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Dissection of general and specific regulatory mechanism of sulfur metabolism in Arabidopsis thaliana

Subject Area Plant Physiology
Term from 2013 to 2024
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 235736350
 
Decrease of growth and translation is a general response of plants to diverse stresses as a trade-off to release energy for stress responses. This project addresses a fundamental question of plant research: How is protein translation and meristem activity regulated under mineral-nutrient deficiency? The coordination of these processes is crucial for acclimation responses such as shifts in shoot-to-root-ratio. In the previous proposal we investigated the sulfate assimilation pathway and its specific regulatory mechanisms in Arabidopsis thaliana. We focused on cysteine since it is the central metabolite that coordinates the assimilation of sulfur with that of carbon and nitrogen. The comparison of mutants that are either limited in flux of the sulfur or carbon/nitrogen branch of the pathway leading to cysteine revealed specific sensing mechanisms by the kinases GCN2 (general control non-derepressible 2) and TOR (target of rapamycin). We showed that both contribute independently to control of translation and growth of shoot and root and that plant TOR senses sulfur availability in leaves via down-regulation of glucose-TOR signaling. The TOR regulated network included induction of autophagy and down-regulation of translation and meristematic activity. These findings provide the basis to unravel the integration of different nutritional cues towards coordinated changes in plant growth regulation. The first part of this study we will address the specificity of TOR regulation upon limitation of diverse mineral nutrients. This will allow us to dissect the signals for the induction of the general response to nutrient limitation orchestrated by TOR from the signals controlling the sulfur deficiency specific response. Further emphasis will be given on the upstream signal transduction machinery for the sulfur deficiency-induced regulation of TOR. In the second part of the study we will unravel how TOR regulates downstream processes to achieve acclimation responses. Prime targets of TOR in this respect are the control of the plasticity of the proteome, the recycling of nutrients by autophagy and the ubiquitin/proteasome system, and the cell cycle in response to sulfur availability. Together, these approaches will explain TOR governed processes that are integral for the understanding of the sulfur regulatory network that can be seen as a role model for primary nutrient metabolism.
DFG Programme Research Grants
 
 

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