# Contributions of TOR Signaling on Photosynthesis
## 2 TOR: A Key Regulator in Photosynthesis
### Role of TOR in Sensing C Nutrient  
Unlike yeast and animals, plants acquired the ability to live outside water, and their most prominent feature is probably their ability to synthesize organic carbon (C) molecules like glucose, sugars (fructose, glucose or sucrose) and starch by using light energy and releasing molecular oxygen into the atmosphere, which is also called photosynthesis. The ability to sense, assimilate, transport, and utilize C nutrients is vital for plant survival and growth. Plants decide whether to store sugars in source leaves or distribute these metabolites to sink organs, such as young organs, roots, or seeds to ensure the supply-demand balance of sugar in plants [48]. Evidence supports that TOR is involved in plant  
Figure 2: Summary of Target of Rapamycin (TOR) signaling in plant photosynthesis, including inputs for the activation of TOR signaling and output processes regulated by the TOR signaling. Light signals and sugars derived from photosynthesis activate TOR signaling and the conserved downstream outputs. The activated TOR downstream outputs regulate photomorphogenesis and leaf development, which eventually influences the efficiency of oxygenic photosynthesis. Abbreviations: COPI, constitutive photomorphogenesis 1; ROP2, Rho-like small GTPase 2; TORC, Target of Rapamycin complex; TOR, Target of Rapamycin; RAPTOR, regulatory-associated protein of mTOR; LST8, lethal with Sec13 protein 8; S6K, S6 kinase; BIN2, brassinosteroid-insensitive 2; BZR1, brassinazole resistance 1; RPS6, ribosomal protein S6; TAP46, type 2A-phosphatase-associated protein 46 kDa; E2 Fa/b, E2 promoter-binding factor a/b; RSH4b, RelA-SpoT homolog gene 4b; ppGpp, guanosine 3\({}^{\prime}\)-diphosphate 5\({}^{\prime}\)-diphosphate; PYL, pyrabactin resistance 1-like; SnRK2, SNF1-related protein kinase 2. C nutrient sensing and serves as an intermediate for the regulation of plant growth by organic carbon (C) sugars [9; 39]. At the photoautotrophic transition checkpoint, 15 mM glucose and sucrose can promote TOR signaling and control root meristem, root elongation, cotyledon expansion, and root hair production activation through glycolysis and mitochondrial bioenergetic. The requirement for glycolysis and mitochondrial bioenergetics to activate TOR protein kinase was monitored by the phosphorylation of its conserved substrates S6K. In this process, other sugars, such as fructose, galactose, and xylose, are much less effective [27; 44]. Recent findings have illustrated that glucose is sufficient to activate TOR kinase in root apexes, whereas glucose and light signals are required for TOR activation in shoot apexes. In shoot apexes, exogenously auxin can replace light to activate TOR and promote leaf development. The small GTPase Rho-related protein 2 (ROP2) transduced light-auxin signal to activate TOR and promotes TOR-dependent phosphorylation and activation of transcription factor E2 Fa/E2 Fb, which eventually enhances root growth and leaf formation [27; 44; 49]. Glucose-activated TOR also controls the accumulation of the brassinosterol (BR)-signaling transcription factor BZR1 (Brassinazole resistance 1). Inhibition of TOR by inducible RNAi reduced expression of BR-responsive genes and abolished sugar-promoted BZR1 accumulation. The growth inhibition caused by TOR inactivation can be partially recovered by exogenously applied BR and the BZR1 gain-of-function mutation _bzr1-1D_. The regulation of BZR1 accumulation by glucose-TOR allows carbon availability to control plant growth [50]. Through genetic approaches and chemical or physiological treatments to either promote or disrupt TOR activity, the results indicated that TOR restricted the plasmodesmata (PD) transport activity in leaves. Further study revealed that TOR was significantly more active in mature leaves photosynthesizing excess sugars (glucose) than in young and growing leaves [51]. In addition to glucose, sucrose is demonstrated to play a pivotal role in TOR activation and development of shoot apical meristem.