Mutations of the AtYAK1 Kinase Suppress TOR Deficiency in Arabidopsis

Archive ouverte

Forzani, Céline | Turqueto Duarte, Gustavo | van Leene, Jelle | Clément, Gilles, G. | Huguet, Stephanie | Paysant-Le Roux, Christine | Mercier, Raphaël | de Jaeger, Geert | Leprince, Anne-Sophie | Meyer, Christian

Edité par CCSD ; Elsevier Inc -

International audience. The target of rapamycin (TOR) kinase is a conserved energy sensor that regulates growth in response to environmental cues. However, little is known about the TOR signaling pathway in plants. We used Arabidopsis lines affected in the lethal with SEC13 protein 8 (LST8-1) gene, a core element of the TOR complex, to search for suppressor mutations. Two suppressor lines with improved growth were isolated that carried mutations in the Yet Another Kinase 1 (AtYAK1) gene encoding a member of the dual-specificity tyrosine phosphorylation-regulated kinase (DYRK) family. Atyakl mutations partly rescued the developmental defects of Ist8-1-1 mutants and conferred resistance to the TOR inhibitor AZD-8055. Moreover, atyakl mutations suppressed the transcriptomic and metabolic perturbations as well as the abscisic acid (ABA) hypersensitivity of the Ist8-1-1 mutants. AtYAK1 interacted with the regulatory-associated protein of TOR (RAPTOR), a component of the TOR complex, and was phosphorylated by TOR. Thus, our findings reveal that AtYAK1 is a TOR effector that probably needs to be switched off to activate plant growth.

• Description
• Sujet/Public
• Outil
• Outil d'anticipation
• Mémoire et thèse
• Gestion