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In all three cases, loss of function of either gene modulated the response of defence compounds. <jats:italic>AtRbohF<\/jats:italic> gene function was necessary for rapid and full induction of salicylic acid (SA) during compatible and incompatible interactions, and for resistance to virulent bacteria. Both <jats:italic>artrboh<\/jats:italic> mutations modulated the effects of intracellular ROS in the <jats:italic>cat2<\/jats:italic> background, although the predominant effect was mediated by <jats:italic>atrbohF<\/jats:italic>. Loss of this gene function increased lesion formation in <jats:italic>cat2<\/jats:italic> but uncoupled this effect from <jats:italic>cat2<\/jats:italic>\u2010triggered induction of SA and camalexin, accumulation of glutathione and disease resistance, all of which were much lower in <jats:italic>cat2 artbohF<\/jats:italic> than in <jats:italic>cat2<\/jats:italic>. A detailed comparison of GC\u2010TOF\u2010MS profiles produced by the three interactions revealed considerable overlap between <jats:italic>cat2<\/jats:italic> effects and those produced by bacterial infection in the wild\u2010type background. Analysis of the impact of the two <jats:italic>atrboh<\/jats:italic> mutations on these profiles provided further evidence that AtRbohF interacts closely with intracellular oxidative stress to tune dynamic metabolic responses during infection. Thus, AtRbohF appears to be a key player not only in HR\u2010related cell death but also in regulating metabolomic responses and resistance. Based on the results obtained during the three types of interaction, a model is proposed of how NADPH oxidases and intracellular ROS interact to determine the outcome of pathogen defence responses.<\/jats:p>","DOI":"10.1111\/j.1365-313x.2011.04816.x","type":"journal-article","created":{"date-parts":[[2011,10,11]],"date-time":"2011-10-11T08:01:03Z","timestamp":1318320063000},"page":"613-627","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":187,"title":["AtRbohF is a crucial modulator of defence\u2010associated metabolism and a key actor in the interplay between intracellular oxidative stress and pathogenesis responses in 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