In close proximity, plants can sense each other’s presence via a decrease in the red to far-red light ratio (low R:FR) in the nearby surroundings. Low R:FR perception by phytochrome photoreceptors triggers strong and rapid elongation growth allowing plants to grow taller than their neighbors and reach better lit areas. This process, known as shade avoidance is mostly orchestrated by the growth hormone auxin. However, although low R:FR promotes elongation growth, it compromises plant defense against pathogens by dampening defense hormone signaling; a phenomenon referred to as shade-induced susceptibility. Furthermore, I recently found that plants exposed to low R:FR conditions accumulate glucose, which accelerates pathogen development in plants tissue. Yet, the involvement of primary metabolism in regulating the shade-induced susceptibility remains to be explored. In eukaryotes, the TARGET OF RAPAMYCIN (TOR) kinase is a master growth regulator integrating the cell energy and carbohydrate status to regulate growth and defense responses. In plants, TOR activity is promoted by auxin and glucose, both strongly induced by low R:FR. Interestingly, I also found TOR gene expression to be induced by low R:FR in a recent RNA-seq study. In this project, I will study if and how low R:FR regulates TOR signaling to promote growth at the expense of defence. I will use genetic and chemical approaches to (I) identify the spatiotemporal dynamics of TOR gene expression and TOR protein activity in response to shade in the model plant Arabidopsis thaliana, (II) identify the dependency of shade-induced auxin levels and sugar accumulation on TOR dynamics and (III) characterize potential links between TOR signaling and defense hormone signaling. The gained insights will be instrumental for understanding how plants use shade signals to balance growth and defense responses and will help to engineer new pathogen-resilient crop varieties, which can be grown optimally at high densities.