Our prior studies found that Arabidopsis seedlings geminated in photosynthesis-restrained (with limited CO 2) and sugar-free liquid medium entered a mitotic quiescent state with arrested primary root growth due to the depletion of endogenous sugars ( 4). In plants, TOR senses both the glucose energy signal and the light-auxin hormone signal to promote the rapid plant growth ( 3– 5), although the key downstream effectors are still largely unknown. The evolutionarily conserved target of rapamycin (TOR) kinase acts as a master regulator that coordinates cell proliferation and growth by integrating nutrient, energy, hormone, and stress signals in all eukaryotes ( 1, 2). Taken together, our results shed light on how carbon and metabolic status can be tightly integrated with the hormone-driven processes to orchestrate complex plant growth programs. Interestingly, dysregulation of TOR or PIN2 disrupts the glucose-promoted low auxin region located in the elongation zone that is essential for cell elongation. We demonstrate that glucose-activated TOR phosphorylates and stabilizes PIN2 and therefore influences the gradient distribution of PIN2 in the Arabidopsis primary root. Here, using a large-scale Arabidopsis mutant screening, we described the identification of PIN2 (PIN-FORMED 2), an auxin efflux facilitator, as a key downstream regulator in glucose-TOR (target of rapamycin) energy signaling. The molecular mechanisms of how such a steep auxin gradient is established and maintained, and how this auxin gradient within the root dynamically adjusts in response to environmental stimuli are still largely unknown. In the primary root of Arabidopsis there is a robust auxin gradient with a peak concentration at the tip of the meristem and a significant decrease throughout the elongation zone.
The plant growth hormone auxin controls cell identity, cell division, and expansion.
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