Figure 7.
Model illustrating the influence of pheophorbide a homeostasis on JA signaling. The middle (wild type [WT]) shows the PAO/phyllobilin pathway under normal senescence conditions, leading to the complete degradation of chl to vacuole-localized phyllobilins. Left and right show modulation of catabolite homeostasis caused by mutations of either nye1-1 or pph-1 (left) or pao1 (right), and the respective observed downstream modulation of the JA response (dashed arrows). Arrow sizes schematically represent relative flux (metabolite) and response (JA signaling) intensities. Among the few genes differentially expressed in nye1-1 and pph-1, jasmonate-ZIM domain genes were downregulated compared to wild type. On the other hand, in pao1, JA biosynthesis and signaling genes as well as some JA bioactive derivatives were induced. DNCC, dioxobilin-type nonfluorescent chlorophyll catabolite; NCC, nonfluorescent chlorophyll catabolite; pFCC, primary fluorescent chlorophyll catabolite.

Model illustrating the influence of pheophorbide a homeostasis on JA signaling. The middle (wild type [WT]) shows the PAO/phyllobilin pathway under normal senescence conditions, leading to the complete degradation of chl to vacuole-localized phyllobilins. Left and right show modulation of catabolite homeostasis caused by mutations of either nye1-1 or pph-1 (left) or pao1 (right), and the respective observed downstream modulation of the JA response (dashed arrows). Arrow sizes schematically represent relative flux (metabolite) and response (JA signaling) intensities. Among the few genes differentially expressed in nye1-1 and pph-1, jasmonate-ZIM domain genes were downregulated compared to wild type. On the other hand, in pao1, JA biosynthesis and signaling genes as well as some JA bioactive derivatives were induced. DNCC, dioxobilin-type nonfluorescent chlorophyll catabolite; NCC, nonfluorescent chlorophyll catabolite; pFCC, primary fluorescent chlorophyll catabolite.

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