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báo cáo khoa học: " Fortunella margarita Transcriptional Reprogramming Triggered by Xanthomonas citri subsp. citri"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Fortunella margarita Transcriptional Reprogramming Triggered by Xanthomonas citri subsp. citri | Khalaf et al. BMC Plant Biology 2011 11 159 http www.biomedcentral.com 1471-2229 11 159 BMC Plant Biology RESEARCH ARTICLE Open Access Fortunella margarita Transcriptional Reprogramming Triggered by Xanthomonas citri subsp. citri 1.2 2 A z- 3 3 1 Abeer A Khalaf 1 Frederick G Gmitter Jr Ana Conesa Joaquin Dopazo and Gloria A Moore Abstract Background Citrus canker disease caused by the bacterial pathogen Xanthomonas citri subsp. citri Xcc has become endemic in areas where high temperature rain humidity and windy conditions provide a favourable environment for the dissemination of the bacterium. Xcc is pathogenic on many commercial citrus varieties but appears to elicit an incompatible reaction on the citrus relative Fortunella margarita Swing kumquat in the form of a very distinct delayed necrotic response. We have developed subtractive libraries enriched in sequences expressed in kumquat leaves during both early and late stages of the disease. The isolated differentially expressed transcripts were subsequently sequenced. Our results demonstrate how the use of microarray expression profiling can help assign roles to previously uncharacterized genes and elucidate plant pathogenesis-response related mechanisms. This can be considered to be a case study in a citrus relative where high throughput technologies were utilized to understand defence mechanisms in Fortunella and citrus at the molecular level. Results cDNAs from sequenced kumquat libraries ESTs made from subtracted RNA populations healthy vs. infected were used to make this microarray. Of 2054 selected genes on a customized array 317 were differentially expressed P 0.05 in Xcc challenged kumquat plants compared to mock-inoculated ones. This study identified components of the incompatible interaction such as reactive oxygen species ROS and programmed cell death PCD . Common defence mechanisms and a number of resistance genes were also identified. In addition there were a considerable number of differentially .