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Fichtner, F.

Publications and source records attributed to Fichtner, F..

11 recordsLinked to original sources

The miR319-targeted TCP transcription factors play crucial roles in the establishment of Arabidopsis thaliana shoot architecture in response to carbon and nitrogen availability.

Shoot branching is a highly plastic developmental process that allows plants to adjust their architecture to environmental conditions, such as carbon and nitrogen availability. Although the class II TCP transcription factor BRANCHED1 is a well-established repressor of shoot branching, the contribution of other TCP factors during this process remains less well understood. Here, we show that the miR319-targeted TCP module promotes shoot branching in Arabidopsis thaliana. Overexpression of miR319 reduced rosette branch production, whereas repression of TCP3 activity or triple knockout (KO) mutation in TCP3, TCP4 and TCP10 inhibited branching. Conversely, expression of a miR319-resistant TCP3 triggered a highly branched phenotype, indicating that TCP3 and related miR319 targets act as positive regulators of shoot branching. Genetic analysis with the strigolactone-deficient max4 mutant showed that strigolactones mediate, at least partly, the reduced branching observed in the miR319 overexpressing line and in the tcp3,4,10 triple mutant. Transcriptomic and DNA-binding analyses indicated indirect effect of TCP3 on strigolactone biosynthesis genes. Instead, miR319 overexpression increased the sensitivity of branching to nitrogen limitation and reduced nitrate uptake, thereby increasing the expression of strigolactone synthesis genes. We further show that carbon starvation reduced the transcription levels of miR319-targeted TCPs, independently of miR319 accumulation, and that TCP3 may connect carbon availability to sugar signalling via HEXOKINASE1. Together, our results identify the miR319-targeted TCP module as a positive regulator of shoot branching that links plant architecture to carbon and nitrogen availability.

plant biology↗

Systemic and local regulation of root growth by vascular trehalose 6-phosphate is correlated with re-allocation of primary metabolites between shoots and roots

Trehalose 6-phoshpate (Tre6P) is a key signalling molecule that reflects carbon status and integrates it with developmental decision making. Tre6P has been demonstrated to regulate various developmental processes, including vegetative growth, shoot branching, flowering, and root branching. Here, we investigate how vasculature-derived Tre6P influences root system architecture by expressing heterologous Tre6P synthase (TPS) or Tre6P phosphatase (TPP) specifically in the plant vasculature. Plants with elevated vascular-derived Tre6P levels had smaller root systems, reduced sucrose levels, and lower root metabolite levels, whereas vascular TPP overexpression had the opposite effect. Using reciprocal grafting experiments, we identified shoot-derived vascular Tre6P to be the main driver of these systemic responses. In lines with increased Tre6P in the shoot vasculature, the shoot-to-root metabolite ratios were consistently increased, indicating that Tre6P modulates metabolite allocation and utilization to balance carbon partitioning between shoot and root growth. Our data further suggest that vascular Tre6P contributed to optimizing the carbon-to-nitrogen ratio to support growth and fitness. Besides this systemic function, this study shows that root-derived Tre6P also plays a critical local role in modulating root development. Collectively, our results demonstrate that Tre6P in the vasculature functions both systemically and locally to coordinate metabolic status with root growth and architecture.

plant biology↗

S1 basic leucine zipper transcription factors shape plant architecture by controlling C/N partitioning to apical and lateral organs

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 S1 basic-leucine-zipper (S1-bZIP) transcription factors in establishing global source-sink interactions. Applying comprehensive molecular, analytical, and genetic approaches, we demonstrate that S1-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, S1-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.

plant biology↗

The transcription factor bZIP11 acts antagonistically with trehalose 6-phosphate to inhibit shoot branching

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.

plant biology↗

Transcription factor HSFA7b controls ethylene signaling and meristem maintenance at the shoot apical meristem during thermomemory

The shoot apical meristem (SAM) is responsible for overall shoot growth by generating all above-ground structures. Recent research identified that the SAM displays an autonomous heat stress (HS) memory of a previous non-lethal HS event. Considering the importance of the SAM for plant growth it is essential to unlock how its thermomemory is mechanistically controlled. Here, we report that HEAT SHOCK TRANSCRIPTION FACTOR A7b (HSFA7b) plays a crucial role in this process in Arabidopsis. We found that HSFA7b directly regulates ethylene response at the SAM by binding to promoters of key regulators of ethylene signaling including ETHYLENE-INSENSITIVE 3 to establish thermotolerance. Moreover, HSFA7b controls maintenance of the SAM stem cell pool during thermomemory by regulating the expression of the master regulator WUSCHEL through direct transcriptional activation of the SPLAYED chromatin remodelling factor.

plant biology↗

Auxin-independent effects of apical dominance induce temporal changes in phytohormones

The inhibition of shoot branching by the growing shoot tip of plants, termed apical dominance, was originally thought to be mediated by auxin. Recently the importance of the shoot tip sink strength during apical dominance has re-emerged with recent studies highlighting roles for sugars in promoting branching. This raises many unanswered questions on the relative roles of auxin and sugars in apical dominance. Here we show that auxin regulation of cytokinins, which promote branching, is significant only after an initial stage of branching we call bud release. During this early bud release stage, rapid cytokinin increases are associated with enhanced sugars. Auxin may also act through strigolactones which have been shown to suppress branching after decapitation, but here we show that strigolactones do not have a significant effect on initial bud outgrowth after decapitation. We report here that when sucrose or cytokinin is abundant, strigolactones are less inhibitory during the bud release stage compared to later stages and that strigolactone treatment rapidly inhibits cytokinin accumulation in pea axillary buds of intact plants. After initial bud release, we find an important role of gibberellin in promoting sustained bud growth downstream of auxin. We are therefore able to suggest a model of apical dominance that integrates auxin, sucrose, strigolactones, cytokinins and gibberellins and describes differences in signalling across stages of bud release to sustained growth.

plant biology↗

Different plasticity of bud outgrowth at cauline and rosette nodes in Arabidopsis thaliana

Shoot branching is a complex mechanism in which secondary shoots grow from buds that are initiated from meristems established in leaf axils. The model plant Arabidopsis thaliana has a rosette leaf growth pattern in the vegetative stage. After flowering initiation, the main stem starts to elongate with the top leaf primordia developing into cauline leaves. Meristems in arabidopsis are initiated in the axils of rosette or cauline leaves, giving rise to rosette or cauline buds, respectively. Plasticity in the process of shoot branching is regulated by resource and nutrient availability as well as by plant hormones. However, few studies have attempted to test whether cauline and rosette branching are subject to the same plasticity. Here, we addressed this question by phenotyping cauline and rosette branching in three arabidopsis ecotypes and several arabidopsis mutants with varied shoot architectures. Our results show that there is no negative correlation between cauline and rosette branch numbers in arabidopsis, demonstrating that there is no trade-off between cauline and rosette bud outgrowth. Through investigation of the altered branching pattern of flowering pathway mutants and arabidopsis ecotypes grown in various photoperiods and light regimes, we further elucidated that the number of cauline branches is closely related to flowering time. The number or rosette branches has an enormous plasticity compared with cauline branches and is influenced by genetic background, flowering time, light intensity and temperature. Our data reveal different plasticity in the regulation of branching at rosette and cauline nodes and promote a framework for future branching analyses. One sentence summaryDifferent plasticity of branching at cauline and rosette nodes of arabidopsis is revealed through detailed correlative analyses of branching under varied genetic and environmental contexts.

plant biology↗

Blocking plasmodesmata in specific phloem cell types reduces axillary bud growth in Arabidopsis thaliana

The plasticity of above ground plant architecture depends on the regulated re-activation and growth of axillary meristems laid down in the axils of leaves along the stem, which often arrest as dormant buds. Plasmodesmata connecting plant cells might control the movement of regulators involved in this developmental switch. Constructs capable of occluding these structures were employed in phloem cell types, because of the importance of phloem in local and systemic trafficking. We show that over-accumulation of callose within companion cells of the Arabidopsis inflorescence reduces the growth rates of activated buds, but does not affect bud activation. Growth rate reductions were not dependent on the phloem-mobile strigolactone receptor, which regulates bud activation. Furthermore, there was no correlation with early bud sugar profiles, which can also affect bud activity and depend on phloem-mediated delivery. It is therefore possible that an as yet unknown mobile signal is involved in modulating branch growth rate.

plant biology↗

Sucrose represses the expression of the strigolactone signalling gene D3/RMS4/MAX2 to promote tillering

- Shoot branching, a major component of shoot architecture, is regulated by multiple signals. Previous studies have indicated that sucrose may promote branching through suppressing the inhibitory effect of the hormone strigolactone (SL). However, the molecular mechanisms underlying this effect are unknown. - Here we used molecular and genetic tools to identify the molecular targets underlying the antagonistic interaction between sucrose and SL. - We showed that sucrose antagonises the suppressive action of SL on tillering in rice and on the degradation of D53, a major target of SL signalling. Sucrose inhibits the expression of D3, the orthologue of the arabidopsis F-box protein MAX2 required for SL signalling. Over-expression of D3 prevents sucrose from inhibiting D53 degradation and enabled the SL inhibition of tillering under high sucrose. Sucrose also prevents SL-induced degradation of D14, the SL receptor involved in D53 degradation. Interestingly, D14 over-expression enhances D53 protein levels and sucrose-induced tillering. - Our results show that sucrose inhibits SL perception by targeting key components of SL signalling and, together with previous studies reporting the inhibition of SL synthesis by nitrate and phosphate, demonstrate the central role played by strigolactones in the regulation of plant architecture by nutrients.

plant biology↗

HEXOKINASE1 interferes with cytokinin synthesis and strigolactone perception during sugar-induced shoot branching

- Plant architecture is controlled by several endogenous signals including hormones and sugars. However, only little is known about the nature and roles of the sugar signalling pathways in this process. Here we test whether the sugar pathway mediated by HEXOKINASE1 (HXK1) is involved in the control of shoot branching. - To test the involvement of HXK1 in the control of shoot architecture we modulated the HXK1 pathway using physiological and genetic approaches in diverse plants, rose, arabidopsis and pea and evaluated impacts of hormonal pathways. - We show that triggering a hexokinase-dependent pathway was able to promote bud outgrowth in pea and rose. In arabidopsis, both HXK1 deficiency and defoliation led to decreased shoot branching and conferred hypersensitivity to auxin. HXK1 expression was positively correlated with sugar availability. HXK1-deficient plants displayed decreased cytokinin levels and increased expression of MAX2 which is required for strigolactone signalling. The branching phenotype of HXK1-deficient plants could be partly restored by cytokinin treatment and strigolactone deficiency could override the negative impact of HXK1 deficiency on shoot branching. - Our observations demonstrate that a HXK1-dependent pathway contributes to the regulation of shoot branching and interact with hormones to modulate plant architecture.

plant biology↗

The role of trehalose 6-phosphate in shoot branching - local and non-local effects on axillary bud outgrowth in arabidopsis rosettes

- Trehalose 6-phosphate (Tre6P) is a sucrose signalling metabolite that has been implicated in regulation of shoot branching, but its precise role is not understood. - We expressed tagged forms of TREHALOSE-6-PHOSPHATE SYNTHASE1 (TPS1) to determine where Tre6P is synthesized in arabidopsis (Arabidopsis thaliana), and investigated the impact of localized changes in Tre6P levels, in axillary buds or vascular tissues, on shoot branching in wild-type and branching mutant backgrounds. - TPS1 is expressed in axillary buds and the subtending vasculature, as well as in the leaf and stem vasculature. Expression of a heterologous trehalose-6-phosphate phosphatase (TPP) to lower Tre6P in axillary buds strongly delayed bud outgrowth in long days and inhibited branching in short days. TPP expression in the vasculature also delayed lateral bud outgrowth and decreased branching. Increased Tre6P in the vasculature enhanced branching and was accompanied by higher expression of FLOWERING LOCUS T (FT) and up-regulation of sucrose transporters. Increased vascular Tre6P levels enhanced branching in branched1 but not in ft mutant backgrounds. - These results provide direct genetic evidence of a local role for Tre6P in regulation of axillary bud outgrowth within the buds themselves, and also connect Tre6P with systemic regulation of shoot branching via FT.

plant biology↗