title: TOR Signaling Promotes Accumulation of BZR1 to Balance Growth with Carbon Availability in Arabidopsis.
abstract: For maintenance of cellular homeostasis, the actions of growth-promoting hormones must be attenuated when nutrient and energy become limiting. The molecular mechanisms that coordinate hormone-dependent growth responses with nutrient availability remain poorly understood in plants [1, 2]. The target of rapamycin (TOR) kinase is an evolutionarily conserved master regulator that integrates nutrient and energy signaling to regulate growth and homeostasis in both animals and plants [3-7]. Here, we show that sugar signaling through TOR controls the accumulation of the brassinosteroid (BR)-signaling transcription factor BZR1, which is essential for growth promotion by multiple hormonal and environmental signals [8-11]. Starvation, caused by shifting of light-grown Arabidopsis seedlings into darkness, as well as inhibition of TOR by inducible RNAi, led to plant growth arrest and reduced expression of BR-responsive genes. The growth arrest caused by TOR inactivation was partially recovered by BR treatment and the gain-of-function mutation bzr1-1D, which causes accumulation of active forms of BZR1 [12]. Exogenous sugar promoted BZR1 accumulation and seedling growth, but such sugar effects were largely abolished by inactivation of TOR, whereas the effect of TOR inactivation on BZR1 degradation is abolished by inhibition of autophagy and by the bzr1-1D mutation. These results indicate that cellular starvation leads sequentially to TOR inactivation, autophagy, and BZR1 degradation. Such regulation of BZR1 accumulation by glucose-TOR signaling allows carbon availability to control the growth promotion hormonal programs, ensuring supply-demand balance in plant growth.
authors.affiliation: Hebei Key Laboratory of Molecular and Cellular Biology, Key Laboratory of Molecular and Cellular Biology of Ministry of Education, College of Life Science, Hebei Normal University, Hebei Collaboration Innovation Center for Cell Signaling, Shijiazhuang, Hebei 050024, China; Center of Basic Forestry and Proteomics, Haixia Institute of Science and Technology (HIST), Fujian Agriculture and Forestry University (FAFU), Fuzhou 350002, China.
authors.forename: Zhenzhen
authors.initials: Z
authors.lastname: Zhang
authors.affiliation: Department of Plant Biology, Carnegie Institution for Science, Stanford, CA 94305, USA.
authors.forename: Jia-Ying
authors.initials: JY
authors.lastname: Zhu
authors.affiliation: Department of Life Science, Chung-Ang University, Seoul 156756, Korea.
authors.forename: Jeehee
authors.initials: J
authors.lastname: Roh
authors.affiliation: IJPB, UMR 1318 INRA-AgroParisTech, ERL CNRS 3559, Saclay Plant Sciences, 78026 Versailles, France.
authors.forename: Chloé
authors.initials: C
authors.lastname: Marchive
authors.affiliation: Department of Life Science, Chung-Ang University, Seoul 156756, Korea.
authors.forename: Seong-Ki
authors.initials: SK
authors.lastname: Kim
authors.affiliation: IJPB, UMR 1318 INRA-AgroParisTech, ERL CNRS 3559, Saclay Plant Sciences, 78026 Versailles, France.
authors.forename: Christian
authors.initials: C
authors.lastname: Meyer
authors.affiliation: Hebei Key Laboratory of Molecular and Cellular Biology, Key Laboratory of Molecular and Cellular Biology of Ministry of Education, College of Life Science, Hebei Normal University, Hebei Collaboration Innovation Center for Cell Signaling, Shijiazhuang, Hebei 050024, China.
authors.forename: Yu
authors.initials: Y
authors.lastname: Sun
authors.affiliation: Center of Basic Forestry and Proteomics, Haixia Institute of Science and Technology (HIST), Fujian Agriculture and Forestry University (FAFU), Fuzhou 350002, China.
authors.forename: Wenfei
authors.initials: W
authors.lastname: Wang
authors.affiliation: Department of Plant Biology, Carnegie Institution for Science, Stanford, CA 94305, USA. Electronic address: zywang24@stanford.edu.
authors.forename: Zhi-Yong
authors.initials: ZY
authors.lastname: Wang
mesh_terms: D017360:Arabidopsis / Q000235:genetics* / Q000254:growth & development / Q000378:metabolism; D029681:Arabidopsis Proteins / Q000235:genetics* / Q000378:metabolism; D002244:Carbon / Q000378:metabolism*; D004268:DNA-Binding Proteins; D009687:Nuclear Proteins / Q000235:genetics* / Q000378:metabolism; D019869:Phosphatidylinositol 3-Kinases / Q000235:genetics* / Q000378:metabolism; D015398:Signal Transduction; D014157:Transcription Factors / Q000235:genetics* / Q000378:metabolism
chemical_list: D029681:Arabidopsis Proteins; D002244:Carbon; D004268:DNA-Binding Proteins; D009687:Nuclear Proteins; D019869:Phosphatidylinositol 3-Kinases; D014157:Transcription Factors; C454444:BZR1 protein, Arabidopsis; C512171:TOR protein, Arabidopsis