@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}
}
@article{AlluBrotmanXueetal.2016,
  author    = {Allu, Annapurna Devi and Brotman, Yariv and Xue, Gang-Ping and Balazadeh, Salma},
  title     = {Transcription factor ANAC032 modulates JA/SA signalling in response to Pseudomonas syringae infection},
  series = {EMBO reports},
  volume    = {17},
  journal   = {EMBO reports},
  publisher = {Wiley-Blackwell},
  address   = {Hoboken},
  issn      = {1469-221X},
  doi       = {10.15252/embr.201642197},
  pages     = {1578 -- 1589},
  year      = {2016},
  abstract  = {Responses to pathogens, including host transcriptional reprogramming, require partially antagonistic signalling pathways dependent on the phytohormones salicylic (SA) and jasmonic (JA) acids. However, upstream factors modulating the interplay of these pathways are not well characterized. Here, we identify the transcription factor ANAC032 from Arabidopsis thaliana as one such regulator in response to the bacterial pathogen Pseudomonas syringae pv. tomato DC3000 (Pst). ANAC032 directly represses MYC2 activation upon Pst attack, resulting in blockage of coronatine-mediated stomatal reopening which restricts entry of bacteria into plant tissue. Furthermore, ANAC032 activates SA signalling by repressing NIMIN1, a key negative regulator of SA-dependent defence. Finally, ANAC032 reduces expression of JA-responsive genes, including PDF1.2A. Thus, ANAC032 enhances resistance to Pst by generating an orchestrated transcriptional output towards key SA- and JA-signalling genes coordinated through direct binding of ANAC032 to the MYC2, NIMIN1 and PDF1.2A promoters.},
  language  = {en}
}