@article{MehrniaBalazadehZanoretal.2013,
  author    = {Mehrnia, Mohammad and Balazadeh, Salma and Zanor, Maria-Ines and M{\"u}ller-R{\"o}ber, Bernd},
  title     = {EBE, an AP2/ERF transcription factor highly expressed in proliferating cells, affects shoot architecture in arabidopsis},
  series = {Plant physiology : an international journal devoted to physiology, biochemistry, cellular and molecular biology, biophysics and environmental biology of plants},
  volume    = {162},
  journal   = {Plant physiology : an international journal devoted to physiology, biochemistry, cellular and molecular biology, biophysics and environmental biology of plants},
  number    = {2},
  publisher = {American Society of Plant Physiologists},
  address   = {Rockville},
  issn      = {0032-0889},
  doi       = {10.1104/pp.113.214049},
  pages     = {842 -- 857},
  year      = {2013},
  abstract  = {We report about ERF BUD ENHANCER (EBE; At5g61890), a transcription factor that affects cell proliferation as well as axillary bud outgrowth and shoot branching in Arabidopsis (Arabidopsis thaliana). EBE encodes a member of the APETALA2/ETHYLENE RESPONSE FACTOR (AP2/ERF) transcription factor superfamily; the gene is strongly expressed in proliferating cells and is rapidly and transiently up-regulated in axillary meristems upon main stem decapitation. Overexpression of EBE promotes cell proliferation in growing calli, while the opposite is observed in EBE-RNAi lines. EBE overexpression also stimulates axillary bud formation and outgrowth, while repressing it results in inhibition of bud growth. Global transcriptome analysis of estradiol-inducible EBE overexpression lines revealed 48 EBE early-responsive genes, of which 14 were up-regulated and 34 were downregulated. EBE activates several genes involved in cell cycle regulation and dormancy breaking, including D-type cyclin CYCD3; 3, transcription regulator DPa, and BRCA1-ASSOCIATED RING DOMAIN1. Among the down-regulated genes were DORMANCY-ASSOCIATED PROTEIN1 (AtDRM1), AtDRM1 homolog, MEDIATOR OF ABA-REGULATED DORMANCY1, and ZINC FINGER HOMEODOMAIN5. Our data indicate that the effect of EBE on shoot branching likely results from an activation of genes involved in cell cycle regulation and dormancy breaking.},
  language  = {en}
}
@article{RaufArifDortayetal.2013,
  author    = {Rauf, Mamoona and Arif, Muhammad and Dortay, Hakan and Matallana-Ramirez, Lilian P. and Waters, Mark T. and Nam, Hong Gil and Lim, Pyung-Ok and M{\"u}ller-R{\"o}ber, Bernd and Balazadeh, Salma},
  title     = {ORE1 balances leaf senescence against maintenance by antagonizing G2-like-mediated transcription},
  series = {EMBO reports},
  volume    = {14},
  journal   = {EMBO reports},
  number    = {4},
  publisher = {Nature Publ. Group},
  address   = {London},
  issn      = {1469-221X},
  doi       = {10.1038/embor.2013.24},
  pages     = {382 -- 388},
  year      = {2013},
  abstract  = {Leaf senescence is a key physiological process in all plants. Its onset is tightly controlled by transcription factors, of which NAC factor ORE1 (ANAC092) is crucial in Arabidopsis thaliana. Enhanced expression of ORE1 triggers early senescence by controlling a downstream gene network that includes various senescence-associated genes. Here, we report that unexpectedly ORE1 interacts with the G2-like transcription factors GLK1 and GLK2, which are important for chloroplast development and maintenance, and thereby for leaf maintenance. ORE1 antagonizes GLK transcriptional activity, shifting the balance from chloroplast maintenance towards deterioration. Our finding identifies a new mechanism important for the control of senescence by ORE1.},
  language  = {en}
}
@article{AlluSojaWuetal.2014,
  author    = {Allu, Annapurna Devi and Soja, Aleksandra Maria and Wu, Anhui and Szymanski, Jedrzej and Balazadeh, Salma},
  title     = {Salt stress and senescence: identification of cross-talk regulatory components},
  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/eru173},
  pages     = {3993 -- 4008},
  year      = {2014},
  abstract  = {Leaf senescence is an active process with a pivotal impact on plant productivity. It results from extensive signalling cross-talk coordinating environmental factors with intrinsic age-related mechanisms. Although many studies have shown that leaf senescence is affected by a range of external parameters, knowledge about the regulatory systems that govern the interplay between developmental programmes and environmental stress is still vague. Salinity is one of the most important environmental stresses that promote leaf senescence and thus affect crop yield. Improving salt tolerance by avoiding or delaying senescence under stress will therefore play an important role in maintaining high agricultural productivity. Experimental evidence suggests that hydrogen peroxide (H2O2) functions as a common signalling molecule in both developmental and salt-induced leaf senescence. In this study, microarray-based gene expression profiling on Arabidopsis thaliana plants subjected to long-term salinity stress to induce leaf senescence was performed, together with co-expression network analysis for H2O2-responsive genes that are mutually up-regulated by salt induced-and developmental leaf senescence. Promoter analysis of tightly co-expressed genes led to the identification of seven cis-regulatory motifs, three of which were known previously, namely CACGTGT and AAGTCAA, which are associated with reactive oxygen species (ROS)-responsive genes, and CCGCGT, described as a stress-responsive regulatory motif, while the others, namely ACGCGGT, AGCMGNC, GMCACGT, and TCSTYGACG were not characterized previously. These motifs are proposed to be novel elements involved in the H2O2-mediated control of gene expression during salinity stress-triggered and developmental senescence, acting through upstream transcription factors that bind to these sites.},
  language  = {en}
}
@article{MuellerRoeberBalazadeh2014,
  author    = {M{\"u}ller-R{\"o}ber, Bernd and Balazadeh, Salma},
  title     = {Auxin and its role in plant senescence},
  series = {Journal of plant growth regulation},
  volume    = {33},
  journal   = {Journal of plant growth regulation},
  number    = {1},
  publisher = {Springer},
  address   = {New York},
  issn      = {0721-7595},
  doi       = {10.1007/s00344-013-9398-5},
  pages     = {21 -- 33},
  year      = {2014},
  abstract  = {Leaf senescence represents a key developmental process through which resources trapped in the photosynthetic organ are degraded in an organized manner and transported away to sustain the growth of other organs including newly forming leaves, roots, seeds, and fruits. The optimal timing of the initiation and progression of senescence are thus prerequisites for controlled plant growth, biomass accumulation, and evolutionary success through seed dispersal. Recent research has uncovered a multitude of regulatory factors including transcription factors, micro-RNAs, protein kinases, and others that constitute the molecular networks that regulate senescence in plants. The timing of senescence is affected by environmental conditions and abiotic or biotic stresses typically trigger a faster senescence. Various phytohormones, including for example ethylene, abscisic acid, and salicylic acid, promote senescence, whereas cytokinins delay it. Recently, several reports have indicated an involvement of auxin in the control of senescence, however, its mode of action and point of interference with senescence control mechanisms remain vaguely defined at present and contrasting observations regarding the effect of auxin on senescence have so far hindered the establishment of a coherent model. Here, we summarize recent studies on auxin-related genes that affect senescence in plants and highlight how these findings might be integrated into current molecular-regulatory models of senescence.},
  language  = {en}
}
@unpublished{Balazadeh2014,
  author    = {Balazadeh, Salma},
  title     = {Stay-green not always stays green},
  series = {Molecular plant},
  volume    = {7},
  journal   = {Molecular plant},
  number    = {8},
  publisher = {Cell Press},
  address   = {Cambridge},
  issn      = {1674-2052},
  doi       = {10.1093/mp/ssu076},
  pages     = {1264 -- 1266},
  year      = {2014},
  language  = {en}
}
@misc{MachensBalazadehMuellerRoeberetal.2017,
  author    = {Machens, Fabian and Balazadeh, Salma and M{\"u}ller-R{\"o}ber, Bernd and Messerschmidt, Katrin},
  title     = {Synthetic Promoters and Transcription Factors for Heterologous Protein Expression in Saccharomyces cerevisiae},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-403804},
  pages     = {11},
  year      = {2017},
  abstract  = {Orthogonal systems for heterologous protein expression as well as for the engineering of synthetic gene regulatory circuits in hosts like Saccharomyces cerevisiae depend on synthetic transcription factors (synTFs) and corresponding cis-regulatory binding sites. We have constructed and characterized a set of synTFs based on either transcription activator-like effectors or CRISPR/Cas9, and corresponding small synthetic promoters (synPs) with minimal sequence identity to the host's endogenous promoters. The resulting collection of functional synTF/synP pairs confers very low background expression under uninduced conditions, while expression output upon induction of the various synTFs covers a wide range and reaches induction factors of up to 400. The broad spectrum of expression strengths that is achieved will be useful for various experimental setups, e.g., the transcriptional balancing of expression levels within heterologous pathways or the construction of artificial regulatory networks. Furthermore, our analyses reveal simple rules that enable the tuning of synTF expression output, thereby allowing easy modification of a given synTF/synP pair. This will make it easier for researchers to construct tailored transcriptional control systems.},
  language  = {en}
}
@article{MachensBalazadehMuellerRoeberetal.2017,
  author    = {Machens, Fabian and Balazadeh, Salma and M{\"u}ller-R{\"o}ber, Bernd and Messerschmidt, Katrin},
  title     = {Synthetic Promoters and Transcription Factors for Heterologous Protein Expression in Saccharomyces cerevisiae},
  series = {Frontiers in Bioengineering and Biotechnology},
  volume    = {5},
  journal   = {Frontiers in Bioengineering and Biotechnology},
  publisher = {Frontiers},
  address   = {Lausanne},
  issn      = {2296-4185},
  doi       = {10.3389/fbioe.2017.00063},
  pages     = {1 -- 11},
  year      = {2017},
  abstract  = {Orthogonal systems for heterologous protein expression as well as for the engineering of synthetic gene regulatory circuits in hosts like Saccharomyces cerevisiae depend on synthetic transcription factors (synTFs) and corresponding cis-regulatory binding sites. We have constructed and characterized a set of synTFs based on either transcription activator-like effectors or CRISPR/Cas9, and corresponding small synthetic promoters (synPs) with minimal sequence identity to the host's endogenous promoters. The resulting collection of functional synTF/synP pairs confers very low background expression under uninduced conditions, while expression output upon induction of the various synTFs covers a wide range and reaches induction factors of up to 400. The broad spectrum of expression strengths that is achieved will be useful for various experimental setups, e.g., the transcriptional balancing of expression levels within heterologous pathways or the construction of artificial regulatory networks. Furthermore, our analyses reveal simple rules that enable the tuning of synTF expression output, thereby allowing easy modification of a given synTF/synP pair. This will make it easier for researchers to construct tailored transcriptional control systems.},
  language  = {en}
}
@article{EbrahimianMotlaghRiboneThirumalaikumaretal.2017,
  author    = {Ebrahimian-Motlagh, Saghar and Ribone, Pamela A. and Thirumalaikumar, Venkatesh P. and Allu, Annapurna Devi and Chan, Raquel L. and Mueller-Roeber, Bernd and Balazadeh, Salma},
  title     = {JUNGBRUNNEN1 Confers Drought Tolerance Downstream of the HD-Zip I Transcription Factor AtHB13},
  series = {Frontiers in plant science},
  volume    = {8},
  journal   = {Frontiers in plant science},
  publisher = {Frontiers Research Foundation},
  address   = {Lausanne},
  issn      = {1664-462X},
  doi       = {10.3389/fpls.2017.02118},
  pages     = {12},
  year      = {2017},
  abstract  = {Low water availability is the major environmental factor limiting growth and productivity of plants and crops and is therefore considered of high importance for agriculture affected by climate change. Identifying regulatory components controlling the response and tolerance to drought stress is thus of major importance. The NAC transcription factor (TF) JUNGBRUNNEN1 (JUB1) from Arabidopsis thaliana extends leaf longevity under non-stress growth conditions, lowers cellular hydrogen peroxide (H2O2) level, and enhances tolerance against heat stress and salinity. Here, we additionally find that JUB1 strongly increases tolerance to drought stress in Arabidopsis when expressed from both, a constitutive (CaMV 35S) and an abiotic stress-induced (RD29A) promoter. Employing a yeast one-hybrid screen we identified HD-Zip class I TF AtHB13 as an upstream regulator of JUB1. AtHB13 has previously been reported to act as a positive regulator of drought tolerance. AtHB13 and JUB1 thereby establish a joint drought stress control module.},
  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}
}
@article{SedaghatmehrMuellerRoeberBalazadeh2016,
  author    = {Sedaghatmehr, Mastoureh and M{\"u}ller-R{\"o}ber, Bernd and Balazadeh, Salma},
  title     = {The plastid metalloprotease FtsH6 and small heat shock protein HSP21 jointly regulate thermomemory in Arabidopsis},
  series = {Nature Communications},
  volume    = {7},
  journal   = {Nature Communications},
  publisher = {Nature Publ. Group},
  address   = {London},
  issn      = {2041-1723},
  doi       = {10.1038/ncomms12439},
  pages     = {14},
  year      = {2016},
  abstract  = {Acquired tolerance to heat stress is an increased resistance to elevated temperature following a prior exposure to heat. The maintenance of acquired thermotolerance in the absence of intervening stress is called 'thermomemory' but the mechanistic basis for this memory is not well defined. Here we show that Arabidopsis HSP21, a plastidial small heat shock protein that rapidly accumulates after heat stress and remains abundant during the thermomemory phase, is a crucial component of thermomemory. Sustained memory requires that HSP21 levels remain high. Through pharmacological interrogation and transcriptome profiling, we show that the plastid-localized metalloprotease FtsH6 regulates HSP21 abundance. Lack of a functional FtsH6 protein promotes HSP21 accumulation during the later stages of thermomemory and increases thermomemory capacity. Our results thus reveal the presence of a plastidial FtsH6-HSP21 control module for thermomemory in plants.},
  language  = {en}
}