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NO way back: nitric oxide and programmed cell death in Arabidopsis thaliana suspension cultures
Author(s) -
Clarke Andrew,
Desikan Radhika,
Hurst Roger D.,
Hancock John T.,
Neill Steven J.
Publication year - 2000
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1046/j.1365-313x.2000.00911.x
Subject(s) - programmed cell death , arabidopsis , microbiology and biotechnology , protein kinase a , arabidopsis thaliana , mapk/erk pathway , hypersensitive response , apoptosis , biology , kinase , nitric oxide , cell culture , chemistry , biochemistry , gene , mutant , genetics , endocrinology
Summary Recent research has implicated nitric oxide (NO) in the induction of the hypersensitive response (HR) during plant–pathogen interactions. Here we demonstrate that Arabidopsis suspension cultures generate elevated levels of NO in response to challenge by avirulent bacteria, and, using NO donors, show that these elevated levels of NO are sufficient to induce cell death in Arabidopsis cells independently of reactive oxygen species (ROS). We also provide evidence that NO‐induced cell death is a form of programmed cell death (PCD), requiring gene expression, and has a number of characteristics of PCD of mammalian cells: NO induced chromatin condensation and caspase‐like activity in Arabidopsis cells, while the caspase‐1 inhibitor, Ac‐YVAD‐CMK, blocked NO‐induced cell death. A well‐established second messenger mediating NO responses in mammalian cells is cGMP, produced by the enzyme guanylate cyclase. A specific inhibitor of guanylate cyclase blocked NO‐induced cell death in Arabidopsis cells, and this inhibition was reversed by the cell‐permeable cGMP analogue, 8Br‐cGMP, although 8Br‐cGMP alone did not induce cell death or potentiate NO‐induced cell death. This suggests that cGMP synthesis is required but not sufficient for NO‐induced cell death in Arabidopsis . In‐gel protein kinase assays showed that NO activates a potential mitogen‐activated protein kinase (MAPK), although a specific inhibitor of mammalian MAPK activation, PD98059, which blocked H 2 O 2 ‐induced cell death, did not inhibit the effects of NO.