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J. Bacteriol. doi:10.1128/JB.00978-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

AvrAC_Xcc8004, a type III effector with a leucine rich repeat domain from Xanthomonas campestris pathovar campestris confers avirulence in vascular tissues of the Arabidopsis thaliana ecotype Col-0

Guangxi Key Laboratory of Subtropical Bioresources Conservation and Utilization, The Key Laboratory of Ministry of Education for Microbial and Plant Genetic Engineering, and College of Life Science and Technology, Guangxi University, 100 Daxue Road, Nanning, Guangxi 530004, People's Republic of China; Laboratoire des Interactions Plantes-Microorganismes, INRA-CNRS, BP52627, 31326 Castanet Cedex, France; Université Paul Sabatier, Toulouse III, Toulouse, France

^* To whom correspondence should be addressed. Email: Matthieu.Arlat{at}toulouse.inra.fr. jltang{at}gxu.edu.cn.

	Abstract

Xanthomonas campestris pathovar campestris causes black rot, a vascular disease on cruciferous plants including Arabidopsis thaliana. The gene XC1553 from the X. campestris pv. campestris strain 8004 encodes a protein containing leucine-rich repeats (LRRs) and appears to be restricted to strains of X. campestris pv. campestris. LRRs are found in a number of type III-secreted effectors in plant and animal pathogens. These prompted us to investigate the role of XC1553 in the interaction between X. campestris pv. campestris and A. thaliana. Translocation assay using the HR-inducing domain of X. campestris pv. campestris AvrBs1 as a reporter revealed that XC1553 is a type III effector. Infiltration of Arabidopsis leaf mesophyll with bacterial suspensions showed no differences between the wild type strain and an XC1553 mutant; both strains induced disease symptoms on Kashmir and Col-0 ecotypes. However, a clear difference was observed when bacteria were introduced into the vascular system by piercing the central vein of leaves. In this case, the wild type strain 8004 caused disease on Kashmir ecotype, but not on ecotype Col-0; the XC1553 mutant became virulent on Col-0 ecotype and still induced disease on Kashmir ecotype. Altogether, these data show that XC1553, which was renamed avrAC_Xcc8004, functions as an avirulence gene whose product seems to be recognized in vascular tissues.

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