Deparment of Plant Pathology and Weed Research, ARO, the Volcani Center, Bet Dagan, Israel.
Phytopathology. 2010 Mar;100(3):252-61. doi: 10.1094/PHYTO-100-3-0252.
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.
采用检测早期感染阶段细菌毒力和宿主防御基因表达的方法,研究了密歇根棒杆菌亚种密歇根ensis 与番茄植株之间的分子相互作用。该研究涉及的密歇根棒杆菌亚种密歇根ensis 基因包括质粒携带的纤维素酶(celA)和丝氨酸蛋白酶(pat-1),以及 chp/tomA 致病性岛(PAI)上的丝氨酸蛋白酶 chpC 和 ppaA。在对 Cmm382(野生型)、Cmm100(缺乏质粒 pCM1 和 pCM2)和 Cmm27(缺乏 PAI)进行番茄接种后,测量了基因表达情况。转录分析表明,celA 和 pat-1 在接种后的最初 12 至 72 小时内显著诱导表达,而 chpC 和 ppaA 仅在接种后 96 小时高度表达。基因表达的相关性研究表明:在缺乏 chp/tomA PAI 的情况下,染色体和质粒定位基因的表达显著减少,而在缺乏毒力质粒的情况下,chpC 和 ppaA 的表达减少。参与细胞壁降解的染色体基因(pelA1、celB、xysA 和 xysB)的转录也在感染早期被诱导。在缺乏 PAI 的情况下,宿主防御基因几丁质酶 II 类和病程相关蛋白-5 同工型的表达在感染早期被诱导,这表明 PAI 定位基因参与抑制番茄的基础防御。