@article{BalazadehSchildhauerAraujoetal.2014,
  author    = {Balazadeh, Salma and Schildhauer, Joerg and Araujo, Wagner L. and Munne-Bosch, Sergi and Fernie, Alisdair R. and Proost, Sebastian and Humbeck, Klaus and M{\"u}ller-R{\"o}ber, Bernd},
  title     = {Reversal of senescence by N resupply to N-starved Arabidopsis thaliana: transcriptomic and metabolomic consequences},
  series = {Journal of experimental botany},
  volume    = {65},
  journal   = {Journal of experimental botany},
  number    = {14},
  publisher = {Oxford Univ. Press},
  address   = {Oxford},
  issn      = {0022-0957},
  doi       = {10.1093/jxb/eru119},
  pages     = {3975 -- 3992},
  year      = {2014},
  abstract  = {Leaf senescence is a developmentally controlled process, which is additionally modulated by a number of adverse environmental conditions. Nitrogen shortage is a well-known trigger of precocious senescence in many plant species including crops, generally limiting biomass and seed yield. However, leaf senescence induced by nitrogen starvation may be reversed when nitrogen is resupplied at the onset of senescence. Here, the transcriptomic, hormonal, and global metabolic rearrangements occurring during nitrogen resupply-induced reversal of senescence in Arabidopsis thaliana were analysed. The changes induced by senescence were essentially in keeping with those previously described; however, these could, by and large, be reversed. The data thus indicate that plants undergoing senescence retain the capacity to sense and respond to the availability of nitrogen nutrition. The combined data are discussed in the context of the reversibility of the senescence programme and the evolutionary benefit afforded thereby. Future prospects for understanding and manipulating this process in both Arabidopsis and crop plants are postulated.},
  language  = {en}
}
@article{KamranfarXueTohgeetal.2018,
  author    = {Kamranfar, Iman and Xue, Gang-Ping and Tohge, Takayuki and Sedaghatmehr, Mastoureh and Fernie, Alisdair R. and Balazadeh, Salma and Mueller-Roeber, Bernd},
  title     = {Transcription factor RD26 is a key regulator of metabolic reprogramming during dark-induced senescence},
  series = {New phytologist : international journal of plant science},
  volume    = {218},
  journal   = {New phytologist : international journal of plant science},
  number    = {4},
  publisher = {Wiley},
  address   = {Hoboken},
  issn      = {0028-646X},
  doi       = {10.1111/nph.15127},
  pages     = {1543 -- 1557},
  year      = {2018},
  abstract  = {Leaf senescence is a key process in plants that culminates in the degradation of cellular constituents and massive reprogramming of metabolism for the recovery of nutrients from aged leaves for their reuse in newly developing sinks. We used molecular-biological and metabolomics approaches to identify NAC transcription factor (TF) RD26 as an important regulator of metabolic reprogramming in Arabidopsis thaliana. RD26 directly activates CHLOROPLAST VESICULATION (CV), encoding a protein crucial for chloroplast protein degradation, concomitant with an enhanced protein loss in RD26 over-expressors during senescence, but a reduced decline of protein in rd26 knockout mutants. RD26 also directly activates LKR/SDH involved in lysine catabolism, and PES1 important for phytol degradation. Metabolic profiling revealed reduced c-aminobutyric acid (GABA) in RD26 overexpressors, accompanied by the induction of respective catabolic genes. Degradation of lysine, phytol and GABA is instrumental for maintaining mitochondrial respiration in carbon-limiting conditions during senescence. RD26 also supports the degradation of starch and the accumulation of mono-and disaccharides during senescence by directly enhancing the expression of AMY1, SFP1 and SWEET15 involved in carbohydrate metabolism and transport. Collectively, during senescence RD26 acts by controlling the expression of genes across the entire spectrum of the cellular degradation hierarchy.},
  language  = {en}
}