Autophagy controls plant basal immunity in a pathogenic lifestyle-dependent manner

Lenz, Heike D.; Haller, Eva; Melzer, Eric; Gust, Andrea A.; Nürnberger, Thorsten

doi:10.4161/auto.7.7.15535

Cited by 34 publications

(41 citation statements)

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“…The response may be associated with autophagy, whose "pro-death" functions provide an essential mechanism for removal of damaged membranes, organelles, oxidized proteins, and other cellular "garbage" and are vital for maintenance of homeostasis (Hofius et al 2011). Autophagy can also serve "anti-death" functions, which are important in innate immunity because they limit the spread of cell death during infection with necrotophic fungal pathogens (Lenz et al 2011). However, when the innate immunity and autophagy are insufficient to control infection and remove garbage, respectively, accumulation of host-cell-derived damage-associated molecular patterns (DAMPs) may trigger accumulation of salicylic acid and pathogenesis-related proteins (Krol et al 2010).…”

Section: Discussionmentioning

confidence: 98%

Involvement of a Class III Peroxidase and the Mitochondrial Protein TSPO in Oxidative Burst Upon Treatment of Moss Plants with a Fungal Elicitor

Lehtonen

Akita²,

Frank³

et al. 2012

MPMI

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Production of apoplastic reactive oxygen species (ROS), or oxidative burst, is among the first responses of plants upon recognition of microorganisms. It requires peroxidase or NADPH oxidase (NOX) activity and factors maintaining cellular redox homeostasis. Here, PpTSPO1 involved in mitochondrial tetrapyrrole transport and abiotic (salt) stress tolerance was tested for its role in biotic stress in Physcomitrella patens, a nonvascular plant (moss). The fungal elicitor chitin caused an immediate oxidative burst in wild-type P. patens but not in the previously described ΔPrx34 mutants lacking the chitin-responsive secreted class III peroxidase (Prx34). Oxidative burst in P. patens was associated with induction of the oxidative stress-related genes AOX, LOX7, and NOX, and also PpTSPO1. The available ΔPpTSPO1 knockout mutants overexpressed AOX and LOX7 constitutively, produced 2.6-fold more ROS than wild-type P. patens, and exhibited increased sensitivity to a fungal necrotrophic pathogen and a saprophyte. These results indicate that Prx34, which is pivotal for antifungal resistance, catalyzes ROS production in P. patens, while PpTSPO1 controls redox homeostasis. The capacity of TSPO to bind harmful free heme and porphyrins and scavenge them through autophagy, as shown in Arabidopsis under abiotic stress, seems important to maintenance of the homeostasis required for efficient pathogen defense.

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Section: Discussionmentioning

confidence: 98%

Involvement of a Class III Peroxidase and the Mitochondrial Protein TSPO in Oxidative Burst Upon Treatment of Moss Plants with a Fungal Elicitor

Lehtonen

Akita²,

Frank³

et al. 2012

MPMI

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“…16 Moreover, during ETI the function Recent reports have shown that plant autophagy is essential for the restriction, and conversely, also for the promotion of HR-PCD at the site of pathogen infection. [11][12][13][14] In tobacco mosaic virus (TMV)-infected Nicotiana benthamiana, knock-down of ATG6 and ATG7 genes resulted in spreading of N-mediated HR genes have been identified in metazoans and yeast, most of which also have counterparts in plants.…”

Section: Autophagy In Plant Innate Immunity-pathogen Life Style Makesmentioning

confidence: 99%

ATG7contributes to plant basal immunity towards fungal infection

Lenz

Vierstra

Nürnberger

et al. 2011

Plant Signaling & Behavior

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A utophagy 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.Plants have evolved a bipartite plant immune system to cope with microbial infections. The first layer of defense relies on the recognition of pathogenassociated molecular patterns (PAMP)

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“…Increased resistance to the virulent biotrophic bacterial pathogen Pseudomonas syringae pv. tomato was also observed in plants harboring mutations in autophagy proteins [25], [26]. These studies suggest a negative effect of plant autophagy in resistance responses toward biotrophic pathogens and are in contrast to N-mediated resistance to tobacco mosaic virus (TMV), which requires functional autophagic machinery for an effective (HR-PCD) defense response [27].…”

Section: Poppies and Charms Can Make Us Sleep As Well [3]mentioning

confidence: 92%

“…Indeed, Arabidopsis ATG5, ATG10, and ATG18a mutants developed spreading necrosis and enhanced disease susceptibility upon infection with necrotrophic fungus Alternaria brassicicola [25], [26]. This includes elevated ROS, which appeared in noninfected regions as well.…”

Section: Poppies and Charms Can Make Us Sleep As Well [3]mentioning

confidence: 99%