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Systemic low temprature signaling in Arabidopsis

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Authors

Gorsuch, Peter A.
Sargeant , Alexander W
Penfield , Steven D
Quick, W Paul
Atkin, Owen

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Japanese Society of Plant Physiologists

Abstract

When leaves are exposed to low temperature, sugars accumulate and transcription factors in the C-repeat binding factor (CBF) family are expressed, which, together with CBF-independent pathways, are known to contribute to the cold acclimation process and an increase in freezing tolerance. What is not known, however, is whether expression of these cold-regulated genes can be induced systemically in response to a localized cold treatment. To address this, pre-existing, mature leaves of warm-grown Arabidopsis thaliana were exposed to a localized cold treatment (near 10°C) whilst conjoined newly developing leaves continued only to experience warmer temperatures. In initial experiments on wild-type A. thaliana (Col-0) using real-time reverse transcriptionPCR (RTPCR) we observed that some genesincluding CBF genes, certain downstream cold-responsive (COR) targets and CBF-independent transcription factorsrespond to a direct 9°C treatment of whole plants. In subsequent experiments, we found that the treatment of expanded leaves with temperatures near 10°C can induce cold-associated genes in conjoined warm-maintained tissues. CBF1 showed a particularly strong systemic response, although CBF-independent transcription factors also responded. Moreover, the localized cold treatment of A. thaliana (C24) plants with a luciferase reporter fused to the promoter region of KIN2 indicated that in warm-maintained leaves, KIN2 might respond to a systemic signal from remote, directly cold-treated leaves. Collectively, our study provides strong evidence that the processes involved in cold acclimation are partially mediated by a signal that acts systemically. This has the potential to act as an early-warning system to enable developing leaves to cope better with the cold environment in which they are growing.

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Plant and Cell Physiology

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Restricted until

2037-12-31