Mutations of the AtYAK1 Kinase Suppress TOR Deficiency in Arabidopsis

Abstract

Summary: 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. Atyak1 mutations partly rescued the developmental defects of lst8-1-1 mutants and conferred resistance to the TOR inhibitor AZD-8055. Moreover, atyak1 mutations suppressed the transcriptomic and metabolic perturbations as well as the abscisic acid (ABA) hypersensitivity of the lst8-1-1 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. : The target of rapamycin (TOR) kinase is conserved in eukaryotes and controls growth and development. Forzani et al. find that mutations of the double-specificity plant YAK1 kinase restore growth of lst8-1 mutants and dampen the effects of TOR deficiency. Moreover, they show that AtYAK1 is phosphorylated by TOR. Keywords: Arabidopsis, TOR kinase, RAPTOR, YAK1 kinase, DYRK kinase, abscisic acid, LST8