Home

About

Advanced Search

Browse by Discipline

Scientific Societies

E-print Alerts

Add E-prints

E-print Network
FAQHELPSITE MAPCONTACT US


  Advanced Search  

 
The Plant Cell, Vol. 15, 93106, January 2003, www.plantcell.org 2002 American Society of Plant Biologists Tandemly Duplicated Arabidopsis Genes That Encode
 

Summary: The Plant Cell, Vol. 15, 93­106, January 2003, www.plantcell.org © 2002 American Society of Plant Biologists
Tandemly Duplicated Arabidopsis Genes That Encode
Polygalacturonase-Inhibiting Proteins Are Regulated
Coordinately by Different Signal Transduction Pathways
in Response to Fungal Infection
Simone Ferrari,a Donatella Vairo,b Frederick M. Ausubel,a Felice Cervone,b and Giulia De Lorenzob,1
a Department of Genetics, Harvard Medical School, and Department of Molecular Biology, Massachusetts General Hospital,
Boston, Massachusetts 02114
b Dipartimento di Biologia Vegetale, Universitą di Roma "La Sapienza," Piazzale Aldo Moro 5, 00185 Rome, Italy
Polygalacturonase-inhibiting proteins (PGIPs) are plant proteins that counteract fungal polygalacturonases, which are
important virulence factors. Like many other plant defense proteins, PGIPs are encoded by gene families, but the roles
of individual genes in these families are poorly understood. Here, we show that in Arabidopsis, two tandemly dupli-
cated PGIP genes are upregulated coordinately in response to Botrytis cinerea infection, but through separate signal
transduction pathways. AtPGIP2 expression is mediated by jasmonate and requires COI1 and JAR1, whereas AtPGIP1
expression is upregulated strongly by oligogalacturonides but is unaffected by salicylic acid, jasmonate, or ethylene.
Both AtPGIP1 and AtPGIP2 encode functional inhibitors of polygalacturonase from Botrytis, and their overexpression in
Arabidopsis significantly reduces Botrytis disease symptoms. Therefore, gene duplication followed by the divergence
of promoter regions may result in different modes of regulation of similar defensive proteins, thereby enhancing the
likelihood of defense gene activation during pathogen infection.
INTRODUCTION

  

Source: Ausubel, Frederick M. - Department of Genetics, Harvard University

 

Collections: Biology and Medicine