@article{ShubchynskyyBonieckaSchweighoferetal.2017,
  author    = {Shubchynskyy, Volodymyr and Boniecka, Justyna and Schweighofer, Alois and Simulis, Justinas and Kvederaviciute, Kotryna and Stumpe, Michael and Mauch, Felix and Balazadeh, Salma and M{\"u}ller-R{\"o}ber, Bernd and Boutrot, Freddy and Zipfel, Cyril and Meskiene, Irute},
  title     = {Protein phosphatase AP2C1 negatively regulates basal resistance and defense responses to Pseudomonas syringae},
  series = {Journal of experimental botany},
  volume    = {68},
  journal   = {Journal of experimental botany},
  number    = {5},
  publisher = {Oxford Univ. Press},
  address   = {Oxford},
  issn      = {0022-0957},
  doi       = {10.1093/jxb/erw485},
  pages     = {1169 -- 1183},
  year      = {2017},
  abstract  = {Mitogen-activated protein kinases (MAPKs) mediate plant immune responses to pathogenic bacteria. However, less is known about the cell autonomous negative regulatory mechanism controlling basal plant immunity. We report the biological role of Arabidopsis thaliana MAPK phosphatase AP2C1 as a negative regulator of plant basal resistance and defense responses to Pseudomonas syringae. AP2C2, a closely related MAPK phosphatase, also negatively controls plant resistance. Loss of AP2C1 leads to enhanced pathogen-induced MAPK activities, increased callose deposition in response to pathogen-associated molecular patterns or to P. syringae pv. tomato (Pto) DC3000, and enhanced resistance to bacterial infection with Pto. We also reveal the impact of AP2C1 on the global transcriptional reprogramming of transcription factors during Pto infection. Importantly, ap2c1 plants show salicylic acid-independent transcriptional reprogramming of several defense genes and enhanced ethylene production in response to Pto. This study pinpoints the specificity of MAPK regulation by the different MAPK phosphatases AP2C1 and MKP1, which control the same MAPK substrates, nevertheless leading to different downstream events. We suggest that precise and specific control of defined MAPKs by MAPK phosphatases during plant challenge with pathogenic bacteria can strongly influence plant resistance.},
  language  = {en}
}
@article{ShahnejatBushehriNobmannAlluetal.2016,
  author    = {Shahnejat-Bushehri, Sara and Nobmann, Barbara and Allu, Annapurna Devi and Balazadeh, Salma},
  title     = {JUB1 suppresses Pseudomonas syringae-induced defense responses through accumulation of DELLA proteins},
  series = {Journal of trace elements in medicine and biology},
  volume    = {11},
  journal   = {Journal of trace elements in medicine and biology},
  publisher = {Elsevier},
  address   = {Philadelphia},
  issn      = {1559-2316},
  doi       = {10.1080/15592324.2016.1181245},
  pages     = {7},
  year      = {2016},
  abstract  = {Phytohormones act in concert to coordinate plant growth and the response to environmental cues. Gibberellins (GAs) are growth-promoting hormones that recently emerged as modulators of plant immune signaling. By regulating the stability of DELLA proteins, GAs intersect with the signaling pathways of the classical primary defense hormones, salicylic acid (SA) and jasmonic acid (JA), thereby altering the final outcome of the immune response. DELLA proteins confer resistance to necrotrophic pathogens by potentiating JA signaling and raise the susceptibility to biotrophic pathogens by attenuating the SA pathway. Here, we show that JUB1, a core element of the GA - brassinosteroid (BR) - DELLA regulatory module, functions as a negative regulator of defense responses against Pseudomonas syringae pv. tomato DC3000 (Pst DC3000) and mediates the crosstalk between growth and immunity.},
  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}
}