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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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PTH11 gene expression in ΔpdeH and ΔpdeL mutants.RNA was extracted from mycelia cultured in liquid CM medium for 2 days. ACTIN was used for normalization, and the values were calculated by 2-ddCT methods with quantitative RT-PCR data. Values represent mean ±SD from two independent experiments with three replicates each. Asterisk indicates significant differences at P = 0.01.
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pone-0017241-g010: PTH11 gene expression in ΔpdeH and ΔpdeL mutants.RNA was extracted from mycelia cultured in liquid CM medium for 2 days. ACTIN was used for normalization, and the values were calculated by 2-ddCT methods with quantitative RT-PCR data. Values represent mean ±SD from two independent experiments with three replicates each. Asterisk indicates significant differences at P = 0.01.

Mentions: To confirm gene expression patterns derived from our microarray experiments, we performed real-time RT-PCR with four selected genes that were down-regulated in the ΔpdeH mutant. Two genes, MPG1 and PTH11, which are required for pathogenesis, were significantly down-regulated (∼10-fold; Figure 4B and 10). Two laccase genes, MGG_11608.6 and MGG_13464.6, were down-regulated to a greater extent (∼100-fold) in the ΔpdeH mutant (Figure 8C). Although the magnitudes of fold changes in laccase gene expression were much higher than the microarray results, the real-time RT-PCR data supported those of the microarray analyses.


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)

PTH11 gene expression in ΔpdeH and ΔpdeL mutants.RNA was extracted from mycelia cultured in liquid CM medium for 2 days. ACTIN was used for normalization, and the values were calculated by 2-ddCT methods with quantitative RT-PCR data. Values represent mean ±SD from two independent experiments with three replicates each. Asterisk indicates significant differences at P = 0.01.
© Copyright Policy
Related In: Results  -  Collection

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

pone-0017241-g010: PTH11 gene expression in ΔpdeH and ΔpdeL mutants.RNA was extracted from mycelia cultured in liquid CM medium for 2 days. ACTIN was used for normalization, and the values were calculated by 2-ddCT methods with quantitative RT-PCR data. Values represent mean ±SD from two independent experiments with three replicates each. Asterisk indicates significant differences at P = 0.01.
Mentions: To confirm gene expression patterns derived from our microarray experiments, we performed real-time RT-PCR with four selected genes that were down-regulated in the ΔpdeH mutant. Two genes, MPG1 and PTH11, which are required for pathogenesis, were significantly down-regulated (∼10-fold; Figure 4B and 10). Two laccase genes, MGG_11608.6 and MGG_13464.6, were down-regulated to a greater extent (∼100-fold) in the ΔpdeH mutant (Figure 8C). Although the magnitudes of fold changes in laccase gene expression were much higher than the microarray results, the real-time RT-PCR data supported those of the microarray analyses.

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