Autophagic components contribute to hypersensitive cell death in Arabidopsis

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Standard

Autophagic components contribute to hypersensitive cell death in Arabidopsis. / Hofius, Daniel; Schultz-Larsen, Torsten; Joensen, Jan; Tsitsigiannis, Dimitrios I; Petersen, Nikolaj H T; Mattsson, Ole; Jørgensen, Lise Bolt; Jones, Jonathan D G; Mundy, John; Petersen, Morten.

In: Cell, Vol. 137, No. 4, 2009, p. 773-83.

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

Harvard

Hofius, D, Schultz-Larsen, T, Joensen, J, Tsitsigiannis, DI, Petersen, NHT, Mattsson, O, Jørgensen, LB, Jones, JDG, Mundy, J & Petersen, M 2009, 'Autophagic components contribute to hypersensitive cell death in Arabidopsis', Cell, vol. 137, no. 4, pp. 773-83. https://doi.org/10.1016/j.cell.2009.02.036

APA

Hofius, D., Schultz-Larsen, T., Joensen, J., Tsitsigiannis, D. I., Petersen, N. H. T., Mattsson, O., Jørgensen, L. B., Jones, J. D. G., Mundy, J., & Petersen, M. (2009). Autophagic components contribute to hypersensitive cell death in Arabidopsis. Cell, 137(4), 773-83. https://doi.org/10.1016/j.cell.2009.02.036

Vancouver

Hofius D, Schultz-Larsen T, Joensen J, Tsitsigiannis DI, Petersen NHT, Mattsson O et al. Autophagic components contribute to hypersensitive cell death in Arabidopsis. Cell. 2009;137(4):773-83. https://doi.org/10.1016/j.cell.2009.02.036

Author

Hofius, Daniel ; Schultz-Larsen, Torsten ; Joensen, Jan ; Tsitsigiannis, Dimitrios I ; Petersen, Nikolaj H T ; Mattsson, Ole ; Jørgensen, Lise Bolt ; Jones, Jonathan D G ; Mundy, John ; Petersen, Morten. / Autophagic components contribute to hypersensitive cell death in Arabidopsis. In: Cell. 2009 ; Vol. 137, No. 4. pp. 773-83.

Bibtex

@article{02a1df205fd111dea8de000ea68e967b,
title = "Autophagic components contribute to hypersensitive cell death in Arabidopsis",
abstract = "Autophagy has been implicated as a prosurvival mechanism to restrict programmed cell death (PCD) associated with the pathogen-triggered hypersensitive response (HR) during plant innate immunity. This model is based on the observation that HR lesions spread in plants with reduced autophagy gene expression. Here, we examined receptor-mediated HR PCD responses in autophagy-deficient Arabidopsis knockout mutants (atg), and show that infection-induced lesions are contained in atg mutants. We also provide evidence that HR cell death initiated via Toll/Interleukin-1 (TIR)-type immune receptors through the defense regulator EDS1 is suppressed in atg mutants. Furthermore, we demonstrate that PCD triggered by coiled-coil (CC)-type immune receptors via NDR1 is either autophagy-independent or engages autophagic components with cathepsins and other unidentified cell death mediators. Thus, autophagic cell death contributes to HR PCD and can function in parallel with other prodeath pathways.",
author = "Daniel Hofius and Torsten Schultz-Larsen and Jan Joensen and Tsitsigiannis, {Dimitrios I} and Petersen, {Nikolaj H T} and Ole Mattsson and J{\o}rgensen, {Lise Bolt} and Jones, {Jonathan D G} and John Mundy and Morten Petersen",
note = "Keywords: Apoptosis; Arabidopsis; Arabidopsis Proteins; Autophagy; DNA-Binding Proteins; Gene Expression Regulation, Plant; Immunity, Innate; Plant Proteins",
year = "2009",
doi = "10.1016/j.cell.2009.02.036",
language = "English",
volume = "137",
pages = "773--83",
journal = "Cell",
issn = "0092-8674",
publisher = "Cell Press",
number = "4",

}

RIS

TY - JOUR

T1 - Autophagic components contribute to hypersensitive cell death in Arabidopsis

AU - Hofius, Daniel

AU - Schultz-Larsen, Torsten

AU - Joensen, Jan

AU - Tsitsigiannis, Dimitrios I

AU - Petersen, Nikolaj H T

AU - Mattsson, Ole

AU - Jørgensen, Lise Bolt

AU - Jones, Jonathan D G

AU - Mundy, John

AU - Petersen, Morten

N1 - Keywords: Apoptosis; Arabidopsis; Arabidopsis Proteins; Autophagy; DNA-Binding Proteins; Gene Expression Regulation, Plant; Immunity, Innate; Plant Proteins

PY - 2009

Y1 - 2009

N2 - Autophagy has been implicated as a prosurvival mechanism to restrict programmed cell death (PCD) associated with the pathogen-triggered hypersensitive response (HR) during plant innate immunity. This model is based on the observation that HR lesions spread in plants with reduced autophagy gene expression. Here, we examined receptor-mediated HR PCD responses in autophagy-deficient Arabidopsis knockout mutants (atg), and show that infection-induced lesions are contained in atg mutants. We also provide evidence that HR cell death initiated via Toll/Interleukin-1 (TIR)-type immune receptors through the defense regulator EDS1 is suppressed in atg mutants. Furthermore, we demonstrate that PCD triggered by coiled-coil (CC)-type immune receptors via NDR1 is either autophagy-independent or engages autophagic components with cathepsins and other unidentified cell death mediators. Thus, autophagic cell death contributes to HR PCD and can function in parallel with other prodeath pathways.

AB - Autophagy has been implicated as a prosurvival mechanism to restrict programmed cell death (PCD) associated with the pathogen-triggered hypersensitive response (HR) during plant innate immunity. This model is based on the observation that HR lesions spread in plants with reduced autophagy gene expression. Here, we examined receptor-mediated HR PCD responses in autophagy-deficient Arabidopsis knockout mutants (atg), and show that infection-induced lesions are contained in atg mutants. We also provide evidence that HR cell death initiated via Toll/Interleukin-1 (TIR)-type immune receptors through the defense regulator EDS1 is suppressed in atg mutants. Furthermore, we demonstrate that PCD triggered by coiled-coil (CC)-type immune receptors via NDR1 is either autophagy-independent or engages autophagic components with cathepsins and other unidentified cell death mediators. Thus, autophagic cell death contributes to HR PCD and can function in parallel with other prodeath pathways.

U2 - 10.1016/j.cell.2009.02.036

DO - 10.1016/j.cell.2009.02.036

M3 - Journal article

C2 - 19450522

VL - 137

SP - 773

EP - 783

JO - Cell

JF - Cell

SN - 0092-8674

IS - 4

ER -

ID: 12794750