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ATG7contributes to plant basal immunity towards fungal infection
- Source :
- Plant Signaling & Behavior. 6:1040-1042
- Publication Year :
- 2011
- Publisher :
- Informa UK Limited, 2011.
-
Abstract
- Autophagy has an important function in cellular homeostasis. In recent years autophagy has been implicated in plant basal immunity and assigned negative (“anti-death”) and positive (“pro-death”) regulatory functions in controlling cell death programs that establish sufficient immunity to microbial infection. We recently showed that Arabidopsis mutants lacking the autophagy-associated (ATG) genes ATG5, ATG10 and ATG18a are compromised in their resistance towards infection with necrotrophic fungal pathogens but display an enhanced resistance towards biotrophic bacterial invaders. Thus, the function of autophagy as either being pro-death or anti-death depends critically on the lifestyle and infection strategy of invading microbes. Here we show that ATG7 contributes to resistance to fungal pathogens. Genetic inactivation of ATG7 results in elevated susceptibility towards the necrotrophic fungal pathogen, Alternaria brassicicola, with atg7 mutants developing spreading necrosis accompanied by production of reactive oxygen intermediates. Likewise, treatment with the fungal toxin fumonisin B1 causes spreading lesion formation in the atg7 mutant. We conclude that ATG7-dependent autophagy constitutes an “anti-death” (“pro-survival”) plant mechanism to control the containment of cell death and immunity to necrophic fungal infection.
- Subjects :
- Alternaria brassicicola
Programmed cell death
Arabidopsis Proteins
ATG5
Autophagy
Arabidopsis
Alternaria
Plant Immunity
Cellular homeostasis
Plant Science
Biology
Plants, Genetically Modified
biology.organism_classification
Fumonisins
Article Addendum
Microbiology
Gene Expression Regulation, Plant
Immunity
Subjects
Details
- ISSN :
- 15592324
- Volume :
- 6
- Database :
- OpenAIRE
- Journal :
- Plant Signaling & Behavior
- Accession number :
- edsair.doi.dedup.....e4016632c511e3229137fedf8cec6211
- Full Text :
- https://doi.org/10.4161/psb.6.7.15605