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Differential effector gene expression underpins epistasis in a plant fungal disease
Author(s) -
Phan Huyen T.T.,
Rybak Kasia,
Furuki Eiko,
Breen Susan,
Solomon Peter S.,
Oliver Richard P.,
Tan KarChun
Publication year - 2016
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/tpj.13203
Subject(s) - pathosystem , biology , effector , quantitative trait locus , epistasis , genetics , septoria , population , locus (genetics) , gene , gene expression , mycosphaerella graminicola , microbiology and biotechnology , botany , demography , sociology
Summary Fungal effector–host sensitivity gene interactions play a key role in determining the outcome of septoria nodorum blotch disease ( SNB ) caused by Parastagonospora nodorum on wheat. The pathosystem is complex and mediated by interaction of multiple fungal necrotrophic effector–host sensitivity gene systems. Three effector sensitivity gene systems are well characterized in this pathosystem; SnToxA– Tsn1 , SnTox1– Snn1 and SnTox3– Snn3 . We tested a wheat mapping population that segregated for Snn1 and Snn3 with SN 15, an aggressive P. nodorum isolate that produces SnToxA, SnTox1 and SnTox3, to study the inheritance of sensitivity to SnTox1 and SnTox3 and disease susceptibility. Interval quantitative trait locus ( QTL ) mapping showed that the SnTox1– Snn1 interaction was paramount in SNB development on both seedlings and adult plants. No effect of the SnTox3– Snn3 interaction was observed under SN 15 infection. The SnTox3– Snn3 interaction was however, detected in a strain of SN 15 in which SnTox1 had been deleted ( tox1–6 ). Gene expression analysis indicates increased SnTox3 expression in tox1–6 compared with SN 15. This indicates that the failure to detect the SnTox3– Snn3 interaction in SN 15 is due – at least in part – to suppressed expression of SnTox3 mediated by SnTox1. Furthermore, infection of the mapping population with a strain deleted in SnToxA , SnTox1 and SnTox3 ( toxa13 ) unmasked a significant SNB QTL on 2 DS where the SnTox2 effector sensitivity gene, Snn2 , is located. This QTL was not observed in SN 15 and tox1–6 infections and thus suggesting that SnToxA and/or SnTox3 were epistatic. Additional QTL s responding to SNB and effectors sensitivity were detected on 2 AS 1 and 3 AL .