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Biology subjects

Weiste, C.

Publications and source records attributed to Weiste, C..

7 recordsLinked to original sources

Under salt stress quinoa stomatal guard cells control transpiration in an ABA-primed manner

O_LIStomatal guard cells, located at the interface between the leaf and the atmosphere, play a key role in transpiration control and photosynthetic CO2 uptake. Halophytes like Chenopodium quinoa tolerate high soil salinity, but the mechanisms governing guard cell responses to salinity stress in relation to the associated epidermal bladder cells (EBCs) remain unknown. C_LIO_LIIn this study, responses of C. quinoa guard cells under salinity stress and external ABA application were analyzed using RNA profiling and voltage-clamp-based electrophysiology. C_LIO_LIUnder salt stress, guard cell RNA profiles reported the activation of ABA synthesis and signaling pathways. However, unlike EBCs, guard cells became transcriptionally insensitive to ABA. Voltage-clamp recordings revealed that under high Na+ concentrations, guard cells activity of K+ uptake channels remained unaffected, while they were impaired in ABA-induced activation of anion channels. As a consequence of a unique guard cell ABA response in salt-adapted plants, stomatal transpiration was reduced and CO2 sensitivity enhanced. C_LIO_LIWe propose that under salt stress, C. quinoa guard cells rewire their hormone signaling to switch from an ABA-sensitive to an ABA-insensitive mode. This adaptation may reflect the halophytes ability to perceive salinity as a non-stressful condition, allowing efficient water usage and sustained growth in saline environments. C_LI

plant biology↗

AFC kinases function as thermosensors that regulate warm temperature-responsive growth in Arabidopsis

Plants respond to elevated temperatures with enhanced elongation growth that depends on rapid transcriptional, post-transcriptional, and post-translational reprogramming. However, it is unclear how temperature information integrates with the splicing machinery to establish warm temperature-dependent splicing patterns. In animals, CDC2-LIKE KINASES (CLKs) function as body temperature sensors that control temperature-dependent splicing via phosphorylation of serine/arginine-rich (SR) proteins. Here we demonstrate that the CLK-homologous ARABIDOPSIS FUS3-COMPLEMENTING (AFC) kinases likewise regulate post-transcriptional RNA processing to control warm temperature-dependent growth in Arabidopsis. The contrasting temperature-activity profiles of the three AFCs depend on specific structural elements, including a conserved activation segment within the kinase domain. Combining protein structure prediction with site-directed mutagenesis, we provide insights into structural features that determine the different temperature-activity profiles of the three AFC paralogs. Analyses of afc mutant plants demonstrate their role in establishing temperature-dependent splicing patterns and thermomorphogenic hypocotyl elongation. Finally, our data indicate SR34 and SR34a as phosphorylation targets mediating temperature-dependent hypocotyl elongation downstream of AFCs. In conclusion, our study provides evidence that temperature-controlled AFC activity is evolutionarily conserved between plants and animals and implicates AFCs in the control of thermomorphogenesis.

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↗

DUF581-9 (At2g44670; FLZ3) negatively regulates SnRK1 activity by interference with T-loop phosphorylation

In plants, SUCROSE NON-FERMENTING RELATED KINASE 1 (SnRK1) is a key energy-sensor that orchestrates large-scale transcriptional reprogramming to maintain cellular homeostasis under energy deficit. SnRK1 activity is under tight negative control, although the exact mechanisms leading to its activation are far from being understood. We show that the Arabidopsis DOMAIN OF UNKNOWN FUNCTION (DUF581) protein DUF581-9/FLZ3 binds to the catalytic SnRK1 subunit KIN10 to inhibit its activation by GRIK-dependent T-loop phosphorylation. Overexpression of DUF581-9 in Arabidopsis dampens SnRK1 signalling and interferes with adaptation to dark-induced starvation. The presence of DUF581-9 significantly reduced SnRK1 activity in protoplasts and in vitro. This was accompanied by a reduction in T175 T-loop phosphorylation and also diminished KIN10 auto-phosphorylation. Furthermore, DUF581-9 reduced binding of the up-stream activating kinase GRIK2 to KIN10, explaining the reduced KIN10 T-loop phosphorylation. Ectopically expressed DUF581-9 protein was rapidly turned over by the proteasome when Arabidopsis plants were subjected to starvation treatment, likely releasing its inhibitory activity on the SnRK1 complex. Taken together, our results support a model in which DUF581-9 negatively regulates SnRK1 activity under energy sufficient conditions. Turnover over of the protein provides a rapid way for SnRK1 activation under energy deficit without the need of de-novo protein synthesis.

plant biology↗

Female gametophyte expressed Arabidopsis thaliana lipid transfer proteins AtLtpI.4 and AtLtpI.8 provide a link between callose homeostasis, pollen tube guidance, and fertilization success

Non-specific lipid transfer proteins (LTPs) represent a sub-class among the large family of Cysteine-rich proteins (CRPs) specific to land plants. LTPs possess a hydrophobic cavity, enabling them to bind and stabilize a variety of lipid molecules outside membranes. In line with the existence of an N-terminal signal peptide, secreted LTPs represent a well-suited mobile signal carrier in the plants extracellular matrix. Thus, LTPs are currently considered as key players to mediate the bulk flow of lipids between membranes/compartments as well as the buildup of lipid barrier polymers including cutin and suberin. Here, we show that floral expressed Arabidopsis thaliana AtLtpI.4 (AtLTP2) and AtLtpI.8 (AtLTP5), mutually control cell-cell communication between growing pollen tubes and ovules during fertilization. Arabidopsis mutants lacking functional AtLtpI.4 and AtLtpI.8 exhibit significantly reduced fertilization success. Cross-pollination and cell biological analyses revealed that AtLtpI.4/I.8 double mutants are impaired in pollen tube guidance towards ovules. Our finding that the AtLtpI.4/I.8 phenotype correlates with aberrant callose depositions in the micropylar region during ovule development suggests that both LTPs represent novel players of a joint signaling pathway that controls callose homeostasis in the female gametophyte.

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↗