Cernadas Raúl Andrés, Camillo Luciana Rodrigues, Benedetti Celso Eduardo
Center for Molecular and Structural Biology, Brazilian Synchrotron Light Laboratory, Campinas, SP, 13083-970, Brazil.
Mol Plant Pathol. 2008 Sep;9(5):609-31. doi: 10.1111/j.1364-3703.2008.00486.x.
Xanthomonas axonopodis pv. citri (Xac) and Xanthomonas axonopodis pv. aurantifolii pathotype C (Xaa) are responsible for citrus canker disease; however, while Xac causes canker on all citrus varieties, Xaa is restricted to Mexican lime, and in sweet oranges it triggers a defence response. To gain insights into the differential pathogenicity exhibited by Xac and Xaa and to survey the early molecular events leading to canker development, a detailed transcriptional analysis of sweet orange plants infected with the pathogens was performed. Using differential display, suppressed subtractive hybridization and microarrays, we identified changes in transcript levels in approximately 2.0% of the approximately 32,000 citrus genes examined. Genes with altered expression in response to Xac/Xaa surveyed at 6 and 48 h post-infection (hpi) were associated with cell-wall modifications, cell division and expansion, vesicle trafficking, disease resistance, carbon and nitrogen metabolism, and responses to hormones auxin, gibberellin and ethylene. Most of the genes that were commonly modulated by Xac and Xaa were associated with basal defences triggered by pathogen-associated molecular patterns, including those involved in reactive oxygen species production and lignification. Significantly, we detected clear changes in the transcriptional profiles of defence, cell-wall, vesicle trafficking and cell growth-related genes in Xac-infected leaves between 6 and 48 hpi. This is consistent with the notion that Xac suppresses host defences early during infection and simultaneously changes the physiological status of the host cells, reprogramming them for division and growth. Notably, brefeldin A, an inhibitor of vesicle trafficking, retarded canker development. In contrast, Xaa triggered a mitogen-activated protein kinase signalling pathway involving WRKY and ethylene-responsive transcriptional factors known to activate downstream defence genes.
柑橘溃疡病菌（Xanthomonas axonopodis pv. citri，简称Xac）和柑橘溃疡病菌致病型C（Xanthomonas axonopodis pv. aurantifolii pathotype C，简称Xaa）是引起柑橘溃疡病的病原菌；然而，Xac能使所有柑橘品种感染溃疡病，而Xaa仅侵染墨西哥莱檬，在甜橙中它会引发防御反应。为深入了解Xac和Xaa表现出的不同致病性，并探究导致溃疡病发生的早期分子事件，我们对感染病原菌的甜橙植株进行了详细的转录分析。通过差异显示、抑制性消减杂交和微阵列技术，我们在大约32000个检测的柑橘基因中，发现约2.0%的基因转录水平发生了变化。在感染后6小时和48小时（hpi）检测到的因Xac/Xaa感染而表达改变的基因，与细胞壁修饰、细胞分裂和扩展、囊泡运输、抗病性、碳氮代谢以及对生长素、赤霉素和乙烯等激素的反应有关。大多数受Xac和Xaa共同调控的基因与由病原体相关分子模式触发的基础防御有关，包括那些参与活性氧产生和木质化的基因。值得注意的是，我们在感染后6至48小时内检测到Xac感染的叶片中，防御、细胞壁、囊泡运输和细胞生长相关基因的转录谱发生了明显变化。这与Xac在感染早期抑制宿主防御并同时改变宿主细胞生理状态，使其重新编程进行分裂和生长的观点一致。值得注意的是，囊泡运输抑制剂布雷菲德菌素A可延缓溃疡病的发展。相比之下，Xaa触发了一条丝裂原活化蛋白激酶信号通路，该通路涉及已知可激活下游防御基因的WRKY和乙烯响应转录因子。
