Proposed model for the interplay of the xanthophyll cycle and plant resistance to <i>Sclerotinia</i>.

<p><i>Sclerotinia</i> secretes oxalate to acidify the infected tissues, which results in increased lumen acidification. Subsequently, the low lumen pH activates NPQ by protonating PsbS protein and VDE. The latter convert violaxanthin (V) to zeaxanthin (Z) via the intermediate antheraxanthin (A) in the xanthophyll cycle. Elevated NPQ and zeaxanthin accumulation have the potential to affect chloroplast redox singling pathways to lower oxidation-derived oxylipins (like jasmonic acid, JA) formation [<a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1004878#ppat.1004878.ref010" target="_blank">10</a>–<a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1004878#ppat.1004878.ref011" target="_blank">11</a>,<a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1004878#ppat.1004878.ref077" target="_blank">77</a>]. On the other hand, the decrease in precursor violaxanthin limits ABA biosynthesis. These aspects, in turn, affects tissue defense responses like ROS induction and callose deposition, which increases plant susceptibility to <i>Sclerotinia</i>.