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

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Standard

Matching NLR immune receptors to autoimmunity in camta3 mutants using antimorphic NLR alleles. / Lolle, Signe; Greeff, Michael Christiaan; Petersen, Klaus; Roux, Milena Edna; Jensen, Michael Krogh; Bressendorff, Simon; Rodriguez Gomes, Eleazar José; Sømark, Kenneth; Mundy, John; Petersen, Morten.

In: Cell Host & Microbe, Vol. 21, No. 4, 2017, p. 518-529.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Lolle, S, Greeff, MC, Petersen, K, Roux, ME, Jensen, MK, Bressendorff, S, Rodriguez Gomes, EJ, Sømark, K, Mundy, J & Petersen, M 2017, 'Matching NLR immune receptors to autoimmunity in camta3 mutants using antimorphic NLR alleles', Cell Host & Microbe, vol. 21, no. 4, pp. 518-529. https://doi.org/10.1016/j.chom.2017.03.005

APA

Lolle, S., Greeff, M. C., Petersen, K., Roux, M. E., Jensen, M. K., Bressendorff, S., Rodriguez Gomes, E. J., Sømark, K., Mundy, J., & Petersen, M. (2017). Matching NLR immune receptors to autoimmunity in camta3 mutants using antimorphic NLR alleles. Cell Host & Microbe, 21(4), 518-529. https://doi.org/10.1016/j.chom.2017.03.005

Vancouver

Lolle S, Greeff MC, Petersen K, Roux ME, Jensen MK, Bressendorff S et al. Matching NLR immune receptors to autoimmunity in camta3 mutants using antimorphic NLR alleles. Cell Host & Microbe. 2017;21(4):518-529. https://doi.org/10.1016/j.chom.2017.03.005

Author

Lolle, Signe ; Greeff, Michael Christiaan ; Petersen, Klaus ; Roux, Milena Edna ; Jensen, Michael Krogh ; Bressendorff, Simon ; Rodriguez Gomes, Eleazar José ; Sømark, Kenneth ; Mundy, John ; Petersen, Morten. / Matching NLR immune receptors to autoimmunity in camta3 mutants using antimorphic NLR alleles. In: Cell Host & Microbe. 2017 ; Vol. 21, No. 4. pp. 518-529.

Bibtex

@article{3e7195ca866e4580a5d883f5649c0b69,
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",
year = "2017",
doi = "10.1016/j.chom.2017.03.005",
language = "English",
volume = "21",
pages = "518--529",
journal = "Cell Host & Microbe",
issn = "1931-3128",
publisher = "Cell Press",
number = "4",

}

RIS

TY - JOUR

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.

UR - http://www.scopus.com/inward/record.url?scp=85017374778&partnerID=8YFLogxK

U2 - 10.1016/j.chom.2017.03.005

DO - 10.1016/j.chom.2017.03.005

M3 - Journal article

C2 - 28407487

AN - SCOPUS:85017374778

VL - 21

SP - 518

EP - 529

JO - Cell Host & Microbe

JF - Cell Host & Microbe

SN - 1931-3128

IS - 4

ER -

ID: 179393643