Extensive alteration of fungal gene transcript accumulation and elevation of G-protein-regulated cAMP levels by a virulence-attenuating hypovirus

Persistent infection of the chestnut blight fungus Cryphonectria parasitica with the prototypic hypovirus CHV1-713 results in attenuation of fungal virulence (hypovirulence) and reduced accumulation of the GTP-binding (G) protein alpha subunit CPG-1. Transgenic cosuppression of CPG-1 accumulation in...

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Veröffentlicht in:Proceedings of the National Academy of Sciences - PNAS 1996-07, Vol.93 (15), p.7996-8000
Hauptverfasser: Chen, B. (University of Maryland, College Park, MD.), Gao, S, Choi, G.H, Nuss, D.L
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container_title Proceedings of the National Academy of Sciences - PNAS
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creator Chen, B. (University of Maryland, College Park, MD.)
Gao, S
Choi, G.H
Nuss, D.L
description Persistent infection of the chestnut blight fungus Cryphonectria parasitica with the prototypic hypovirus CHV1-713 results in attenuation of fungal virulence (hypovirulence) and reduced accumulation of the GTP-binding (G) protein alpha subunit CPG-1. Transgenic cosuppression of CPG-1 accumulation in the absence of virus infection also confers hypovirulence. We now report the use of mRNA differential display to examine the extent to which virus infection alters fungal gene transcript accumulation and to assess the degree to which modification of CPG-1 signal transduction contributes to this alteration. More than 400 PCR products were identified that either increased (296 products) or decreased (127 products) in abundance as a result of virus infection. Significantly, 65% of these products exhibited similar changes as a result of CPG-1 cosuppression in the absence of virus infection. We also report that both virus infection and CPG-1 cosuppression elevate cAMP levels 3- to 5-fold. Additionally, it was possible to mimic the effect of virus infection and CPG-1 cosuppression on transcript accumulation for representative fungal genes by drug-induced elevation of cAMP levels. These results strengthen and extend previous indications that hypovirus infection causes a significant and persistent alteration of fungal gene expression/transcript accumulation. They further show that this alteration is primarily mediated through modification of the CPG-1 signaling pathway and suggest that, similar to mammalian Gi; alpha subunits, CPG-1 functions as negative modulator of adenylyl cyclase. Finally, these results suggest a role for G-protein-regulated cAMP accumulation in hypovirus-mediated alteration of fungal gene expression
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(University of Maryland, College Park, MD.) ; Gao, S ; Choi, G.H ; Nuss, D.L</creator><creatorcontrib>Chen, B. (University of Maryland, College Park, MD.) ; Gao, S ; Choi, G.H ; Nuss, D.L</creatorcontrib><description>Persistent infection of the chestnut blight fungus Cryphonectria parasitica with the prototypic hypovirus CHV1-713 results in attenuation of fungal virulence (hypovirulence) and reduced accumulation of the GTP-binding (G) protein alpha subunit CPG-1. Transgenic cosuppression of CPG-1 accumulation in the absence of virus infection also confers hypovirulence. We now report the use of mRNA differential display to examine the extent to which virus infection alters fungal gene transcript accumulation and to assess the degree to which modification of CPG-1 signal transduction contributes to this alteration. More than 400 PCR products were identified that either increased (296 products) or decreased (127 products) in abundance as a result of virus infection. Significantly, 65% of these products exhibited similar changes as a result of CPG-1 cosuppression in the absence of virus infection. We also report that both virus infection and CPG-1 cosuppression elevate cAMP levels 3- to 5-fold. Additionally, it was possible to mimic the effect of virus infection and CPG-1 cosuppression on transcript accumulation for representative fungal genes by drug-induced elevation of cAMP levels. These results strengthen and extend previous indications that hypovirus infection causes a significant and persistent alteration of fungal gene expression/transcript accumulation. They further show that this alteration is primarily mediated through modification of the CPG-1 signaling pathway and suggest that, similar to mammalian Gi; alpha subunits, CPG-1 functions as negative modulator of adenylyl cyclase. 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(University of Maryland, College Park, MD.)</creatorcontrib><creatorcontrib>Gao, S</creatorcontrib><creatorcontrib>Choi, G.H</creatorcontrib><creatorcontrib>Nuss, D.L</creatorcontrib><title>Extensive alteration of fungal gene transcript accumulation and elevation of G-protein-regulated cAMP levels by a virulence-attenuating hypovirus</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>Persistent infection of the chestnut blight fungus Cryphonectria parasitica with the prototypic hypovirus CHV1-713 results in attenuation of fungal virulence (hypovirulence) and reduced accumulation of the GTP-binding (G) protein alpha subunit CPG-1. Transgenic cosuppression of CPG-1 accumulation in the absence of virus infection also confers hypovirulence. We now report the use of mRNA differential display to examine the extent to which virus infection alters fungal gene transcript accumulation and to assess the degree to which modification of CPG-1 signal transduction contributes to this alteration. More than 400 PCR products were identified that either increased (296 products) or decreased (127 products) in abundance as a result of virus infection. Significantly, 65% of these products exhibited similar changes as a result of CPG-1 cosuppression in the absence of virus infection. We also report that both virus infection and CPG-1 cosuppression elevate cAMP levels 3- to 5-fold. Additionally, it was possible to mimic the effect of virus infection and CPG-1 cosuppression on transcript accumulation for representative fungal genes by drug-induced elevation of cAMP levels. These results strengthen and extend previous indications that hypovirus infection causes a significant and persistent alteration of fungal gene expression/transcript accumulation. They further show that this alteration is primarily mediated through modification of the CPG-1 signaling pathway and suggest that, similar to mammalian Gi; alpha subunits, CPG-1 functions as negative modulator of adenylyl cyclase. 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Transgenic cosuppression of CPG-1 accumulation in the absence of virus infection also confers hypovirulence. We now report the use of mRNA differential display to examine the extent to which virus infection alters fungal gene transcript accumulation and to assess the degree to which modification of CPG-1 signal transduction contributes to this alteration. More than 400 PCR products were identified that either increased (296 products) or decreased (127 products) in abundance as a result of virus infection. Significantly, 65% of these products exhibited similar changes as a result of CPG-1 cosuppression in the absence of virus infection. We also report that both virus infection and CPG-1 cosuppression elevate cAMP levels 3- to 5-fold. Additionally, it was possible to mimic the effect of virus infection and CPG-1 cosuppression on transcript accumulation for representative fungal genes by drug-induced elevation of cAMP levels. These results strengthen and extend previous indications that hypovirus infection causes a significant and persistent alteration of fungal gene expression/transcript accumulation. They further show that this alteration is primarily mediated through modification of the CPG-1 signaling pathway and suggest that, similar to mammalian Gi; alpha subunits, CPG-1 functions as negative modulator of adenylyl cyclase. Finally, these results suggest a role for G-protein-regulated cAMP accumulation in hypovirus-mediated alteration of fungal gene expression</abstract><cop>United States</cop><pub>National Academy of Sciences of the United States of America</pub><pmid>8755591</pmid><doi>10.1073/pnas.93.15.7996</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record>
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subjects 1-Methyl-3-isobutylxanthine - pharmacology
ADENOSINE MONOPHOSPHATE
ADENOSINMONOFOSFATO
ARN MENSAJERO
ARN MESSAGER
Caffeine - pharmacology
CRYPHONECTRIA PARASITICA
Cyclic AMP - metabolism
EXPRESION GENICA
EXPRESSION DES GENES
Fungal genes
Fungal Proteins - biosynthesis
Fungi
Genes, Fungal
GENETICA
GENETIQUE
GTP-Binding Protein alpha Subunits, Gi-Go
GTP-Binding Proteins - biosynthesis
Heterotrimeric GTP-Binding Proteins
hypovirus
Infections
Messenger RNA
Microbiology
NUCLEOTIDE
NUCLEOTIDOS
Parasitism
PATHOGENESE
PATOGENESIS
PATOGENICIDAD
Polymerase Chain Reaction
POUVOIR PATHOGENE
Product category rules
Product displays
PROTEINAS AGLUTINANTES
PROTEINE DE LIAISON
Proteins
Ribonucleic acid
RNA
RNA Viruses - physiology
RNA, Fungal - biosynthesis
RNA, Messenger - biosynthesis
Signal Transduction
Theophylline - pharmacology
TRANSCRIPCION
TRANSCRIPTION
Transcription, Genetic
Virulence
VIRUS DE LAS PLANTAS
VIRUS DES VEGETAUX
Virus Replication
Viruses
Xylariales - pathogenicity
Xylariales - physiology
Xylariales - virology
title Extensive alteration of fungal gene transcript accumulation and elevation of G-protein-regulated cAMP levels by a virulence-attenuating hypovirus
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