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Sequential Expression of Bacterial Virulence and Plant Defense Genes During Infection of Tomato with Clavibacter michiganensis subsp. michiganensis

March 2010 , Volume 100 , Number  3
Pages  252 - 261

L. Chalupowicz, M. Cohen-Kandli, O. Dror, R. Eichenlaub, K.-H. Gartemann, G. Sessa, I. Barash, and S. Manulis-Sasson

First, second, third, and eighth authors: Department of Plant Pathology and Weed Research, ARO, the Volcani Center, Bet Dagan, Israel; first, second, sixth, and seventh authors: Department of Plant Sciences, Tel Aviv University, Israel; and fourth and fifth authors: Fakultät für Biologie, Gentechnologie/Mikrobiologie, Universität Bielefeld, Germany.

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Accepted for publication 21 October 2009.

The molecular interactions between Clavibacter michiganensis subsp. michiganensis and tomato plant were studied by following the expression of bacterial virulence and host-defense genes during early stages of infection. The C. michiganensis subsp. michiganensis genes included the plasmid-borne cellulase (celA) and the serine protease (pat-1), and the serine proteases chpC and ppaA, residing on the chp/tomA pathogenicity island (PAI). Gene expression was measured following tomato inoculation with Cmm382 (wild type), Cmm100 (lacking the plasmids pCM1 and pCM2), and Cmm27 (lacking the PAI). Transcriptional analysis revealed that celA and pat-1 were significantly induced in Cmm382 at initial 12 to 72 h, whereas chpC and ppaA were highly expressed only 96 h after inoculation. Interdependence between the expression of chromosomal and of plasmid-located genes was revealed: expression of celA and pat-1 was substantially reduced in the absence of the chp/tomA PAI, whereas chpC and ppaA expressions were reduced in the absence of the virulence plasmids. Transcription of chromosomal genes involved in cell wall degradation (i.e., pelA1, celB, xysA, and xysB), was also induced at early stages of infection. Expression of the host-defense genes, chitinase class II and pathogenesis-related protein-5 isoform was induced in the absence of the PAI at early stages of infection, suggesting that PAI-located genes are involved in suppression of tomato basal defenses.

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