ONE (2011)

Bottom Line: As a second messenger, cAMP is important in the activation of downstream effector molecules.This is in contrast to PdeH whose mutation resulted in major defects in conidial morphology, cell wall integrity, and surface hydrophobicity, as well as a significant reduction in pathogenicity.Moreover, microarray data revealed new insights into the underlying cAMP regulatory mechanisms that may help to identify potential pathogenicity factors for the development of new disease management strategies.

View Article: PubMed Central - PubMed

Affiliation: Department of Plant Pathology, College of Plant Protection, Nanjing Agricultural University, and Key Laboratory of Monitoring and Management of Crop Diseases and Pest Insects, Ministry of Agriculture, Nanjing, China.

ABSTRACT
Cyclic AMP (cAMP) signaling plays an important role in regulating multiple cellular responses, such as growth, morphogenesis, and/or pathogenicity of eukaryotic organisms such as fungi. As a second messenger, cAMP is important in the activation of downstream effector molecules. The balance of intracellular cAMP levels depends on biosynthesis by adenylyl cyclases (ACs) and hydrolysis by cAMP phosphodiesterases (PDEases). The rice blast fungus Magnaporthe oryzae contains a high-affinity (PdeH/Pde2) and a low-affinity (PdeL/Pde1) PDEases, and a previous study showed that PdeH has a major role in asexual differentiation and pathogenicity. Here, we show that PdeL is required for asexual development and conidial morphology, and it also plays a minor role in regulating cAMP signaling. This is in contrast to PdeH whose mutation resulted in major defects in conidial morphology, cell wall integrity, and surface hydrophobicity, as well as a significant reduction in pathogenicity. Consistent with both PdeH and PdeL functioning in cAMP signaling, disruption of PDEH only partially rescued the mutant phenotype of ΔmagB and Δpka1. Further studies suggest that PdeH might function through a feedback mechanism to regulate the expression of pathogenicity factor Mpg1 during surface hydrophobicity and pathogenic development. Moreover, microarray data revealed new insights into the underlying cAMP regulatory mechanisms that may help to identify potential pathogenicity factors for the development of new disease management strategies.

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Related in: MedlinePlus

ΔpdeH mutants have a defect in cell-wall integrity.Growth of wild type and mutant strains on complete media (CM) without 1 M sorbitol (top); growth of strains on CM with 1 M sorbitol (middle); growth of strains on straw decoction and corn media (SDC) without sorbitol (bottom). The ΔpdeH and ΔpdeH ΔpdeL mutants undergo progressive autolysis on CM in the absence of osmotic stabilization. Radial growth rates are identical to those of the wild-type strains.
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pone-0017241-g002: ΔpdeH mutants have a defect in cell-wall integrity.Growth of wild type and mutant strains on complete media (CM) without 1 M sorbitol (top); growth of strains on CM with 1 M sorbitol (middle); growth of strains on straw decoction and corn media (SDC) without sorbitol (bottom). The ΔpdeH and ΔpdeH ΔpdeL mutants undergo progressive autolysis on CM in the absence of osmotic stabilization. Radial growth rates are identical to those of the wild-type strains.

Mentions: While the growth of the ΔpdeH mutant appeared normal on CM agar plates (Table 2), the ΔpdeH mutant did undergo progressive autolysis of mycelia after prolonged incubation for at least 14 days (Figure 2, top panel). Autolysis began at the center of the colony and radiated outward. The autolysis of the ΔpdeH mutant can be suppressed by addition of 1 M sorbitol to the culture medium (Figure 2, middle panel). The autolysis tended to be more severe in the ΔpdeLΔpdeH mutant than ΔpdeH, similar to the Δmps1 and Δmck1 mutants that exhibited a defect in cell wall integrity [62], [63]. Interestingly, the ΔpdeH mutant did not undergo autolysis on DSC medium under the same conditions (Figure 2, bottom panel), indicating that PdeH may also be involved in sensing nutrients in the maintenance of cell wall integrity.


Two phosphodiesterase genes, PDEL and PDEH, regulate development and pathogenicity by modulating intracellular cyclic AMP levels in Magnaporthe oryzae.

Zhang H, Liu K, Zhang X, Tang W, Wang J, Guo M, Zhao Q, Zheng X, Wang P, Zhang Z - PLoS ONE (2011)

ΔpdeH mutants have a defect in cell-wall integrity.Growth of wild type and mutant strains on complete media (CM) without 1 M sorbitol (top); growth of strains on CM with 1 M sorbitol (middle); growth of strains on straw decoction and corn media (SDC) without sorbitol (bottom). The ΔpdeH and ΔpdeH ΔpdeL mutants undergo progressive autolysis on CM in the absence of osmotic stabilization. Radial growth rates are identical to those of the wild-type strains.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3046207&req=5

pone-0017241-g002: ΔpdeH mutants have a defect in cell-wall integrity.Growth of wild type and mutant strains on complete media (CM) without 1 M sorbitol (top); growth of strains on CM with 1 M sorbitol (middle); growth of strains on straw decoction and corn media (SDC) without sorbitol (bottom). The ΔpdeH and ΔpdeH ΔpdeL mutants undergo progressive autolysis on CM in the absence of osmotic stabilization. Radial growth rates are identical to those of the wild-type strains.
Mentions: While the growth of the ΔpdeH mutant appeared normal on CM agar plates (Table 2), the ΔpdeH mutant did undergo progressive autolysis of mycelia after prolonged incubation for at least 14 days (Figure 2, top panel). Autolysis began at the center of the colony and radiated outward. The autolysis of the ΔpdeH mutant can be suppressed by addition of 1 M sorbitol to the culture medium (Figure 2, middle panel). The autolysis tended to be more severe in the ΔpdeLΔpdeH mutant than ΔpdeH, similar to the Δmps1 and Δmck1 mutants that exhibited a defect in cell wall integrity [62], [63]. Interestingly, the ΔpdeH mutant did not undergo autolysis on DSC medium under the same conditions (Figure 2, bottom panel), indicating that PdeH may also be involved in sensing nutrients in the maintenance of cell wall integrity.

Bottom Line: As a second messenger, cAMP is important in the activation of downstream effector molecules.This is in contrast to PdeH whose mutation resulted in major defects in conidial morphology, cell wall integrity, and surface hydrophobicity, as well as a significant reduction in pathogenicity.Moreover, microarray data revealed new insights into the underlying cAMP regulatory mechanisms that may help to identify potential pathogenicity factors for the development of new disease management strategies.

View Article: PubMed Central - PubMed

Affiliation: Department of Plant Pathology, College of Plant Protection, Nanjing Agricultural University, and Key Laboratory of Monitoring and Management of Crop Diseases and Pest Insects, Ministry of Agriculture, Nanjing, China.

ABSTRACT
Cyclic AMP (cAMP) signaling plays an important role in regulating multiple cellular responses, such as growth, morphogenesis, and/or pathogenicity of eukaryotic organisms such as fungi. As a second messenger, cAMP is important in the activation of downstream effector molecules. The balance of intracellular cAMP levels depends on biosynthesis by adenylyl cyclases (ACs) and hydrolysis by cAMP phosphodiesterases (PDEases). The rice blast fungus Magnaporthe oryzae contains a high-affinity (PdeH/Pde2) and a low-affinity (PdeL/Pde1) PDEases, and a previous study showed that PdeH has a major role in asexual differentiation and pathogenicity. Here, we show that PdeL is required for asexual development and conidial morphology, and it also plays a minor role in regulating cAMP signaling. This is in contrast to PdeH whose mutation resulted in major defects in conidial morphology, cell wall integrity, and surface hydrophobicity, as well as a significant reduction in pathogenicity. Consistent with both PdeH and PdeL functioning in cAMP signaling, disruption of PDEH only partially rescued the mutant phenotype of ΔmagB and Δpka1. Further studies suggest that PdeH might function through a feedback mechanism to regulate the expression of pathogenicity factor Mpg1 during surface hydrophobicity and pathogenic development. Moreover, microarray data revealed new insights into the underlying cAMP regulatory mechanisms that may help to identify potential pathogenicity factors for the development of new disease management strategies.

Show MeSH
Related in: MedlinePlus