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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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Appressorium formation assays.(A) Conidia of each strain were incubated on hydrophobic surfaces for 24 hours (up panel); hyphal plugs of each strain were incubated on hydrophobic surfaces for 48 hours (bottom panel). (B) Conidia of each strain were incubated on hydrophilic surfaces for 24 hours.
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pone-0017241-g006: Appressorium formation assays.(A) Conidia of each strain were incubated on hydrophobic surfaces for 24 hours (up panel); hyphal plugs of each strain were incubated on hydrophobic surfaces for 48 hours (bottom panel). (B) Conidia of each strain were incubated on hydrophilic surfaces for 24 hours.

Mentions: Physical cues of inductive surfaces, such as hardness and hydrophobicity, are necessary for appressorium formation [53]. The wild-type strain is unable to form appressoria on non-inductive surfaces, except in the presence of exogenous cAMP or inhibitors of PDEases [70]. To verify the effects of increased cAMP levels in the ΔpdeL and ΔpdeH mutants, we examined appressorium formation on inductive and non-inductive surfaces. The conidia and hyphal tips of the ΔpdeL and ΔpdeH mutants formed normal melanized appressoria on inductive surfaces, similar to the wild-type strain (Figure 6A, Table 2). However, the ΔpdeH mutant was able to form normal melanized appressoria on non-inductive surfaces (Figure 6B, Table 2), indicating that PdeH is an important negative regulator of appressorium formation.


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)

Appressorium formation assays.(A) Conidia of each strain were incubated on hydrophobic surfaces for 24 hours (up panel); hyphal plugs of each strain were incubated on hydrophobic surfaces for 48 hours (bottom panel). (B) Conidia of each strain were incubated on hydrophilic surfaces for 24 hours.
© Copyright Policy
Related In: Results  -  Collection

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

pone-0017241-g006: Appressorium formation assays.(A) Conidia of each strain were incubated on hydrophobic surfaces for 24 hours (up panel); hyphal plugs of each strain were incubated on hydrophobic surfaces for 48 hours (bottom panel). (B) Conidia of each strain were incubated on hydrophilic surfaces for 24 hours.
Mentions: Physical cues of inductive surfaces, such as hardness and hydrophobicity, are necessary for appressorium formation [53]. The wild-type strain is unable to form appressoria on non-inductive surfaces, except in the presence of exogenous cAMP or inhibitors of PDEases [70]. To verify the effects of increased cAMP levels in the ΔpdeL and ΔpdeH mutants, we examined appressorium formation on inductive and non-inductive surfaces. The conidia and hyphal tips of the ΔpdeL and ΔpdeH mutants formed normal melanized appressoria on inductive surfaces, similar to the wild-type strain (Figure 6A, Table 2). However, the ΔpdeH mutant was able to form normal melanized appressoria on non-inductive surfaces (Figure 6B, Table 2), indicating that PdeH is an important negative regulator of appressorium formation.

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