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Edinburgh, Scotland, United Kingdom - TAIR

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Autophagic components contribute to hypersensitive<br />

cell death in Arabidopsis<br />

Recent studies implicate autophagy as a pro-survival mechanism in plants that<br />

restricts programmed cell death (PCD) associated with the pathogen-triggered<br />

hypersensitive response (HR). This model is based on the observation that HR<br />

lesions show unrestricted spreading in tobacco and Arabidopsis plants with<br />

RNAi-mediated reduction of autophagy gene expression. We examined HR PCD<br />

responses in autophagy-deficient Arabidopsis knockout mutants (atg), and report<br />

that infection-induced lesions are contained in atg mutants. HR PCD conditioned<br />

by one class of innate immune receptors through the defense regulator EDS1 is<br />

suppressed in atg mutants. Furthermore, we demonstrate that PCD triggered by<br />

immune receptors via NDR1 is either autophagy-independent or engages<br />

autophagic components with cathepsins and other unidentified cell death<br />

mediators. Thus, autophagic cell death contributes to HR PCD and can function<br />

in parallel with other pro-death pathways.<br />

80<br />

C29<br />

Thursday 15:45 - 16:00<br />

Plant Defence<br />

Daniel Hofius1<br />

Torsten Schultz-Larsen2<br />

Jan Joensen1<br />

Dimitrios Tsitsigiannis3<br />

Ole Mattsson1<br />

Nikolaj Petersen4<br />

Lise Jørgensen1<br />

Jonathan D G Jones2<br />

John Mundy1<br />

Morten Petersen1<br />

1Copenhagen University,<br />

Copenhagen<br />

Denmark<br />

2Sainsbury Laboratory<br />

Norwich<br />

UK<br />

3Agricultural University<br />

Athens<br />

Greece<br />

4Danish Cancer Society<br />

Copenhagen<br />

Denmark

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