Plant hormones (Literature sources on phytohormones and plant signalling)
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The role of long-distance mobile metabolites in the plant stress response and signaling - Review

The role of long-distance mobile metabolites in the plant stress response and signaling - Review | Plant hormones (Literature sources on phytohormones and plant signalling) | Scoop.it
Authors: Jianghua Cai, Dongqi Li and Asaph Aharoni

The Plant Journal (2023)

Abstract: "Plants developed sophisticated mechanisms to perceive environmental stimuli and generate appropriate signals to maintain optimal growth and stress responses. A fascinating strategy employed by plants is the use of long-distance mobile signals which can trigger local and distant responses across the entire plant. Some metabolites play a central role as long-distance mobile signals allowing plants to communicate across tissues and mount robust stress responses. In this review, we summarize the current knowledge regarding the various long-distance mobile metabolites and their functions in stress response and signaling pathways. We also raise questions with respect to how we can identify new mobile metabolites and engineer them to improve plant health and resilience."
Julio Retamales's insight:
This excellent review is part of a special issue ("Regulation of Metabolism"), which contains other relevant reviews.
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Scooped by Julio Retamales
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Identification of new potential downstream transcriptional targets of the strigolactone pathway including glucosinolate biosynthesis

Identification of new potential downstream transcriptional targets of the strigolactone pathway including glucosinolate biosynthesis | Plant hormones (Literature sources on phytohormones and plant signalling) | Scoop.it
Authors: Alicia M. Hellens, Tinashe G. Chabikwa, Franziska Fichtner, Philip B. Brewer and Christine A. Beveridge.

Plant Direct (2023)

Abstract: "Strigolactones regulate shoot branching and many aspects of plant growth, development, and allelopathy. Strigolactones are often discussed alongside auxin because they work together to inhibit shoot branching. However, the roles and mechanisms of strigolactones and how they act independently of auxin are still elusive. Additionally, there is still much in general to be discovered about the network of molecular regulators and their interactions in response to strigolactones. Here, we conducted an experiment in Arabidopsis with physiological treatments and strigolactone mutants to determine transcriptional pathways associated with strigolactones. The three physiological treatments included shoot tip removal with and without auxin treatment and treatment of intact plants with the auxin transport inhibitor, N-1-naphthylphthalamic acid (NPA). We identified the glucosinolate biosynthesis pathway as being upregulated across strigolactone mutants indicating strigolactone–glucosinolate crosstalk. Additionally, strigolactone application cannot restore the highly branched phenotype observed in glucosinolate biosynthesis mutants, placing glucosinolate biosynthesis downstream of strigolactone biosynthesis. Oxidative stress genes were enriched across the experiment suggesting that this process is mediated through multiple hormones. Here, we also provide evidence supporting non-auxin-mediated, negative feedback on strigolactone biosynthesis. Increases in strigolactone biosynthesis gene expression seen in strigolactone mutants could not be fully restored by auxin. By contrast, auxin could fully restore auxin-responsive gene expression increases, but not sugar signaling-related gene expression. Our data also point to alternative roles of the strigolactone biosynthesis genes and potential new signaling functions of strigolactone precursors. In this study, we identify a strigolactone-specific regulation of glucosinolate biosynthesis genes indicating that the two are linked and may work together in regulating stress and shoot ranching responses in Arabidopsis. Additionally, we provide evidence for non-auxin-mediated feedback on strigolactone biosynthesis and discuss this in the context of sugar signaling."
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