English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Zendy Plus

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Zendy Tools

Zendy Open

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 .

Differential effector gene expression underpins epistasis in a plant fungal disease