On April 21, 2026, Nature Communications published online a research article entitled “Sucrose-activated TOR and phyA signaling alleviates shade-mediated inhibition of leaf development in Arabidopsis” by Professor Lin Li’s research group from the School of Life Sciences at Fudan University.
After preparation, Arabidopsis seeds were transferred into a JIUPO BPC500DH Plant Growth Chamber, where the temperature was set at 22°C. Continuous simulated white light was provided using a dedicated JIUPO plant growth LED lighting system. The seeds were initially cultivated for 3 days, with the red, blue, and far-red light intensities maintained at predefined experimental standards.
The seedlings were subsequently divided into two groups for cultivation: one group was transferred to a light environment simulating field canopy shade conditions, while the other group was continuously maintained under the original simulated white-light conditions for normal growth.
Using the model plant Arabidopsis thaliana as the experimental system, this study revealed that the interaction between sucrose-activated TOR signaling and the phyA-mediated light signaling pathway plays a crucial role in alleviating shade-induced inhibition of leaf development. These findings provide new theoretical insights and potential genetic targets for breeding crops with improved shade tolerance under high-density planting conditions and enhancing crop productivity in intensive cultivation systems.
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1. TOR and phyA are essential components mediating sucrose-induced recovery of leaf development under shade conditions
The research team first established experimental light systems simulating white light (R/FR = 4) and shade conditions (R/FR = 0.17). They found that the development of true leaves in wild-type Arabidopsis was significantly inhibited under shade conditions, whereas exogenous sucrose application substantially increased the area of the first true leaf and reactivated cell division activity in the shoot apical meristem, as demonstrated by the pCYCB1;1::GUS reporter system.
When plants were treated with the TOR-specific inhibitor Torin 2 or subjected to induced suppression of TOR expression, the sucrose-mediated recovery effect on leaf development was completely abolished, demonstrating that TOR activity is indispensable for this regulatory process.
Further screening of mutants associated with shade signaling pathways revealed that phyA mutants completely lost their sucrose-dependent leaf developmental response under shade conditions, whereas phyB and pif7 mutants retained their ability to respond to sucrose and promote leaf growth.
Moreover, this regulatory effect displayed clear tissue specificity: phyA specifically regulates sucrose-induced leaf development but does not affect sucrose-induced hypocotyl elongation, whereas phyB and PIF7 are responsible for regulating sucrose responses during hypocotyl elongation.
Through analyses of multiple mutant combinations and complementation experiments, the researchers ultimately demonstrated that TOR and phyA jointly mediate the sucrose-induced restoration of leaf development under shade conditions.
Figure 1: TOR and phyA participate in mediating sucrose-induced recovery of leaf development under shade conditions
2. PHYA directly interacts with the TOR complex and the two components mutually regulate each other
The Arabidopsis TOR complex consists of TOR, RAPTOR, and LST8. Plants with loss-of-function mutations in RAPTOR or LST8 failed to exhibit sucrose-mediated regulation of leaf development under shade conditions.
Genetic analyses demonstrated that both functional phyA signaling and TOR activation are essential for sucrose-induced restoration of leaf development, indicating that neither component can compensate for the absence of the other.
Pull-down assays, luciferase complementation imaging (LCI), and co-immunoprecipitation (Co-IP) experiments confirmed that PHYA directly interacts with LST8, a component of the TOR complex.
Using S6K1 phosphorylation status as an indicator of TOR activity, the researchers found that shade conditions suppressed TOR activity, whereas sucrose treatment restored TOR activation. Importantly, this sucrose-induced TOR activation was dependent on phyA signaling.
In vitro kinase assays further demonstrated that TOR can directly phosphorylate PHYA, revealing a bidirectional regulatory interaction between TOR and phyA.
Figure 2: Validation of the interaction and reciprocal regulation between PHYA and the TOR complex
3. The sucrose–TOR signaling pathway promotes post-transcriptional accumulation of PHYA protein under shade conditions
The study revealed that sucrose treatment under shade conditions significantly increased PHYA protein accumulation. This effect was abolished by Torin 2 treatment, while the transcriptional level of PHYA remained unchanged following sucrose application, indicating that sucrose regulates PHYA stability through a post-transcriptional mechanism rather than transcriptional activation.
In mutants lacking functional components of the TOR complex, sucrose failed to induce PHYA accumulation, further confirming that this process is dependent on TOR activity.
Subcellular localization analysis and nuclear–cytoplasmic fractionation experiments showed that sucrose treatment promoted PHYA accumulation in the nucleus.
To investigate the protein degradation mechanism, the researchers examined the autophagy pathway. Autophagy-defective mutants or treatment with autophagy inhibitors increased only the basal level of PHYA protein but did not affect sucrose-induced PHYA accumulation.
These results indicate that autophagy regulates the basal degradation of PHYA, whereas sucrose-mediated PHYA stabilization occurs independently of the autophagy pathway.
Figure 3: Sucrose–TOR signaling promotes PHYA accumulation and nuclear localization under shade conditions
4. Sucrose-mediated stabilization of PHYA depends on the COP1/SPA E3 ubiquitin ligase complex
Under white-light conditions, PHYA is degraded through the 26S proteasome pathway mediated by the COP1/SPA complex.
The researchers found that sucrose treatment significantly delayed PHYA degradation after plants were transferred from shade conditions to white light. This stabilization effect was comparable to that observed with the proteasome inhibitor MG132, indicating that sucrose suppresses proteasome-dependent degradation of PHYA.
In cop1 and spa quadruple mutants, sucrose failed to promote PHYA accumulation, demonstrating that this process requires the COP1/SPA complex.
Co-IP experiments further showed that sucrose weakened the interaction between PHYA and COP1, and this effect was abolished by Torin 2 treatment, indicating that:
Sucrose activates TOR signaling, which disrupts the PHYA–COP1/SPA interaction and prevents PHYA ubiquitination and subsequent degradation.
Genetic experiments revealed that cop1 and spa multiple mutants displayed enhanced sucrose-induced leaf developmental responses, whereas this enhancement was significantly reduced in the phyA mutant background.
These findings establish that COP1/SPA functions upstream of phyA in regulating this signaling pathway.
Figure 4: Sucrose-mediated PHYA accumulation depends on the COP1/SPA complex
5. Sucrose and phyA synergistically regulate the expression of genes associated with leaf development under shade conditions
To investigate the molecular mechanisms underlying sucrose- and phyA-mediated regulation, the researchers performed shoot transcriptome analysis using wild-type plants and phyA mutants treated with sucrose under shade conditions.
The analysis revealed that, in wild-type plants, 714 genes were upregulated and 857 genes were downregulated in response to sucrose treatment, whereas sucrose-responsive gene expression changes were significantly weakened in the phyA mutants.
Using mfuzz clustering analysis, sucrose-responsive genes were classified into three major groups. Among these, phyA-dependent upregulated genes were significantly enriched in pathways associated with cytokinin biosynthesis, signal transduction, and cell wall biosynthesis, which are closely related to leaf development.
In contrast, phyA-dependent downregulated genes were mainly enriched in leaf senescence-related pathways.
Further validation experiments demonstrated that the sucrose-induced expression of positive regulators involved in leaf development requires the coordinated action of both TOR and phyA. Treatment with the tor mutant background or the TOR inhibitor Torin 2 significantly suppressed this induction effect, confirming that TOR and phyA act synergistically to regulate the transcription of downstream genes involved in leaf development.
Figure 5: Transcriptomic analysis reveals the synergistic regulation of shade-responsive leaf development genes by sucrose and phyA
6. The sucrose–phyA module regulates leaf development under shade conditions through activation of the cytokinin pathway
Previous studies have demonstrated that shade conditions inhibit leaf development by accelerating cytokinin degradation.
In this study, the researchers found that sucrose treatment under shade conditions reversed the shade-induced downregulation of genes involved in cytokinin biosynthesis and signaling pathways, while simultaneously suppressing the induction of the cytokinin degradation gene CKX6. Importantly, this regulatory process was entirely dependent on phyA.
Genetic analyses showed that the ckx6 mutant accumulated higher endogenous cytokinin levels, exhibited larger leaf primordia under shade conditions, and displayed reduced sensitivity to sucrose treatment.
Furthermore, both the phyA ckx6 double mutant and exogenous application of 6-benzylaminopurine (6-BA) successfully restored the leaf developmental defects observed in the phyA mutant.
These results demonstrate that the sucrose–phyA module positively regulates leaf development under shade conditions by controlling cytokinin metabolism and signaling pathways.
Figure 6: The sucrose–phyA module regulates shade-induced leaf development through activation of the cytokinin pathway
This study provides the first evidence that phyA directly interacts with TOR, revealing a previously unknown regulatory pathway in which light and carbon signals are integrated through coordinated TOR–phyA signaling to control shade-mediated leaf development.
The study further clarifies the functional differentiation of different photoreceptors in specific plant tissues, expands the current understanding of plant shade avoidance regulation mechanisms, and provides new molecular targets for breeding crops with enhanced tolerance to high-density planting conditions.
Manipulation of the TOR–phyA regulatory module may offer promising strategies for improving photosynthetic efficiency and crop yield under dense planting systems.