@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}
}
@article{FrancoObregonCambriaGreutertetal.2018,
  author    = {Franco-Obregon, Alfredo and Cambria, Elena and Greutert, Helen and Wernas, Timon and Hitzl, Wolfgang and Egli, Marcel and Sekiguchi, Miho and Boos, Norbert and Hausmann, Oliver and Ferguson, Stephen J. and Kobayashi, Hiroshi and W{\"u}rtz-Kozak, Karin},
  title     = {TRPC6 in simulated microgravity of intervertebral disc cells},
  series = {European Spine Journal},
  volume    = {27},
  journal   = {European Spine Journal},
  number    = {10},
  publisher = {Springer},
  address   = {New York},
  issn      = {0940-6719},
  doi       = {10.1007/s00586-018-5688-8},
  pages     = {2621 -- 2630},
  year      = {2018},
  abstract  = {Purpose Prolonged bed rest and microgravity in space cause intervertebral disc (IVD) degeneration. However, the underlying molecular mechanisms are not completely understood. Transient receptor potential canonical (TRPC) channels are implicated in mechanosensing of several tissues, but are poorly explored in IVDs. Methods Primary human IVD cells from surgical biopsies composed of both annulus fibrosus and nucleus pulposus (passage 1-2) were exposed to simulated microgravity and to the TRPC channel inhibitor SKF-96365 (SKF) for up to 5days. Proliferative capacity, cell cycle distribution, senescence and TRPC channel expression were analyzed. Results Both simulated microgravity and TRPC channel antagonism reduced the proliferative capacity of IVD cells and induced senescence. While significant changes in cell cycle distributions (reduction in G1 and accumulation in G2/M) were observed upon SKF treatment, the effect was small upon 3days of simulated microgravity. Finally, downregulation of TRPC6 was shown under simulated microgravity. Conclusions Simulated microgravity and TRPC channel inhibition both led to reduced proliferation and increased senescence. Furthermore, simulated microgravity reduced TRPC6 expression. IVD cell senescence and mechanotransduction may hence potentially be regulated by TRPC6 expression. This study thus reveals promising targets for future studies.},
  language  = {en}
}
@article{WatanabeTohgeBalazadehetal.2018,
  author    = {Watanabe, Mutsumi and Tohge, Takayuki and Balazadeh, Salma and Erban, Alexander and Giavalisco, Patrick and Kopka, Joachim and Mueller-Roeber, Bernd and Fernie, Alisdair R. and Hoefgen, Rainer},
  title     = {Comprehensive Metabolomics Studies of Plant Developmental Senescence},
  series = {Plant Senescence: Methods and Protocols},
  volume    = {1744},
  journal   = {Plant Senescence: Methods and Protocols},
  publisher = {Humana Press},
  address   = {Totowa},
  isbn      = {978-1-4939-7672-0},
  issn      = {1064-3745},
  doi       = {10.1007/978-1-4939-7672-0_28},
  pages     = {339 -- 358},
  year      = {2018},
  abstract  = {Leaf senescence is an essential developmental process that involves diverse metabolic changes associated with degradation of macromolecules allowing nutrient recycling and remobilization. In contrast to the significant progress in transcriptomic analysis of leaf senescence, metabolomics analyses have been relatively limited. A broad overview of metabolic changes during leaf senescence including the interactions between various metabolic pathways is required to gain a better understanding of the leaf senescence allowing to link transcriptomics with metabolomics and physiology. In this chapter, we describe how to obtain comprehensive metabolite profiles and how to dissect metabolic shifts during leaf senescence in the model plant Arabidopsis thaliana. Unlike nucleic acid analysis for transcriptomics, a comprehensive metabolite profile can only be achieved by combining a suite of analytic tools. Here, information is provided for measurements of the contents of chlorophyll, soluble proteins, and starch by spectrophotometric methods, ions by ion chromatography, thiols and amino acids by HPLC, primary metabolites by GC/TOF-MS, and secondary metabolites and lipophilic metabolites by LC/ESI-MS. These metabolite profiles provide a rich catalogue of metabolic changes during leaf senescence, which is a helpful database and blueprint to be correlated to future studies such as transcriptome and proteome analyses, forward and reverse genetic studies, or stress-induced senescence studies.},
  language  = {en}
}