@article{SedaghatmehrThirumalaikumarKamranfaretal.2019,
  author    = {Sedaghatmehr, Mastoureh and Thirumalaikumar, Venkatesh P. and Kamranfar, Iman and Marmagne, Anne and Masclaux-Daubresse, Celine and Balazadeh, Salma},
  title     = {A regulatory role of autophagy for resetting the memory of heat stress in plants},
  series = {Plant, cell \& environment : cell physiology, whole-plant physiology, community physiology},
  volume    = {42},
  journal   = {Plant, cell \& environment : cell physiology, whole-plant physiology, community physiology},
  number    = {3},
  publisher = {Wiley},
  address   = {Hoboken},
  issn      = {0140-7791},
  doi       = {10.1111/pce.13426},
  pages     = {1054 -- 1064},
  year      = {2019},
  abstract  = {As sessile life forms, plants are repeatedly confronted with adverse environmental conditions, which can impair development, growth, and reproduction. During evolution, plants have established mechanisms to orchestrate the delicate balance between growth and stress tolerance, to reset cellular biochemistry once stress vanishes, or to keep a molecular memory, which enables survival of a harsher stress that may arise later. Although there are several examples of memory in diverse plants species, the molecular machinery underlying the formation, duration, and resetting of stress memories is largely unknown so far. We report here that autophagy, a central self-degradative process, assists in resetting cellular memory of heat stress (HS) in Arabidopsis thaliana. Autophagy is induced by thermopriming (moderate HS) and, intriguingly, remains high long after stress termination. We demonstrate that autophagy mediates the specific degradation of heat shock proteins at later stages of the thermorecovery phase leading to the accumulation of protein aggregates after the second HS and a compromised heat tolerance. Autophagy mutants retain heat shock proteins longer than wild type and concomitantly display improved thermomemory. Our findings reveal a novel regulatory mechanism for HS memory in plants.},
  language  = {en}
}
@article{NaseriBalazadehMachensetal.2017,
  author    = {Naseri, Gita and Balazadeh, Salma and Machens, Fabian and Kamranfar, Iman and Messerschmidt, Katrin and M{\"u}ller-R{\"o}ber, Bernd},
  title     = {Plant-Derived Transcription Factors for Orthologous Regulation of Gene Expression in the Yeast Saccharomyces cerevisiae},
  series = {ACS synthetic biology},
  volume    = {6},
  journal   = {ACS synthetic biology},
  publisher = {American Chemical Society},
  address   = {Washington},
  issn      = {2161-5063},
  doi       = {10.1021/acssynbio.7b00094},
  pages     = {1742 -- 1756},
  year      = {2017},
  abstract  = {Control of gene expression by transcription factors (TFs) is central in many synthetic biology projects for which a tailored expression of one or multiple genes is often needed. As TFs from evolutionary distant organisms are unlikely to affect gene expression in a host of choice, they represent excellent candidates for establishing orthogonal control systems. To establish orthogonal regulators for use in yeast (Saccharomyces cerevisiae), we chose TFs from the plant Arabidopsis thaliana. We established a library of 106 different combinations of chromosomally integrated TFs, activation domains (yeast GAL4 AD, herpes simplex virus VP64, and plant EDLL) and synthetic promoters harboring cognate cis regulatory motifs driving a yEGFP reporter. Transcriptional output of the different driver/reporter combinations varied over a wide spectrum, with EDLL being a considerably stronger transcription activation domain in yeast than the GAL4 activation domain, in particular when fused to Arabidopsis NAC TFs. Notably, the strength of several NAC-EDLL fusions exceeded that of the strong yeast TDH3 promoter by 6- to 10-fold. We furthermore show that plant TFs can be used to build regulatory systems encoded by centromeric or episomal plasmids. Our library of TF-DNA binding site combinations offers an excellent tool for diverse synthetic biology applications in yeast.},
  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}
}
@phdthesis{Kamranfar2015,
  author    = {Kamranfar, Iman},
  title     = {Functional analysis of gene regulatory networks controlled by stress responsive transcription factors in Arabidopsis thaliana},
  school      = {Universit{\"a}t Potsdam},
  pages     = {151},
  year      = {2015},
  language  = {en}
}