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Plant and Cell Physiology Advance Access published online on February 8, 2007
Plant and Cell Physiology, doi:10.1093/pcp/pcm021
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© The Author 2007. Published by Oxford University Press on behalf of Japanese Society of Plant Physiologists. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

MAP kinases function at the downstream of HSP90 and upstream of mitochondria in TMV-resistance gene N-mediated hypersensitive cell death

Reona Takabatake1, Yuko Ando1, Shigemi Seo1, Shinpei Katou1, Shinya Tsuda2, Yuko Ohashi1 and Ichiro Mitsuhara1,*

1National Institute of Agrobiological Sciences, 2-1-2 Kannondai, Tsukuba, Ibaraki, 305-8602, Japan
2National Agricultural Research Center, Tsukuba Ibaraki 305-8666, Japan

*For correspondence (fax +81 029 8387469; e-mail mituhara{at}affrc.go.jp).


  Abstract

Although the involvement of HSP90, mitogen-activated protein kinase (MAPK) cascades, and organelle dysfunction in plant hypersensitive cell death has been suggested, the mutual relationship among them has not been elucidated. Here, we show that the molecular network of HSP90, WIPK/SIPK-mediated MAPK cascade, and mitochondrial dysfunction in Tobacco mosaic virus (TMV) resistance gene N-dependent cell death. p50, the Avr component for N, NtMEK2DD, a constitutively active form of a MAPK kinase of WIPK/SIPK, and a mammalian pro-apoptotic factor Bax were used for cell death induction. Suppression of HSP90 and treatment with geldanamycin, a specific inhibitor of HSP90, compromised p50- but not NtMEK2DD– or Bax-mediated cell death accompanying the reduction of NtMEK2, WIPK, and SIPK activation. In WIPK/SIPK-double knockdown plants, p50- and NtMEK2DD– but not Bax-mediated cell death was suppressed. All three types of cell death induced mitochondrial dysfunction, but they were similarly suppressed by Bcl-xL, which is a mammalian anti-apoptotic factor, and prevents mitochondrial dysfunction in plants as animals in cell death signal pathway. Taken together with the expression profile of hypersensitive reaction marker genes, it was indicated that the MAPK cascade functions downstream of HSP90 and transduces the cell death signal to mitochondria for the N gene-dependent cell death.

Furthermore, we found that WIPK and SIPK are functionally redundant in cell death signaling using WIPK/SIPK single or double knockdown plants.

Keywords: heat shock protein 90 - mitochondria - mitogen-activated protein kinase - programmed cell death - signal transduction - transient expression


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