Biology subjects

Confraria, A.

Publications and source records attributed to Confraria, A..

4 recordsLinked to original sources

bioRxiv2026

Phosphate Deficiency Attenuates SnRK1 Activity to Modulate the Phosphate Starvation Response in Arabidopsis thaliana

Phosphate starvation requires extensive metabolic and developmental reprogramming, yet how this response is coordinated with cellular energy status remains poorly understood. The energy sensor SnRK1 regulates plant growth and metabolism in response to energy availability, but its contribution to the regulation and deployment of the phosphate starvation response (PSR) remains unclear. To address this, we combined physiological, proteomic and metabolomic analyses with genetic manipulation of SnRK1 activity in Arabidopsis thaliana to determine how SnRK1 influences plant responses to phosphate starvation. We found that phosphate starvation reduced SnRK1 activity and activation-loop (T-loop) phosphorylation, while altering SnRK1 activity changed the timing and magnitude of physiological, proteomic and metabolic responses to phosphate limitation. Reduced SnRK1 activity was generally associated with earlier and stronger deployment of PSR-associated responses, whereas increased SnRK1 activity delayed or attenuated several components of the response. These effects were tissue- and time-dependent and were accompanied by distinct metabolic configurations. Our findings support a model in which SnRK1 acts as a quantitative metabolic brake on the PSR, coordinating the metabolic investment required for phosphate-starvation adaptation with growth.

plant biology↗

bioRxiv2025

TPS Proteins coordinate plant growth with sugar availability via the SnRK1 Kinase

The ability to sense and respond to nutrients determines adaptation and survival in all organisms. In plants, sucrose stimulates growth and developmental progression via the signalling sugar trehalose 6-phosphate (T6P) which reflects sucrose availability. T6P acts, at least partly, by inhibiting the protein kinase SUCROSE NON-FERMENTING 1 (SNF1)-RELATED KINASE 1 (SnRK1) but the underlying mechanisms are poorly understood. Here, we identify a group of catalytically inactive T6P synthase (TPS) proteins, TPS5/6/7, as important factors for coupling the T6P signal to SnRK1 activity. In Arabidopsis thaliana, lack of TPS5/6/7 causes severe growth defects, particularly in roots. This is accompanied by a metabolic signature that is suggestive of T6P insensitivity and impaired sucrose utilization. Using a combination of genetics, SnRK1 activity assays, and imaging, we demonstrate that the growth defects of the tps5/6/7 mutant are due to SnRK1 misregulation and are reverted by knocking-down SnRK1 in this background. Co-immunoprecipitation assays further show that T6P promotes the interaction of TPS proteins with SnRK1 in a highly specific and dose-dependent manner. Our results support a model where TPS proteins act as T6P sensors, inhibiting non-nuclear SnRK1 activity when sucrose is abundant to promote biosynthetic processes and growth.

plant biology↗

bioRxiv2023

HOS1 promotes plant tolerance to low-energy stress via the SnRK1 protein kinase

Plants need to integrate internal and environmental signals to mount adequate stress responses. The NUCLEAR PORE COMPLEX (NPC) component HIGH EXPRESSION OF OSMOTICALLY RESPONSIVE GENES 1 (HOS1) is emerging as such an integrator, affecting responses to cold, heat, light and salinity. Stress conditions often converge in a low-energy signal that activates SUCROSE NON-FERMENTING 1-RELATED KINASE 1 (SnRK1) to promote stress tolerance and survival. Here, we explored the role of HOS1 in the SnRK1-dependent response to low-energy stress in Arabidopsis thaliana, using darkness as a treatment and a combination of genetic, biochemical and phenotypic assays. We show that the induction of starvation genes and plant tolerance to prolonged darkness are defective in the hos1 mutant. HOS1 interacts physically with the SnRK11 catalytic subunit in yeast-two-hybrid and in planta, and the nuclear accumulation of SnRK11 is reduced in the hos1 mutant. Likewise, another NPC mutant, nup160, exhibits lower activation of starvation genes and decreased tolerance to prolonged darkness. Importantly, defects in low-energy responses in the hos1 background are rescued by fusing SnRK11 to a potent nuclear localization signal, or by sugar supplementation during the dark treatment. Altogether, this work demonstrates the importance of HOS1 for the nuclear accumulation of SnRK11, which is key for plant tolerance to low-energy conditions.

plant biology↗

bioRxiv2023

Sugar signaling modulates SHOOT MERISTEMLESS expression and meristem function in Arabidopsis

In plants, development of all above-ground tissues is controlled by the shoot apical meristem (SAM) which balances cell proliferation and differentiation to allow life-long growth. To maximize fitness and survival, meristem activity is adjusted to the prevailing conditions through a poorly understood integration of developmental signals with environmental and nutritional information. Here, we show that sugar signals influence SAM function by altering the protein levels of SHOOT MERISTEMLESS (STM), a key regulator of meristem maintenance. STM is less abundant in the inflorescence meristems of plants grown or treated under limiting light conditions, with lower STM levels correlating with lower sugar content in these meristems. Additionally, sucrose but not light is sufficient to sustain STM accumulation in excised inflorescences. Plants overexpressing the 1-subunit of SUCROSE-NON-FERMENTING1-RELATED KINASE 1 (SnRK1) accumulate less STM protein under optimal light conditions, despite higher sugar accumulation in the meristem. Furthermore, SnRK11 interacts physically with STM, suggesting a direct local repression. Surprisingly, silencing SnRK1 in the meristem leads to reduced STM expression and severe developmental phenotypes previously associated with STM loss-of-function. Altogether, we demonstrate that sugars promote STM accumulation and that the SnRK1 sugar sensor plays a dual role in the SAM, limiting STM abundance under unfavorable conditions but being required for overall meristem organization and integrity. This highlights the importance of sugars and SnRK1 signaling for the proper coordination of meristem activities.

plant biology↗