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Identification of a putative voltage‐gated Ca 2+ channel as a key regulator of elicitor‐induced hypersensitive cell death and mitogen‐activated protein kinase activation in rice
Author(s) -
Kurusu Takamitsu,
Yagala Toshikazu,
Miyao Akio,
Hirochika Hirohiko,
Kuchitsu Kazuyuki
Publication year - 2005
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 - 10.1111/j.1365-313x.2005.02415.x
Subject(s) - elicitor , hypersensitive response , microbiology and biotechnology , protein kinase a , biology , mapk/erk pathway , programmed cell death , kinase , biochemistry , apoptosis , gene
Summary Elicitor‐triggered transient membrane potential changes and Ca 2+ influx through the plasma membrane are thought to be important during defense signaling in plants. However, the molecular bases for the Ca 2+ influx and its regulation remain largely unknown. Here we tested effects of overexpression as well as retrotransposon ( Tos17 )‐insertional mutagenesis of the rice two‐pore channel 1 (OsTPC1), a putative voltage‐gated Ca 2+ ‐permeable channel, on a proteinaceous fungal elicitor‐induced defense responses in rice cells. The overexpressor showed enhanced sensitivity to the elicitor to induce oxidative burst, activation of a mitogen‐activated protein kinase (MAPK), OsMPK2, as well as hypersensitive cell death. On the contrary, a series of defense responses including the cell death and activation of the MAPK were severely suppressed in the insertional mutant, which was complemented by overexpression of the wild‐type gene. These results suggest that the putative Ca 2+ ‐permeable channel determines sensitivity to the elicitor and plays a role as a key regulator of elicitor‐induced defense responses, activation of MAPK cascade and hypersensitive cell death.