Phytohormones are not only instrumental in regulating developmental processes in plants but also play important roles for the plant's responses to biotic and abiotic stresses. In particular, abscisic acid, ethylene, jasmonic acid, and salicylic acid have been shown to possess crucial functions in mediating or orchestrating stress responses in plants. Here, we review the role of salicylic acid and jasmonic acid in pathogen defence responses with special emphasis on their function in the solanaceous plant potato.

A change regarding the extent of adhesion − hereafter referred to as adhesion plasticity − between adhesive and less-adhesive states of mammalian cells is important for their behavior. To investigate adhesion plasticity, we have selected a stable isogenic subpopulation of human MDA-MB-468 breast carcinoma cells growing in suspension. These suspension cells are unable to re-adhere to various matrices or to contract three-dimensional collagen lattices. By using transcriptome analysis, we identified the focal adhesion protein tensin3 (Tns3) as a determinant of adhesion plasticity. Tns3 is strongly reduced at mRNA and protein levels in suspension cells. Furthermore, by transiently challenging breast cancer cells to grow under non-adherent conditions markedly reduces Tns3 protein expression, which is regained upon re-adhesion. Stable knockdown of Tns3 in parental MDA-MB-468 cells results in defective adhesion, spreading and migration. Tns3-knockdown cells display impaired structure and dynamics of focal adhesion complexes as determined by immunostaining. Restoration of Tns3 protein expression in suspension cells partially rescues adhesion and focal contact composition. Our work identifies Tns3 as a crucial focal adhesion component regulated by, and functionally contributing to, the switch between adhesive and non-adhesive states in MDA-MB-468 cancer cells.

The tapetal major facilitator NPF2.8 is required for accumulation of flavonol glycosides on the pollen surface of Arabidopsis thaliana.

27 The formation and accumulation of methylglyoxal (MGO) is associated with age-related 28 diseases such as diabetes, cancer and neurodegenerative disorders. MGO is the major 29 precursor of non-enzymatic glycation of macromolecules affecting their function and 30 structure. We now show for the first time that MGO stress not only led to cellular aging 31 responses like DNA double-strand breaks indicated by an accumulation of γH2AX in the 32 nucleus. We also observed an immediate increase of Ser15 phosphorylated p53 in the nucleus 33 of MGO treated cell lines which will change the cellular expression pattern with adverse 34 effects on the cell cycle and other cellular functions not necessarily related to aging. Introduction36 The formation and accumulation of methylglyoxal (MGO), the most potent glycating agent in 37 humans, is associated with age-related diseases such as diabetes, obesity, atherosclerosis, 38 cancer and neurodegenerative disorders [1]. Methylglyoxal is mainly formed by the non-39 enzymatic degradation of triose phosphates, glyceraldehyde-3-phosphate (G3P) and 40 dihydroxyacetone-phosphate (DHAP), as a byproduct of glycolysis. It takes place in all cells 41 and organisms. [2, 3]. The actual concentration of MGO in the cell depends on several factors 42 like the rate of detoxification by glyoxalases, the phosphate pool of the cell and the rate of 43 influx of carbon sources [4]. 44 MGO is the major precursor of non-enzymatic glycation of proteins, lipids and DNA, 45 subsequently leading to the formation of a heterogeneous group of molecules, collectively 46 called AGEs (advanced glycation endproducts) [1, 3, 5]. The glycation reactions can cause 3 47 the formation of complexes and irreversible adducts of these macromolecules affecting their 48 function and structure. Accumulation of AGEs compromises cellular processes resulting in 49 mitochondrial dysfunction, genomic instability, loss of proteostasis, inflammaging and 50 cellular senescence [6]. Moreover, other studies revealed that elevated MGO levels may also 51 have beneficial effects in cancer and lifespan [7, 8]. 52 Tumor cells differ from non-tumor cells concerning their high glycolytic rates under 53 anaerobic conditions (Warburg effect). This inefficient energy production, cause a high rate 54 of glucose uptake and glycolysis in tumors resulting in elevated MGO levels [9]. Loarca et al. 55 reported that treatment of hepatocellular carcinoma (HCC) cell lines with MGO promote the 56 localization of p53 into the nucleus whereas total cellular p53 levels are not altered [10]. p5357 is a well-known tumor suppressor that is mutated in many tumor cells [11]. It functions as a 58 transcription factor, which is involved in the regulation of the cell cycle, DNA repair and 59 apoptosis. Upon cellular stress such as DNA damage, hypoxia or viral infection p53 is 60 activated and stabilized by different post-translational modifications interfering with its 61 degradation [12]. It was shown that DNA damage induces phosphorylation of p53 on Ser15 62 [13]....

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