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Two putatively homoeologous wheat genes mediate recognition of SnTox3 to confer effector‐triggered susceptibility to Stagonospora nodorum
Author(s) -
Zhang Zengcui,
Friesen Timothy L.,
Xu Steven S.,
Shi Gongjun,
Liu Zhaohui,
Rasmussen Jack B.,
Faris Justin D.
Publication year - 2011
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/j.1365-313x.2010.04407.x
Subject(s) - biology , genetics , locus (genetics) , effector , gene , plant disease resistance , brachypodium distachyon , genome , powdery mildew , common wheat , xanthomonas oryzae , chromosome , botany , microbiology and biotechnology
Summary The pathogen Stagonospora nodorum produces multiple effectors, also known as host‐selective toxins (HSTs), that interact with corresponding host sensitivity genes in an inverse gene‐for‐gene manner to cause the disease Stagonospora nodorum blotch (SNB) in wheat. In this study, a sensitivity gene was identified in Aegilops tauschii , the diploid D‐genome donor of common wheat. The gene was mapped to the short arm of chromosome 5D and mediated recognition of the effector SnTox3, which was previously shown to be recognized by the wheat gene Snn3 on chromosome arm 5BS. Comparative mapping suggested that Snn3 and the gene on 5DS are probably homoeologous and derived from a common ancestor. Therefore, we propose to designate these genes as Snn3‐B1 and Snn3‐D1 , respectively. Compatible Snn3‐D1 –SnTox3 interactions resulted in more severe necrosis in both effector infiltration and spore inoculation experiments than compatible Snn3‐B1 –SnTox3 interactions, indicating that Snn3‐B1 and Snn3‐D1 may have different affinities in SnTox3 recognition or signal transduction. Wheat bin‐mapped expressed sequence tags and good levels of collinearity among the wheat Snn3 regions, rice ( Oryza sativa ), and Brachypodium distachyon were exploited for saturation and fine mapping of the Snn3‐D1 locus. Markers delineating the Snn3‐D1 locus to a 1.4 cM interval will be useful for initiating positional cloning. Further characterization of how these homoeologous genes mediate recognition of the same pathogen effector should enhance understanding of host manipulation by necrotrophic pathogens in causing disease.