Matching NLR immune receptors to autoimmunity in camta3 mutants using antimorphic NLR alleles

Signe Lolle; Michael Christiaan Greeff; Klaus Petersen; Milena Edna Roux; Michael Krogh Jensen; Simon Bressendorff; Eleazar José Rodriguez Gomes; Kenneth Sømark; John Mundy; Morten Petersen

doi:10.1016/j.chom.2017.03.005

Matching NLR immune receptors to autoimmunity in camta3 mutants using antimorphic NLR alleles

Signe Lolle, Michael Christiaan Greeff, Klaus Petersen, Milena Edna Roux, Michael Krogh Jensen, Simon Bressendorff, Eleazar José Rodriguez Gomes, Kenneth Sømark, John Mundy, Morten Petersen^*

^*Corresponding author for this work

Functional Genomics

34 Citations (Scopus)

Abstract

To establish infection, pathogens deploy effectors to modify or remove host proteins. Plant immune receptors with nucleotide-binding, leucine-rich repeat domains (NLRs) detect these modifications and trigger immunity. Plant NLRs thus guard host “guardees.” A corollary is that autoimmunity may result from inappropriate NLR activation because mutations in plant guardees could trigger corresponding NLR guards. To explore these hypotheses, we expressed 108 dominant-negative (DN) Arabidopsis NLRs in various lesion mimic mutants, including camta3, which exhibits autoimmunity. CAMTA3 was previously described as a negative regulator of immunity, and we find that autoimmunity in camta3 is fully suppressed by expressing DNs of two NLRs, DSC1 and DSC2. Additionally, expression of either NLR triggers cell death that can be suppressed by CAMTA3 expression. These findings support a model in which DSC1 and DSC2 guard CAMTA3, and they suggest that other negative regulators of immunity may similarly represent guardees.

Original language	English
Journal	Cell Host & Microbe
Volume	21
Issue number	4
Pages (from-to)	518-529
Number of pages	12
ISSN	1931-3128
DOIs	https://doi.org/10.1016/j.chom.2017.03.005
Publication status	Published - 2017

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title = "Matching NLR immune receptors to autoimmunity in camta3 mutants using antimorphic NLR alleles",

abstract = "To establish infection, pathogens deploy effectors to modify or remove host proteins. Plant immune receptors with nucleotide-binding, leucine-rich repeat domains (NLRs) detect these modifications and trigger immunity. Plant NLRs thus guard host “guardees.” A corollary is that autoimmunity may result from inappropriate NLR activation because mutations in plant guardees could trigger corresponding NLR guards. To explore these hypotheses, we expressed 108 dominant-negative (DN) Arabidopsis NLRs in various lesion mimic mutants, including camta3, which exhibits autoimmunity. CAMTA3 was previously described as a negative regulator of immunity, and we find that autoimmunity in camta3 is fully suppressed by expressing DNs of two NLRs, DSC1 and DSC2. Additionally, expression of either NLR triggers cell death that can be suppressed by CAMTA3 expression. These findings support a model in which DSC1 and DSC2 guard CAMTA3, and they suggest that other negative regulators of immunity may similarly represent guardees.",

author = "Signe Lolle and Greeff, {Michael Christiaan} and Klaus Petersen and Roux, {Milena Edna} and Jensen, {Michael Krogh} and Simon Bressendorff and {Rodriguez Gomes}, {Eleazar Jos{\'e}} and Kenneth S{\o}mark and John Mundy and Morten Petersen",

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doi = "10.1016/j.chom.2017.03.005",

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T1 - Matching NLR immune receptors to autoimmunity in camta3 mutants using antimorphic NLR alleles

AU - Lolle, Signe

AU - Greeff, Michael Christiaan

AU - Petersen, Klaus

AU - Roux, Milena Edna

AU - Jensen, Michael Krogh

AU - Bressendorff, Simon

AU - Rodriguez Gomes, Eleazar José

AU - Sømark, Kenneth

AU - Mundy, John

AU - Petersen, Morten

PY - 2017

Y1 - 2017

N2 - To establish infection, pathogens deploy effectors to modify or remove host proteins. Plant immune receptors with nucleotide-binding, leucine-rich repeat domains (NLRs) detect these modifications and trigger immunity. Plant NLRs thus guard host “guardees.” A corollary is that autoimmunity may result from inappropriate NLR activation because mutations in plant guardees could trigger corresponding NLR guards. To explore these hypotheses, we expressed 108 dominant-negative (DN) Arabidopsis NLRs in various lesion mimic mutants, including camta3, which exhibits autoimmunity. CAMTA3 was previously described as a negative regulator of immunity, and we find that autoimmunity in camta3 is fully suppressed by expressing DNs of two NLRs, DSC1 and DSC2. Additionally, expression of either NLR triggers cell death that can be suppressed by CAMTA3 expression. These findings support a model in which DSC1 and DSC2 guard CAMTA3, and they suggest that other negative regulators of immunity may similarly represent guardees.

AB - To establish infection, pathogens deploy effectors to modify or remove host proteins. Plant immune receptors with nucleotide-binding, leucine-rich repeat domains (NLRs) detect these modifications and trigger immunity. Plant NLRs thus guard host “guardees.” A corollary is that autoimmunity may result from inappropriate NLR activation because mutations in plant guardees could trigger corresponding NLR guards. To explore these hypotheses, we expressed 108 dominant-negative (DN) Arabidopsis NLRs in various lesion mimic mutants, including camta3, which exhibits autoimmunity. CAMTA3 was previously described as a negative regulator of immunity, and we find that autoimmunity in camta3 is fully suppressed by expressing DNs of two NLRs, DSC1 and DSC2. Additionally, expression of either NLR triggers cell death that can be suppressed by CAMTA3 expression. These findings support a model in which DSC1 and DSC2 guard CAMTA3, and they suggest that other negative regulators of immunity may similarly represent guardees.

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SP - 518

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JF - Cell Host & Microbe

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ER -

Matching NLR immune receptors to autoimmunity in camta3 mutants using antimorphic NLR alleles

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