TY - JOUR
T1 - A novel membrane fusion-mediated plant immunity against bacterial pathogens
AU - Hatsugai, Noriyuki
AU - Iwasaki, Shinji
AU - Tamura, Kentaro
AU - Kondo, Maki
AU - Fuji, Kentaro
AU - Ogasawara, Kimi
AU - Nishimura, Mikio
AU - Hara-Nishimura, Ikuko
PY - 2009/11/1
Y1 - 2009/11/1
N2 - Plants have developed their own defense strategies because they have no immune cells. A common plant defense strategy involves programmed cell death (PCD) at the infection site, but how the PCD-associated cell-autonomous immunity is executed in plants is not fully understood. Here we provide a novel mechanism underlying cell-autonomous immunity, which involves the fusion of membranes of a large central vacuole with the plasma membrane, resulting in the discharge of vacuolar antibacterial proteins to the outside of the cells, where bacteria proliferate. The extracellular fluid that was discharged from the vacuoles of infected leaves had both antibacterial activity and cell death-inducing activity. We found that a defect in proteasome function abolished the membrane fusion associated with both disease resistance and PCD in response to avirulent bacterial strains but not to a virulent strain. Furthermore, RNAi plants with a defective proteasome subunit PBA1 have reduced DEVDase activity, which is an activity associated with caspase-3, one of the executors of animal apoptosis. The plant counterpart of caspase-3 has not yet been identified. Our results suggest that PBA1 acts as a plant caspase-3-like enzyme. Thus, this novel defense strategy through proteasome-regulating membrane fusion of the vacuolar and plasma membranes provides plants with a mechanism for attacking intercellular bacterial pathogens.
AB - Plants have developed their own defense strategies because they have no immune cells. A common plant defense strategy involves programmed cell death (PCD) at the infection site, but how the PCD-associated cell-autonomous immunity is executed in plants is not fully understood. Here we provide a novel mechanism underlying cell-autonomous immunity, which involves the fusion of membranes of a large central vacuole with the plasma membrane, resulting in the discharge of vacuolar antibacterial proteins to the outside of the cells, where bacteria proliferate. The extracellular fluid that was discharged from the vacuoles of infected leaves had both antibacterial activity and cell death-inducing activity. We found that a defect in proteasome function abolished the membrane fusion associated with both disease resistance and PCD in response to avirulent bacterial strains but not to a virulent strain. Furthermore, RNAi plants with a defective proteasome subunit PBA1 have reduced DEVDase activity, which is an activity associated with caspase-3, one of the executors of animal apoptosis. The plant counterpart of caspase-3 has not yet been identified. Our results suggest that PBA1 acts as a plant caspase-3-like enzyme. Thus, this novel defense strategy through proteasome-regulating membrane fusion of the vacuolar and plasma membranes provides plants with a mechanism for attacking intercellular bacterial pathogens.
KW - Caspase activity
KW - Cell-autonomous immunity
KW - Hypersensitive response
KW - Membrane fusion
KW - Programmed cell death
KW - Proteasome
UR - http://www.scopus.com/inward/record.url?scp=70350655656&partnerID=8YFLogxK
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U2 - 10.1101/gad.1825209
DO - 10.1101/gad.1825209
M3 - Article
C2 - 19833761
AN - SCOPUS:70350655656
SN - 0890-9369
VL - 23
SP - 2496
EP - 2506
JO - Genes and Development
JF - Genes and Development
IS - 21
ER -