|Scofield, Steven - Steve|
Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 9/25/2007
Publication Date: 12/1/2007
Citation: Faris, J.D., Friesen, T.L., Lu, H., Reddy, L., Zhang, Z., Liu, Z., Xu, S.S., Meinhardt, S.W., Fellers, J.P., Oliver, R.P., Solomon, P.S., Chao, S., Chu, C., Abeysekara, N., Scofield, S.R. 2007. Genetic analysis of host-toxin interactions in the wheat-Stagonospora nodorum pathosystem. Meeting Abstract. National Wheat Genomics Conference abstracts pg. 11
Technical Abstract: Stagonospora nodorum, causal agent of Stagonospora nodorum blotch (SNB) in wheat, produces multiple necrosis-inducing host-selective toxins (HSTs) that interact with dominant host sensitivity genes to cause disease. Absence of either the toxin or the dominant host gene precludes recognition and results in an incompatible (resistant) response. Therefore, these host-toxin interactions are mirror images of classical gene-for-gene interactions. One of the first HSTs identified in this system was SnToxA, which was horizontally transferred from S. nodorum to the tan spot pathogen Pyrenophora tritici-repentis around 1941. This event is considered to have been significant for the establishment of tan spot as a pathogen. Sensitivity to SnToxA is governed by the Tsn1 gene on the long arm of chromosome 5B. To date, eight additional toxins designated SnTox1 thru SnTox8 have been identified, and their corresponding host sensitivity genes designated Snn1 thru Snn8 have been mapped to wheat chromosome arms 1BS, 2DS, 5BS, 4BL, 5BS, 6AL, 5DS, and 3DL, respectively. Genetic analysis of several host-toxin interactions indicates that they play important roles in the development of disease in adult plants as well as seedlings, and their effects are mostly additive, but some espistasis has also been observed. To gain a better understanding of compatible host-toxin interactions at the molecular level, we have embarked on the positional cloning of two host-sensitivity genes: Tsn1 on 5BL and Snn1 on 1BS. Toward the map-based cloning of Tsn1 on chromosome 5B, we sequenced and assembled chromosome 5A and 5B BAC contigs spanning the gene. Evaluation of gene content and micro-colinearity between the orthologous regions of 5A, 5B, and rice chromosome 9 indicated the 5A region and rice share a higher level of micro-colinearity than the 5B region does with rice due to the presence of numerous transpositions, deletions, and rearrangements present in the wheat 5B region. In addition, the 5B Tsn1 candidate region is nearly 4 times larger than the corresponding region of 5A due to the presence of additional genes and transposable elements. At least ten genes exist within the 360 kb Tsn1 candidate gene region, and they are currently being validated by comparative sequence analysis of Tsn1-disrupted mutants and virus-induced gene silencing (VIGS). An important applied by-product of this research is the development of efficient PCR-based markers for Tsn1, which are being used to introgress SnToxA insensitivity into adapted germplasm. Overall, this research demonstrates the potential of the wheat-S. nodorum pathosystem to be an excellent toxin-based inverse gene-for-gene model.