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The emerging role of TARGET OF RAPAMYCIN in the shade-driven pathogen susceptibility in plants.

Applicant Dr. Sarah Courbier
Subject Area Plant Physiology
Term since 2022
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 513924299
 
The exponential human population growth, coupled with arable land losses due to intensive farming, forces growers to produce more yield with less land. One strategy used to promote yield is to grow plants closer together. However, at high planting densities, plants will eventually shade each other. Plants detect shade via a reduction of the ratio between red and far-red light (low R:FR). Low R:FR perception by phytochrome photoreceptors triggers strong and rapid growth responses, mostly driven by the growth hormone auxin, known as shade avoidance, allowing plants to outcompete their neighbours for light. In addition to eliciting growth responses, low R:FR promotes plant susceptibility to pathogens via a dampening of defence hormone signalling referred to as the shade-induced susceptibility (Courbier et al., 2021). Recently, we also found that plants experiencing low R:FR accumulate sugars, which is closely associated with faster lesion development by pathogens (Courbier et al., 2020). Yet, the molecular mechanism behind how sugar accumulation leads to increased pathogen susceptibility remains elusive. In our recent RNA-sequencing dataset, I found that TARGET OF RAPAMYCIN (TOR) is upregulated in response to low R:FR. In eukaryotes, TOR is a master growth regulator activated by glucose and auxin, both strongly elevated in shaded plants, too. The proposed research project is divided into three main work packages which aim to (I) identify the spatiotemporal dynamics of TOR gene expression, TOR protein abundance and activity in response to shade and/or pathogen infection in Arabidopsis thaliana, (II) identify the dependency of shade-induced auxin signalling and glucose accumulation on TOR dynamics, and then (III) unravel potential links between TOR signalling and defence hormone signalling. This way, I aim to identify if and how sugar accumulation during plant shading controls TOR and the subsequent growth-defence trade-off. The gained insights will be instrumental for understanding how plants use light signals coming from neighbouring plants to balance growth and defence in a competing environment. In addition, the obtained results can pinpoint TOR as a molecular breeding target for crop varieties with higher disease resistance when grown in higher densities.
DFG Programme WBP Position
 
 

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