|Zhang, Zengcui - North Dakota State University|
|Rasmussen, Jack - North Dakota State University|
Submitted to: Molecular Plant-Microbe Interactions
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/7/2011
Publication Date: 12/1/2011
Citation: Faris, J.D., Zhang, Z., Rasmussen, J.B., Friesen, T.L. 2011. Variable expression of the Stagonospora nodorum effector SnToxA among isolates is correlated with levels of disease susceptibility in wheat. Molecular Plant-Microbe Interactions. 24:1419-1426.
Interpretive Summary: Many plant necrotrophic pathogens such as Stagonospora nodorum, which causes the disease Stagonospora nodorum blotch in wheat, produce toxins that, when recognized by specific genes in wheat, cause cell death allowing the pathogen to grow and complete their life cycle. Thus, wheat genes that mediate recognition of pathogen toxins are considered susceptibility genes. Two of the toxins produced by Stagonospora nodorum are SnToxA and SnTox2, which are recognized by the wheat genes Tsn1 and Snn2,respectively. The Tsn1-SnToxA and Snn2-SnTox2 interactions are both known to cause extensive cell death and lead to disease susceptibility. Here, we used genetics and molecular techniques to analyze these two interactions in two different strains (isolates) of the pathogen to determine if the different pathogenic strains varied in their utilization of the two toxins. The results indicated that one strain (Sn4) utilized both toxins equally because the Tsn1-SnToxA and Snn2-SnTox2 interactions contributed equally to disease development. However, the other strain (Sn5) utilized SnToxA much more than SnTox2 because the Tsn1-SnToxA interaction contributed substantially more to disease development than did the Snn2-SnTox2 interaction. DNA sequence analysis of the SnToxA gene from both pathogen strains indicated that genetic variation in the toxin-producing genes did not contribute to the differences observed. However, further analysis indicated that the Sn5 strain produced much more SnToxA than did the Sn4 strain, and this difference in toxin expression was likely responsible for the increase in disease caused by the Tsn1-SnToxA interaction in Sn5. This work furthers our knowledge regarding the mechanisms of pathogen susceptibility, and strengthens the notion that toxin sensitivity genes should be eliminated from modern wheat varieties to obtain enhanced resistance to diseases caused by necrotrophic pathogens.
Technical Abstract: Most research on host-pathogen interactions is focused on mechanisms of resistance, but less is known regarding mechanisms of susceptibility. The wheat-Stagonospora nodorum pathosystem involves pathogen-produced effectors, also known as host-selective toxins, that interact with corresponding dominant host genes to cause disease. Recognition of the S. nodorum effectors SnToxA and SnTox2 is mediated by the wheat genes Tsn1 and Snn2,respectively. Here, we inoculated a population of wheat recombinant inbred lines that segregates for Tsn1 and Snn2 with conidia from two S. nodorum isolates, Sn4 and Sn5, which both produce SnToxA and SnTox2 to compare the effects of compatible Tsn1-SnToxA and Snn2-SnTox2 interactions between the two isolates. Genetic analysis revealed that the two interactions contribute equally to disease susceptibility caused by isolate Sn4, but the Tsn1-SnToxA interaction contributed substantially more to disease conferred by Sn5 than did the Snn2-SnTox2 interaction. Sequence analysis of the SnToxA locus from Sn4 and Sn5 indicated they were 99.5% identical with no polymorphisms in the coding region or the predicted promoters. Analysis of transcription levels showed that expression levels of SnToxA peaked at 48 hours post inoculation for both isolates, but SnToxA expression in Sn5 was 2.5-fold higher than in Sn4. This work demonstrates that necrotrophic effectors of different isolates can be expressed at different levels in planta, and it strongly suggests that higher levels of expression lead to increased levels of disease susceptibility in the wheat-S. nodorum pathosystem.