Actin as deathly switch? How auxin can suppress cell-death related defence.
Plant innate immunity is composed of two layers--a basal immunity, and a specific effector-triggered immunity, which is often accompanied by hypersensitive cell death. Initiation of cell death depends on a complex network of signalling pathways. The phytohormone auxin as central regulator of plant growth and development represents an important component for the modulation of plant defence. In our previous work, we showed that cell death is heralded by detachment of actin from the membrane. Both, actin response and cell death, are triggered by the bacterial elicitor harpin in grapevine cells. In this study we investigated, whether harpin-triggered actin bundling is necessary for harpin-triggered cell death. Since actin organisation is dependent upon auxin, we used different auxins to suppress actin bundling. Extracellular alkalinisation and transcription of defence genes as the basal immunity were examined as well as cell death. Furthermore, organisation of actin was observed in response to pharmacological manipulation of reactive oxygen species and phospholipase D. We find that induction of defence genes is independent of auxin. However, auxin can suppress harpin-induced cell death and also counteract actin bundling. We integrate our findings into a model, where harpin interferes with an auxin dependent pathway that sustains dynamic cortical actin through the activity of phospholipase D. The antagonism between growth and defence is explained by mutual competition for signal molecules such as superoxide and phosphatidic acid. Perturbations of the auxin-actin pathway might be used to detect disturbed integrity of the plasma membrane and channel defence signalling towards programmed cell death.
Department of Plant Pathology, Agricultural College, Sichuan Agricultural University, Chengdu 611130, P. R. China.
Xiaoli
X
Chang
Molecular Cell Biology, Botanical Institute, Karlsruhe Institute of Technology, Kaiserstr. 2, D-76128 Karlsruhe, Germany.
Michael
M
Riemann
Molecular Cell Biology, Botanical Institute, Karlsruhe Institute of Technology, Kaiserstr. 2, D-76128 Karlsruhe, Germany.
Qiong
Q
Liu
Molecular Cell Biology, Botanical Institute, Karlsruhe Institute of Technology, Kaiserstr. 2, D-76128 Karlsruhe, Germany.
Peter
P
Nick
D000199:Actins / Q000235:genetics* / Q000276:immunology / Q000378:metabolism; D001425:Bacterial Outer Membrane Proteins / Q000037:antagonists & inhibitors* / Q000302:isolation & purification / Q000494:pharmacology; D018929:Cell Culture Techniques; D016923:Cell Death / Q000187:drug effects / Q000235:genetics; D002462:Cell Membrane / Q000187:drug effects / Q000378:metabolism / Q000648:ultrastructure; D002470:Cell Survival / Q000187:drug effects / Q000235:genetics; D018506:Gene Expression Regulation, Plant; D007210:Indoleacetic Acids / Q000494:pharmacology*; D010712:Phosphatidic Acids / Q000276:immunology / Q000378:metabolism; D010739:Phospholipase D / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D059828:Plant Cells / Q000187:drug effects / Q000276:immunology / Q000378:metabolism* / Q000648:ultrastructure; D010937:Plant Growth Regulators / Q000494:pharmacology*; D057865:Plant Immunity / Q000235:genetics; D018515:Plant Leaves / Q000187:drug effects / Q000235:genetics / Q000276:immunology; D010940:Plant Proteins / Q000235:genetics* / Q000276:immunology / Q000378:metabolism; D044224:Pseudomonas syringae / Q000737:chemistry; D017382:Reactive Oxygen Species / Q000276:immunology / Q000378:metabolism; D015398:Signal Transduction; D013481:Superoxides / Q000276:immunology / Q000378:metabolism; D014158:Transcription, Genetic; D027843:Vitis / Q000187:drug effects / Q000235:genetics / Q000276:immunology
D000199:Actins; D001425:Bacterial Outer Membrane Proteins; D007210:Indoleacetic Acids; D010712:Phosphatidic Acids; D010937:Plant Growth Regulators; D010940:Plant Proteins; D017382:Reactive Oxygen Species; D013481:Superoxides; C087295:HrpZ protein, Pseudomonas syringae; D010739:Phospholipase D