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Plant Signaling and Behavior
Sharabi-Schwager, M., Department of Postharvest Science of Fresh Produce, ARO, the Volcani Center, Bet Dagan, Israel
Samach, A., Institute of Plant Sciences and Genetics in Agriculture, Faculty of Agricultural, Food and Environmental Quality Sciences
The Hebrew University of Jerusalem, Rehovot, Israel
Porat, R., Department of Postharvest Science of Fresh Produce, ARO, the Volcani Center, Bet Dagan, Israel
CBF1-3 (C-repeat binding factors) are transcriptional activators governing plant responses to low temperatures. Overexpression of CBF1-3 genes enhances plant frost tolerance, but also causes various pleiotropic effects regarding plant growth and development, mainly growth retardation, and delay of flowering and senescence. In a recent study, we reported that overexpression of CBF2 suppressed leaf senescence induced by the stress hormone ethylene. Here we show that overexpression of CBF2 also suppressed chlorophyll breakdown and leaf senescence induced by the phytohormones abscisic acid (ABA), salicylic acid (SA) and methyl jasmonate (MeJA), which indicates its broader role in suppressing hormone-induced leaf senescence. As previously reported for ethylene, the observed decrease in responsiveness to ABA in CBF2-overexpressing plants was specific to leaf senescence, since other responses to ABA were similar to those of wild-type plants. Transcript profiling analysis of hormone metabolism and responsive genes revealed that overexpression of CBF2 induced expression of ABAbiosynthesis and ABA-responsive genes and suppressed SA- and JA-related genes. Overall, in light of the adverse effects of CBF2 on ABA metabolism and responsiveness, on the one hand, and SA and JA metabolism and responsiveness, on the other hand, we conclude that overexpression of CBF2 suppresses hormone-induced leaf senescence by directly counteracting the hormone effects on leaf senescence and not by general suppression of their synthesis or signal transduction pathways. © 2010 Landes Bioscience.
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Overexpression of the CBF2 transcriptional activator in Arabidopsis counteracts hormone activation of leaf senescence
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Sharabi-Schwager, M., Department of Postharvest Science of Fresh Produce, ARO, the Volcani Center, Bet Dagan, Israel
Samach, A., Institute of Plant Sciences and Genetics in Agriculture, Faculty of Agricultural, Food and Environmental Quality Sciences
The Hebrew University of Jerusalem, Rehovot, Israel
Porat, R., Department of Postharvest Science of Fresh Produce, ARO, the Volcani Center, Bet Dagan, Israel
Overexpression of the CBF2 transcriptional activator in Arabidopsis counteracts hormone activation of leaf senescence
CBF1-3 (C-repeat binding factors) are transcriptional activators governing plant responses to low temperatures. Overexpression of CBF1-3 genes enhances plant frost tolerance, but also causes various pleiotropic effects regarding plant growth and development, mainly growth retardation, and delay of flowering and senescence. In a recent study, we reported that overexpression of CBF2 suppressed leaf senescence induced by the stress hormone ethylene. Here we show that overexpression of CBF2 also suppressed chlorophyll breakdown and leaf senescence induced by the phytohormones abscisic acid (ABA), salicylic acid (SA) and methyl jasmonate (MeJA), which indicates its broader role in suppressing hormone-induced leaf senescence. As previously reported for ethylene, the observed decrease in responsiveness to ABA in CBF2-overexpressing plants was specific to leaf senescence, since other responses to ABA were similar to those of wild-type plants. Transcript profiling analysis of hormone metabolism and responsive genes revealed that overexpression of CBF2 induced expression of ABAbiosynthesis and ABA-responsive genes and suppressed SA- and JA-related genes. Overall, in light of the adverse effects of CBF2 on ABA metabolism and responsiveness, on the one hand, and SA and JA metabolism and responsiveness, on the other hand, we conclude that overexpression of CBF2 suppresses hormone-induced leaf senescence by directly counteracting the hormone effects on leaf senescence and not by general suppression of their synthesis or signal transduction pathways. © 2010 Landes Bioscience.
Scientific Publication
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