Abstract
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.
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Abstract
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.
Competing Interest Statement
The authors have declared no competing interest.
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