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Transcriptional responses toward diffusible signals from symbiotic microbes reveal MtNFP- and MtDMI3-dependent reprogramming of host gene expression by arbuscular mycorrhizal fungal lipochitooligosaccharides.

Identifieur interne : 001F56 ( Main/Corpus ); précédent : 001F55; suivant : 001F57

Transcriptional responses toward diffusible signals from symbiotic microbes reveal MtNFP- and MtDMI3-dependent reprogramming of host gene expression by arbuscular mycorrhizal fungal lipochitooligosaccharides.

Auteurs : Lisa F. Czaja ; Claudia Hogekamp ; Patrick Lamm ; Fabienne Maillet ; Eduardo Andres Martinez ; Eric Samain ; Jean Dénarié ; Helge Küster ; Natalija Hohnjec

Source :

RBID : pubmed:22652128

English descriptors

Abstract

The formation of root nodules and arbuscular mycorrhizal (AM) roots is controlled by a common signaling pathway including the calcium/calmodulin-dependent kinase Doesn't Make Infection3 (DMI3). While nodule initiation by lipochitooligosaccharide (LCO) Nod factors is well characterized, diffusible AM fungal signals were only recently identified as sulfated and nonsulfated LCOs. Irrespective of different outcomes, the perception of symbiotic LCOs in Medicago truncatula is mediated by the LysM receptor kinase M. truncatula Nod factor perception (MtNFP). To shed light on transcriptional responses toward symbiotic LCOs and their dependence on MtNFP and Ca(2+) signaling, we performed genome-wide expression studies of wild-type, Nod-factor-perception mutant1, and dmi3 mutant roots challenged with Myc- and Nod-LCOs. We show that Myc-LCOs lead to transient, quick responses in the wild type, whereas Nod-LCOs require prolonged incubation for maximal expression activation. While Nod-LCOs are most efficient for an induction of persistent transcriptional changes, sulfated Myc-LCOs are less active, and nonsulfated Myc-LCOs display the lowest capacity to activate and sustain expression. Although all symbiotic LCOs up-regulated a common set of genes, discrete subsets were induced by individual LCOs, suggesting common and specific functions for these in presymbiotic signaling. Surprisingly, even sulfated fungal Myc-LCOs and Sinorhizobium meliloti Nod-LCOs, having very similar structures, each elicited discrete subsets of genes, while a mixture of both Myc-LCOs activated responses deviating from those induced by single treatments. Focusing on the precontact phase, we identified signaling-related and transcription factor genes specifically up-regulated by Myc-LCOs. Comparative gene expression studies in symbiotic mutants demonstrated that transcriptional reprogramming by AM fungal LCOs strictly depends on MtNFP and largely requires MtDMI3.

DOI: 10.1104/pp.112.195990
PubMed: 22652128
PubMed Central: PMC3425205

Links to Exploration step

pubmed:22652128

Le document en format XML

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<term>Diffusion (drug effects)</term>
<term>Gene Expression Regulation, Plant (drug effects)</term>
<term>Genes, Plant (genetics)</term>
<term>Host-Pathogen Interactions (drug effects)</term>
<term>Host-Pathogen Interactions (genetics)</term>
<term>Kinetics (MeSH)</term>
<term>Lipopolysaccharides (pharmacology)</term>
<term>Medicago truncatula (drug effects)</term>
<term>Medicago truncatula (genetics)</term>
<term>Medicago truncatula (microbiology)</term>
<term>Models, Biological (MeSH)</term>
<term>Mutation (genetics)</term>
<term>Mycorrhizae (drug effects)</term>
<term>Mycorrhizae (physiology)</term>
<term>Plant Proteins (genetics)</term>
<term>Plant Proteins (metabolism)</term>
<term>Plant Roots (drug effects)</term>
<term>Plant Roots (genetics)</term>
<term>Plant Roots (microbiology)</term>
<term>Promoter Regions, Genetic (genetics)</term>
<term>Reproducibility of Results (MeSH)</term>
<term>Signal Transduction (drug effects)</term>
<term>Signal Transduction (genetics)</term>
<term>Symbiosis (drug effects)</term>
<term>Symbiosis (genetics)</term>
<term>Transcription Factors (genetics)</term>
<term>Transcription Factors (metabolism)</term>
<term>Transcription, Genetic (drug effects)</term>
<term>Transcriptional Activation (drug effects)</term>
<term>Transcriptional Activation (genetics)</term>
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<term>Plant Proteins</term>
<term>Transcription Factors</term>
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<term>Plant Proteins</term>
<term>Transcription Factors</term>
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<term>Lipopolysaccharides</term>
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<term>Diffusion</term>
<term>Gene Expression Regulation, Plant</term>
<term>Host-Pathogen Interactions</term>
<term>Medicago truncatula</term>
<term>Mycorrhizae</term>
<term>Plant Roots</term>
<term>Signal Transduction</term>
<term>Symbiosis</term>
<term>Transcription, Genetic</term>
<term>Transcriptional Activation</term>
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<term>Host-Pathogen Interactions</term>
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<term>Mutation</term>
<term>Plant Roots</term>
<term>Promoter Regions, Genetic</term>
<term>Signal Transduction</term>
<term>Symbiosis</term>
<term>Transcriptional Activation</term>
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<term>Plant Roots</term>
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<div type="abstract" xml:lang="en">The formation of root nodules and arbuscular mycorrhizal (AM) roots is controlled by a common signaling pathway including the calcium/calmodulin-dependent kinase Doesn't Make Infection3 (DMI3). While nodule initiation by lipochitooligosaccharide (LCO) Nod factors is well characterized, diffusible AM fungal signals were only recently identified as sulfated and nonsulfated LCOs. Irrespective of different outcomes, the perception of symbiotic LCOs in Medicago truncatula is mediated by the LysM receptor kinase M. truncatula Nod factor perception (MtNFP). To shed light on transcriptional responses toward symbiotic LCOs and their dependence on MtNFP and Ca(2+) signaling, we performed genome-wide expression studies of wild-type, Nod-factor-perception mutant1, and dmi3 mutant roots challenged with Myc- and Nod-LCOs. We show that Myc-LCOs lead to transient, quick responses in the wild type, whereas Nod-LCOs require prolonged incubation for maximal expression activation. While Nod-LCOs are most efficient for an induction of persistent transcriptional changes, sulfated Myc-LCOs are less active, and nonsulfated Myc-LCOs display the lowest capacity to activate and sustain expression. Although all symbiotic LCOs up-regulated a common set of genes, discrete subsets were induced by individual LCOs, suggesting common and specific functions for these in presymbiotic signaling. Surprisingly, even sulfated fungal Myc-LCOs and Sinorhizobium meliloti Nod-LCOs, having very similar structures, each elicited discrete subsets of genes, while a mixture of both Myc-LCOs activated responses deviating from those induced by single treatments. Focusing on the precontact phase, we identified signaling-related and transcription factor genes specifically up-regulated by Myc-LCOs. Comparative gene expression studies in symbiotic mutants demonstrated that transcriptional reprogramming by AM fungal LCOs strictly depends on MtNFP and largely requires MtDMI3.</div>
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<AbstractText>The formation of root nodules and arbuscular mycorrhizal (AM) roots is controlled by a common signaling pathway including the calcium/calmodulin-dependent kinase Doesn't Make Infection3 (DMI3). While nodule initiation by lipochitooligosaccharide (LCO) Nod factors is well characterized, diffusible AM fungal signals were only recently identified as sulfated and nonsulfated LCOs. Irrespective of different outcomes, the perception of symbiotic LCOs in Medicago truncatula is mediated by the LysM receptor kinase M. truncatula Nod factor perception (MtNFP). To shed light on transcriptional responses toward symbiotic LCOs and their dependence on MtNFP and Ca(2+) signaling, we performed genome-wide expression studies of wild-type, Nod-factor-perception mutant1, and dmi3 mutant roots challenged with Myc- and Nod-LCOs. We show that Myc-LCOs lead to transient, quick responses in the wild type, whereas Nod-LCOs require prolonged incubation for maximal expression activation. While Nod-LCOs are most efficient for an induction of persistent transcriptional changes, sulfated Myc-LCOs are less active, and nonsulfated Myc-LCOs display the lowest capacity to activate and sustain expression. Although all symbiotic LCOs up-regulated a common set of genes, discrete subsets were induced by individual LCOs, suggesting common and specific functions for these in presymbiotic signaling. Surprisingly, even sulfated fungal Myc-LCOs and Sinorhizobium meliloti Nod-LCOs, having very similar structures, each elicited discrete subsets of genes, while a mixture of both Myc-LCOs activated responses deviating from those induced by single treatments. Focusing on the precontact phase, we identified signaling-related and transcription factor genes specifically up-regulated by Myc-LCOs. Comparative gene expression studies in symbiotic mutants demonstrated that transcriptional reprogramming by AM fungal LCOs strictly depends on MtNFP and largely requires MtDMI3.</AbstractText>
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