Premium
A high‐throughput screen of cell‐death‐inducing factors in Nicotiana benthamiana identifies a novel MAPKK that mediates INF1‐induced cell death signaling and non‐host resistance to Pseudomonas cichorii
Author(s) -
Takahashi Yoshihiro,
Nasir Khairun Hisam Bin,
Ito Akiko,
Kanzaki Hiroyuki,
Matsumura Hideo,
Saitoh Hiromasa,
Fujisawa Shizuko,
Kamoun Sophien,
Terauchi Ryohei
Publication year - 2007
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.2006.03022.x
Subject(s) - nicotiana benthamiana , biology , programmed cell death , microbiology and biotechnology , elicitor , gene silencing , hypersensitive response , mapk/erk pathway , protein kinase a , schneider 2 cells , kinase , rna interference , apoptosis , gene , genetics , rna
Summary A high‐throughput overexpression screen of Nicotiana benthamiana cDNAs identified a gene for a mitogen‐activated protein kinase kinase (MAPKK) as a potent inducer of the hypersensitive response (HR)‐like cell death. NbMKK1 protein is localized to the nucleus, and the N‐terminal putative MAPK docking site of NbMKK1 is required for its function as a cell‐death inducer. NbMKK1 ‐mediated leaf‐cell death was compromised in leaves where NbSIPK expression was silenced by virus‐induced gene silencing. A yeast two‐hybrid assay showed that NbMKK1 and NbSIPK physically interact, suggesting that NbSIPK is one of the downstream targets of NbMKK1. Phytophthora infestans INF1 elicitor‐mediated HR was delayed in NbMKK1 ‐silenced plants, indicating that NbMKK1 is involved in this HR pathway. Furthermore, the resistance of N. benthamiana to a non‐host pathogen Pseudomonas cichorii was compromised in NbMKK1 ‐silenced plants. These results demonstrate that MAPK cascades involving NbMKK1 control non‐host resistance including HR cell death.