A CLV3-WUS positive feedback loop in individual cells enhances shoot stem cell thermotolerance in Arabidopsis.

Gibberellic Acids and ethylene antagonistically regulate stem growth via SlGAI-SlERF1B-SlXTH19 module in tomato.

Stem growth and development greatly influence on plant architecture and yield, which are intimately associated with cell wall remodeling. However, the regulatory mechanisms governing cell-wall remodeling in crops remain poorly understood. Xyloglucan endotransglucosylase/hydrolase (XTH) plays a pivotal role in xyloglucan metabolism. Here, we demonstrated that SlXTH19 controls cell wall remodeling and stem growth. Knockout or knockdown of SlXTH19 decreased cell wall thickness and cellulose and hemicellulose content in tomato stems. We demonstrated that ETHYLENE RESPONSE FACTOR (ERF) transcription factor SlERF1B binds directly to the SlXTH19 promoter, repressing its expression. Knockdown of SlERF1B showed greater stem growth and cell wall composition, whereas SlERF1B-overexpressing plants had a shorter plant heights and thinner stems than the wild type. Further investigation revealed that SlERF1B directly binds to the SlGA3ox1 promoter and represses production of GA. In addition, SlGAI, the core negative regulator of GA signaling, interacts with SlERF1B, and these interactions enhanced the inhibitory effect of SlERF1B on its downstream targets SlXTH19 and SlGA3ox1. Collectively, these results reveal a signaling module in which GA signaling modulates the degradation of SlGAI, attenuates ethylene (ETH) signaling to inhibit SlXTH19 expression, and regulates stem growth in tomato plants.

The BZR1-BLH1-PIF4 feedback module acts as a molecular amplifier for precise thermomorphogenesis in Arabidopsis

Global increases in the intensity and frequency of elevated temperatures is threatening ecosystem stability and crop yield. Understanding plant thermomorphogenesis is critical for developing climate-resilient crops, yet the underlying mechanisms remain to be clarified. Here, we identify the BEL1-LIKE HOMEODOMAIN transcription factor BLH1 as a critical negative regulator of thermomorphogenesis that modulates the key BRASSINAZOLE-RESISTANT 1 (BZR1)-PHYTOCHROME INTERACTING FACTOR 4 (PIF4) thermomorphogenic regulatory module. Overexpression of BLH1 or its homologs confers high-temperature (HT) insensitivity, whereas blh higher-order mutants exhibit HT hypersensitivity. BLH1 expression is directly repressed by BZR1 and is down-regulated by HT. We further demonstrate that BLH1 directly binds to the PIF4 promoter to repress its transcription and concurrently interacts with the PIF4 protein to inhibit its activity. Overexpression of BLH1 rescues the elongated hypocotyl phenotype in bzr1-1D or PIF4 overexpression plants. Our findings define a BZR1-BLH1-PIF4 regulatory axis that modulates the BZR1-PIF4-auxin-BR-BZR1 positive feedback loop, ensuring a balanced thermomorphogenic response to HT. High temperatures trigger plant growth responses that can compromise crop yield. Here the authors report that the BLH1 protein acts as a brake to fine-tune the heat response, offering a target for breeding climate-resilient crops.

LF1 mediates brassinosteroid signaling to regulate leaf angle development in rice.

CYCLING DOF FACTOR 2 (LdCDF2) functions as a positive regulator integrating GA signaling and biosynthesis to drive bulb germination in Lilium.

The dormancy release and initiation of germination in underground storage organs are critical for plant adaptation and agriculture. Gibberellin (GA) promotes germination, but how GA signaling achieves self-amplification at the early stage of germination to drive rapid germination remains unknown. In particular, the molecular hub that connects GA perception and biosynthesis has yet to be identified. Here, we identified CYCLING DOF FACTOR 2 (LdCDF2) from Lilium davidii var. unicolor as a novel positive regulator of germination. Using stable genetic transformation, protein‒protein interaction assays, and cell-free degradation assays, we revealed a germination module wherein LdCDF2 directly couples GA signaling with biosynthesis. Mechanistically, LdCDF2 directly activates the transcription of LdGA3ox2/3, thereby promoting GA biosynthesis. Moreover, the DELLA protein LdSLR1 interacts with LdCDF2, inhibiting the transcriptional activity of LdCDF2 and accelerating its degradation via the 26S proteasome, thereby exerting a dual inhibitory effect on germination. When GA signaling degrades LdSLR1, LdCDF2 is released, reactivating GA synthesis and enabling GA signal self-amplification. Genetic evidence revealed that stable silencing of LdCDF2 reduced the germination rate by 76.0% and endogenous GA3 level to 57.69% of that of the control, while overexpression increased the rate by 2.7-fold and the GA3 level by 6.29-fold. In summary, this study identifies LdCDF2 as a hub linking GA signaling and biosynthesis and elucidates how the DELLA-LdCDF2 dual switch mediates GA self-amplification. This discovery advances our understanding of underground organ germination mechanisms and provides new molecular targets for studying plant hormone signaling cascades and precisely controlling bulbous plant germination timing.

Arabidopsis HY5 enhances jasmonate responses by directly suppressing the expression of the JAZ1 gene in a FIN219/JAR1-dependent manner

Light is a key environmental signal that regulates plant growth and development. ELONGATED HYPOCOTYL 5 (HY5), a bZIP transcription factor, is a central positive regulator of photomorphogenesis in Arabidopsis thaliana, integrating light and hormone signaling pathways. However, the molecular role of HY5 in jasmonate (JA) signaling remains unclear. Here, we show that methyl jasmonate (MeJA) substantially induces HY5 protein accumulation in a FIN219/JAR1-dependent manner. Genetic evidence indicates that HY5 and FIN219 act synergistically to inhibit hypocotyl growth and coordinate defense-related transcriptional networks. Loss of HY5 function results in hypersensitivity to MeJA-mediated inhibition of hypocotyl elongation, and transcriptomic analyses reveal disturbances in numerous light- and JA-responsive genes. HY5 represses JAZ1 expression by binding to its G-box-containing promoter and physically interacts with JAZ1, suggesting both transcriptional and post-translational regulation. Furthermore, HY5 and MYC2 compete for binding at the JAZ1 promoter, modulating JA responses under far-red light. Together, our findings uncover a regulatory mechanism in which HY5 fine-tunes JA signaling and seedling development by integrating light and hormone cues. This work provides new insights into HY5-mediated crosstalk and identifies potential targets to improve stress resilience in crops.

A Regulatory Circuit between AGL103 and TCPs Balances Growth and Stress Tolerance in Arabidopsis thaliana.

Plants must balance growth with stress adaptation, yet the transcriptional mechanisms governing this trade-off remain incompletely defined. Here, we identify the MADS-box transcription factor (TF) AGL103 as a promoter of growth but a negative regulator of drought and salt tolerance in Arabidopsis thaliana. agl103 mutants exhibit enhanced germination, root elongation, and survival under mannitol-induced osmotic stress and salt stress, whereas AGL103-overexpressing plants are hypersensitive. Transcriptomic and molecular analyses show that AGL103 directly represses MYB15 and MYB102 by binding CArG motifs in their promoters. Notably, AGL103 also physically interacts with Teosinte branched 1/Cycloidea/ Proliferating cell factor (TCP) proteins TCP14 and TCP15, forming a repressor complex that reinforces MYB15/MYB102 suppression and antagonizes TCP14-mediated transcriptional activation. Furthermore, TCP14, but not TCP15, feeds back to repress AGL103 transcription, establishing a regulatory loop that fine-tunes plant growth and stress responses. This AGL103-TCPs module integrates developmental and stress signaling, offering mechanistic insight into how plants balance growth and resilience and highlighting potential targets for engineering stress-tolerant crops.