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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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Functional categorization of the consensus genes.(A) Expression profiles were combined and showing PdeL- and PdeH-dependent. (B) Up-regulation and down-regulation of more than two-fold change genes were grouped according to their putative function (see Supplemental data for details).
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pone-0017241-g009: Functional categorization of the consensus genes.(A) Expression profiles were combined and showing PdeL- and PdeH-dependent. (B) Up-regulation and down-regulation of more than two-fold change genes were grouped according to their putative function (see Supplemental data for details).

Mentions: To identify genes regulated by PdeL and PdeH, we compared gene expression profiles of ΔpdeL, ΔpdeH, and ΔpdeLΔpdeH mutants with the wild-type strain during the hyphal stage. In total, 1582 genes were up-regulated and 1724 genes were down-regulated in ΔpdeL, ΔpdeH, and ΔpdeLΔpdeH mutants (Figure 9A). Of the 1582 up-regulated genes, we found 373 that were regulated by PdeL, 459 by PdeH, and 1248 by PdeL and PdeH together. Of the 1724 down-regulated genes, the corresponding numbers were 509, 652, and 1450, respectively. Those genes in which the expression ratio was greater than 2-fold were functionally grouped into GO categories as described in the Materials and Methods (Figure 9B, Tables S2, S3 and S4). Overall, we noted that genes associated with protein and amino acid degradation, lipid degradation, secondary metabolism including melanin biosynthesis, and cellular transportation exhibited marked decreases in expression. Among genes that were up-regulated by PdeL, PdeH, or PdeL and PdeH, we were able to positively assign two genes, MGG_07881.6 and MGG_03508.6, to PdeH, in contrast to many by PdeL or PdeL and PdeH (Table S5).


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)

Functional categorization of the consensus genes.(A) Expression profiles were combined and showing PdeL- and PdeH-dependent. (B) Up-regulation and down-regulation of more than two-fold change genes were grouped according to their putative function (see Supplemental data for details).
© Copyright Policy
Related In: Results  -  Collection

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

pone-0017241-g009: Functional categorization of the consensus genes.(A) Expression profiles were combined and showing PdeL- and PdeH-dependent. (B) Up-regulation and down-regulation of more than two-fold change genes were grouped according to their putative function (see Supplemental data for details).
Mentions: To identify genes regulated by PdeL and PdeH, we compared gene expression profiles of ΔpdeL, ΔpdeH, and ΔpdeLΔpdeH mutants with the wild-type strain during the hyphal stage. In total, 1582 genes were up-regulated and 1724 genes were down-regulated in ΔpdeL, ΔpdeH, and ΔpdeLΔpdeH mutants (Figure 9A). Of the 1582 up-regulated genes, we found 373 that were regulated by PdeL, 459 by PdeH, and 1248 by PdeL and PdeH together. Of the 1724 down-regulated genes, the corresponding numbers were 509, 652, and 1450, respectively. Those genes in which the expression ratio was greater than 2-fold were functionally grouped into GO categories as described in the Materials and Methods (Figure 9B, Tables S2, S3 and S4). Overall, we noted that genes associated with protein and amino acid degradation, lipid degradation, secondary metabolism including melanin biosynthesis, and cellular transportation exhibited marked decreases in expression. Among genes that were up-regulated by PdeL, PdeH, or PdeL and PdeH, we were able to positively assign two genes, MGG_07881.6 and MGG_03508.6, to PdeH, in contrast to many by PdeL or PdeL and PdeH (Table S5).

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