ORCID Profile
0000-0001-9715-8012
Current Organisations
The University of Auckland
,
University of Queensland
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Publisher: Wiley
Date: 03-2023
DOI: 10.1002/PLD3.486
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 branching responses in Arabidopsis. Additionally, we provide evidence for non‐auxin‐mediated feedback on strigolactone biosynthesis and discuss this in the context of sugar signaling.
Publisher: Cold Spring Harbor Laboratory
Date: 24-05-2023
DOI: 10.1101/2023.05.23.541964
Abstract: Plants exhibit an immense plasticity in their architecture. While the impact of hormonal regulation is well-characterised, the importance of sugar-signalling has just recently emerged. Here, we addressed which sugar-signalling components mediate the trade-off between growth of apical versus lateral meristems and how they control organ sink-strength. Thereby, we unravelled a novel developmental function of the sugar-controlled S 1 basic-leucine-zipper (S 1 -bZIP) transcription factors in establishing global source-sink interactions. Applying comprehensive molecular, analytical, and genetic approaches, we demonstrate that S 1 -bZIPs operate in a redundant manner to control tissue-specific expression of defined SWEET sugar-transporters and the GAT1_2.1 glutaminase. By these means, S 1 -bZIPs control carbohydrate (C)-channelling from source leaves to apical shoot and root organs and tune systemic organic nitrogen (N)-supply to restrict lateral organ formation by C/N depletion. Knowledge of the underlying mechanisms controlling plant C/N partitioning is of pivotal importance for breeding strategies to generate plants with desired architectural and nutritional characteristics.
Publisher: Cold Spring Harbor Laboratory
Date: 24-05-2023
DOI: 10.1101/2023.05.23.542007
Abstract: The ontogenetic regulation of shoot branching allows plants to adjust their architecture in accordance with the environment. This process is due to the regulation of axillary bud outgrowth into branches, which can be induced by increasing sugar availability to the buds through decapitation of the shoot tip. Different sugar signalling components have been identified in the induction of shoot branching. However, the molecular components that maintain bud dormancy in response to sugar starvation remain largely unknown. Here, we show at the genetic level that basic leucine zipper 11 (bZIP11), a transcription factor that plays important roles in response to sugar starvation in plants, inhibits shoot branching in Arabidopsis thaliana . Physiology experiments demonstrated that bZIP11 protein levels are decreased by decapitation. Molecular and genetic evidence suggests that bZIP11 acts in a negative feedback loop with trehalose 6-phosphate (Tre6P), a sugar signal that promotes shoot branching. Our data also suggest that the central energy sensor SUCROSE NON-FERMENTING 1 RELATED KINASE1 (SnRK1), alleviates the inhibitory effect of Tre6P on bZIP11 protein accumulation and inhibits shoot branching. Altogether, these data provide a working model that involves bZIP11, Tre6P and SnRK1 in the regulation of shoot branching.
Location: United Kingdom of Great Britain and Northern Ireland
Location: United Kingdom of Great Britain and Northern Ireland
No related grants have been discovered for Alicia May Hellens.