|VAN DE MORTEL, MARTIJN|
Submitted to: Biennial Conference on Molecular and Cellular Biology of the Soybean
Publication Type: Abstract Only
Publication Acceptance Date: 6/1/2008
Publication Date: N/A
Technical Abstract: Asian soybean rust (ASR) is now a threat to soybean production in all major growing regions in the world. This potentially devastating disease is caused by the obligate fungal pathogen Phakopsora pachyrhizi and resistance in soybean germplasm is limited. Moreover, this resistance is generally observed as low compatibility to the fungus, which occurs at a much later time (approximately 3 days after infection), compared to more typical resistance displayed as a hypersensitive reaction within the first 24h after infection. We have started to decipher the interactions between host and pathogen at the molecular level and categorized genes responsive to P. pachyrhizi in the Rpp2, Rpp3, and Rpp4 genetic backgrounds and in susceptible genotypes. Microscopic and gene expression analyses conducted at time points spanning early infection to symptom development have allowed us to correlate P. pachyrhizi growth and development with the timing of molecular events in the host. We observe that P. pachyrhizi induces a strong non-specific defense response upon infection, after which the fungus grows virtually undetected until haustoria form. The onset and magnitude of a second phase of differential gene expression patterns appear to be major determinants of resistance. In addition, we observe different classes of regulatory proteins differentially expressed in the various Rpp backgrounds, indicating these three resistance genes may activate specific signal transduction pathways. We hypothesize that the early responses represent an ineffective basal defense response. Rpp2, Rpp3, or Rpp4 subsequently mediates an effective resistance response after P. pachyrhizi forms haustoria and secretes effector proteins.