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Journal of Bacteriology, January 2008, p. 343-355, Vol. 190, No. 1
0021-9193/08/$08.00+0     doi:10.1128/JB.00978-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

AvrACXcc8004, a Type III Effector with a Leucine-Rich Repeat Domain from Xanthomonas campestris Pathovar campestris Confers Avirulence in Vascular Tissues of Arabidopsis thaliana Ecotype Col-0{triangledown} ,{dagger}

Rong-Qi Xu,1,{ddagger} Servane Blanvillain,2,{ddagger} Jia-Xun Feng,1 Bo-Le Jiang,1 Xian-Zhen Li,1 Hong-Yu Wei,1 Thomas Kroj,2 Emmanuelle Lauber,2 Dominique Roby,2 Baoshan Chen,1 Yong-Qiang He,1 Guang-Tao Lu,1 Dong-Jie Tang,1 Jacques Vasse,2 Matthieu Arlat,2,3* and Ji-Liang Tang1*

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,1 Laboratoire des Interactions Plantes-Microorganismes, INRA-CNRS, BP52627, 31326 Castanet Cedex, France,2 Université Paul Sabatier, Toulouse III, Toulouse, France3

Received 20 June 2007/ Accepted 10 October 2007

Xanthomonas campestris pathovar campestris causes black rot, a vascular disease on cruciferous plants, including Arabidopsis thaliana. The gene XC1553 from 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 the XC1553 gene in the interaction between X. campestris pv. campestris and A. thaliana. Translocation assays using the hypersensitive-reaction-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 gene 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 the Kashmir ecotype, but not on ecotype Col-0; the XC1553 gene mutant became virulent on the Col-0 ecotype and still induced disease on the Kashmir ecotype. Altogether, these data show that the XC1553 gene, which was renamed avrACXcc8004, functions as an avirulence gene whose product seems to be recognized in vascular tissues.

* Corresponding author. Mailing address for M. Arlat: Laboratoire des Interactions Plantes-Microorganismes, INRA-CNRS, BP52627, 31326 Castanet Cedex, France. Phone: 33-561-285047. Fax: 33-561-285061. E-mail: Matthieu.Arlat{at}toulouse.inra.fr. Mailing address for J.-L. Tang: College of Life Science and Technology, Guangxi University, 100 Daxue Road, Nanning, Guangxi 530004, People's Republic of China. Phone: 86-771-3239566. Fax: 86-771-3239413. E-mail: jltang{at}gxu.edu.cn

{triangledown} Published ahead of print on 19 October 2007.

{dagger} Supplemental material for this article may be found at http://jb.asm.org/.

{ddagger} Rong-Qi Xu and Servane Blanvillain contributed equally to this work.

Journal of Bacteriology, January 2008, p. 343-355, Vol. 190, No. 1
0021-9193/08/$08.00+0     doi:10.1128/JB.00978-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



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