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Molecular Plant Advance Access originally published online on April 29, 2008
Molecular Plant 2008 1(3):482-495; doi:10.1093/mp/ssn013
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© The Author 2008. Published by the Molecular Plant Shanghai Editorial Office in association with Oxford University Press on behalf of CSPP and IPPE, SIBS, CAS.

Kunitz Trypsin Inhibitor: An Antagonist of Cell Death Triggered by Phytopathogens and Fumonisin B1 in Arabidopsis

Jing Lia,b, Günter Bradera and E. Tapio Palvaa,1

a Viikki Biocenter, Department of Biological and Environmental Sciences, Division of Genetics, University of Helsinki, POB 56, FIN-00014, Helsinki, Finland
b Current address: Sainsbury Laboratory, John Innes Centre, Colney, Norwich NR4 7UH, United Kingdom

1 To whom correspondence should be addressed. E-mail tapio.palva{at}helsinki.fi, fax +358-9–191–59076, tel. +358-9-191-59600.

Programmed cell death (PCD) is a central regulatory process in both plant development and in plant responses to pathogens. PCD requires a coordinate activation of pro-apoptotic factors such as proteases and suppressors inhibiting and modulating these processes. In plants, various caspase-like cysteine proteases as well as serine proteases have been implicated in PCD. Here, we show that a serine protease (Kunitz trypsin) inhibitor (KTI1) of Arabidopsis acts as a functional KTI when produced in bacteria and in planta. Expression of AtKTI1 is induced late in response to bacterial and fungal elicitors and to salicylic acid. RNAi silencing of the AtKTI1 gene results in enhanced lesion development after infiltration of leaf tissue with the PCD-eliciting fungal toxin fumonisin B1 (FB1) or the avirulent bacterial pathogen Pseudomonas syringae pv tomato DC3000 carrying avrB (Pst avrB). Overexpression of AtKTI1 results in reduced lesion development after Pst avrB and FB1 infiltration. Interestingly, RNAi silencing of AtKTI1 leads to enhanced resistance to the virulent pathogen Erwinia carotovora subsp. carotovora SCC1, while overexpression of AtKTI1 leads to higher susceptibility towards this pathogen. Together, these data indicate that AtKTI1 is involved in modulating PCD in plant–pathogen interactions.


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