Thursday, April 22, 2021
2pm – visioconference (zoom)
BPMP, “Water, signaling and hydraulic architecture” team (Aqua)
Regulation of plant energy signaling by components of the abscisic acid pathway
The capacity to sense and react to fluctuations in nutrient availability is crucial for the survival of all living organisms. In eukaryotes, two highly evolutionarily conserved protein complexes, the Snf1/AMPK/SnRK1 and the TOR protein kinases, play an essential role in the control of energy homeostasis. Low-energy conditions activate the Snf1/AMPK/SnRK1 system, which thereby initiates a transcriptional and metabolic reprogramming to favor catabolic (energy producing) over anabolic (energy consuming) processes and ultimately restore energy homeostasis. One of the main targets of Snf1/AMPK/SnRK1 is the growth-promoting TOR kinase, which is inhibited in conditions of energy deficit that cannot sustain growth. Snf1/AMPK/SnRK1 and TOR constitute the Snf1/AMPK/SnRK1-TOR functional axis, which translates the cellular energy/nutritional status into growth outputs. The capacity to sense the energy status enables the Snf1/AMPK/SnRK1-TOR axis to react to a diversity of stress conditions that impinge on primary energy metabolism.
In unicellular organisms the Snf1/AMPK/SnRK1-TOR axis responds mainly to energy and nutrient availability while, with the onset of multicellularity, it evolved the ability to respond to systemic signals, like hormones and growth factors, to coordinate whole-organism physiology and growth. In addition to its role in stress responses, the Snf1/AMPK/SnRK1-TOR axis plays pivotal roles in developmental regulation. In plants the SnRK1-TOR axis has been implicated in the response to the main phytohormones, including ABA, but how these pathways are interconnected at the molecular level is poorly understood. The work that is going to be presented addressed the connection between SnRK1 and ABA signaling, identifying two core components of ABA signaling as novel regulators of the SnRK1 pathway. First, clade A PP2C phosphatases (established negative regulators of ABA signaling) were found to be necessary to reset SnRK1 signaling, with lack of these phosphatases causing defective SnRK1 repression when energy levels are restored after stress. Repression of kinase activity is exerted via direct binding to the SnRK1 α-catalytic subunit through dephosphorylation and physical obstruction. As a consequence of such regulation, SnRK1 signaling is activated by ABA in a PP2C-dependent manner. Second, SnRK2 kinases (established positive regulators of ABA signaling) were found to act as repressors of SnRK1 signaling under normal growth conditions. SnRK2s are required to form SnRK1 repressor complexes that are responsive to ABA, but not to energy deficit. In the presence of ABA, on the other hand, these SnRK2-containing complexes dissociate through canonical ABA signaling, releasing SnRK1 and SnRK2 kinases to drive stress responses and growth inhibition. One major outcome of this release is the inhibition of TOR and growth (post-germination growth and lateral root development). Therefore SnRK2s play a dual role in SnRK1 regulation: in control conditions they inhibit SnRK1 signaling contributing to normal growth and development, while, in response to ABA, they act in concert with SnRK1 to drive stress responses and growth repression.
Conclusively, this work describes novel mechanisms of how the SnRK1-TOR axis is regulated by ABA signals, contributing molecular knowledge into how plant growth and development are shaped by the environment.
Contact : Mattia Adamo