@article{TomeNaegeleAdamoetal.2014,
  author    = {Tome, Filipa and N{\"a}gele, Thomas and Adamo, Mattia and Garg, Abhroop and Marco-Ilorca, Carles and Nukarinen, Ella and Pedrotti, Lorenzo and Peviani, Alessia and Simeunovic, Andrea and Tatkiewicz, Anna and Tomar, Monika and Gamm, Magdalena},
  title     = {The low energy signaling network},
  series = {Frontiers in Plant Science},
  volume    = {5},
  journal   = {Frontiers in Plant Science},
  number    = {353},
  issn      = {1664-462X},
  doi       = {10.3389/fpls.2014.00353},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-115813},
  year      = {2014},
  abstract  = {Stress impacts negatively on plant growth and crop productivity, causing extensive losses to agricultural production worldwide. Throughout their life, plants are often confronted with multiple types of stress that affect overall cellular energy status and activate energy-saving responses. The resulting low energy syndrome (LES) includes transcriptional, translational, and metabolic reprogramming and is essential for stress adaptation. The conserved kinases sucrose-non-fermenting-1-related protein kinase-1 (SnRK1) and target of rapamycin (TOR) play central roles in the regulation of LES in response to stress conditions, affecting cellular processes and leading to growth arrest and metabolic reprogramming. We review the current understanding of how TOR and SnRK1 are involved in regulating the response of plants to low energy conditions. The central role in the regulation of cellular processes, the reprogramming of metabolism, and the phenotypic consequences of these two kinases will be discussed in light of current knowledge and potential future developments.},
  language  = {en}
}
@article{NukarinenNaegelePedrottietal.2016,
  author    = {Nukarinen, Ella and N{\"a}gele, Thomas and Pedrotti, Lorenzo and Wurzinger, Bernhard and Mair, Andrea and Landgraf, Ramona and B{\"o}rnke, Frederik and Hanson, Johannes and Teige, Markus and Baena-Gonzalez, Elena and Dr{\"o}ge-Laser, Wolfgang and Weckwerth, Wolfram},
  title     = {Quantitative phosphoproteomics reveals the role of the AMPK plant ortholog SnRK1 as a metabolic master regulator under energy deprivation},
  series = {Scientific Reports},
  volume    = {6},
  journal   = {Scientific Reports},
  number    = {31697},
  doi       = {10.1038/srep31697},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-167638},
  year      = {2016},
  abstract  = {Since years, research on SnRK1, the major cellular energy sensor in plants, has tried to define its role in energy signalling. However, these attempts were notoriously hampered by the lethality of a complete knockout of SnRK1. Therefore, we generated an inducible amiRNA::SnRK1α2 in a snrk1α1 knock out background (snrk1α1/α2) to abolish SnRK1 activity to understand major systemic functions of SnRK1 signalling under energy deprivation triggered by extended night treatment. We analysed the in vivo phosphoproteome, proteome and metabolome and found that activation of SnRK1 is essential for repression of high energy demanding cell processes such as protein synthesis. The most abundant effect was the constitutively high phosphorylation of ribosomal protein S6 (RPS6) in the snrk1α1/α2 mutant. RPS6 is a major target of TOR signalling and its phosphorylation correlates with translation. Further evidence for an antagonistic SnRK1 and TOR crosstalk comparable to the animal system was demonstrated by the in vivo interaction of SnRK1α1 and RAPTOR1B in the cytosol and by phosphorylation of RAPTOR1B by SnRK1α1 in kinase assays. Moreover, changed levels of phosphorylation states of several chloroplastic proteins in the snrk1α1/α2 mutant indicated an unexpected link to regulation of photosynthesis, the main energy source in plants.},
  language  = {en}
}