The role of potassium in quality of grapes after harvest

Author(s):  
Amnon Lichter ◽  
David Obenland ◽  
Nirit Bernstein ◽  
Jennifer Hashim ◽  
Joseph Smilanick

Objectives: The objectives of the proposal were to study how potassium (K) enters the berry and in what tissues it accumulates, to determine what is the sensitive phenological stage that is responsive to K, to study the influence of K on sugar translocation, to determine if K has effects on expression of genes in source and sink organs and to study applied aspects of the responses to K at the vineyard level. During the research it was realized that K acts externally so a major part of the original objectives had to be deserted and new ones, i.e. the role of K in enhancing water loss from the berry, had to be developed. In addition, the US partners developed practical objectives of understanding the interaction of K application and water deficit as well as application of growth regulators. Background: In our preliminary data we showed that application of K at mid-ripening enhanced sugar accumulation of table grapes. This finding is of major implications to both early and late harvested grapes and it was essential to understand the mode of action of this treatment. Our major hypothesis was that K enters the berry and by that increases sugar translocation into the berry. In addition it was important to cover practical issues of the application which may influence its efficacy and its reproducibility. Conclusions: The major conclusion from the research was that our initial hypothesis was wrong. Mineral analysis of pulp tissue indicated that upon application of K there was a significant increase in most of the major minerals. Subsequently, we developed a new hypothesis that K acts by increasing the water loss from the berry. In vitro studies of K-treated berries corroborated this hypothesis showing greater weight-loss of treated berries. This was not necessarily expressed in the vineyard as in some experiments berry weight remained unchanged, suggesting that the vine compensated for the enhanced water loss. Importantly, we also discovered that the efficacy of different K salts was strongly correlated to the pH of the salt solution: basic K salts had better efficacy than neutral or acidic salts and modifying the pH of the same salt changed its efficacy. It was therefore suggested that K changes the properties of the cuticle making it more susceptible to water loss. Of the practical aspects it was found that application of K to the clusters was sufficient to trigger its affect and that dual application of K had a stronger effect than single application. With regard to timing, it was realized that application of K after veraison was affective and the berries responded also when ripe. While the effect of K application was significant at harvest, it was mostly insignificant one week after application, suggesting that prolonged exposure to K was required. Implications: The scientific implications of the study are that the external mineral composition of the berry may have a significant role in sugar accumulation and that water loss may have an important role in sugar accumulation in grapes. It is not entirely clear how K modulates the cuticle but according to the literature its incorporation into the cuticle may increase its polarity and facilitate generation of "water bridges" between the flesh and the environment. The practical implications of this study are very significant because realizing the mode of action of K can facilitate a much more efficient application strategy. For example, it can be understood that sprays must be directed to the clusters rather than the whole vines and it can be predicted that the length of exposure is important. Also, by increasing the pH of simple K salts, the efficacy of the treatment can be enhanced, saving in the costs of the treatment. Finally, the ability of grape growers to apply K in a safe and knowledgeable way can have significant impact on the length of the season of early grape cultivars and improve the flavor of high grape yields which may otherwise have compromised sugar levels.

Diabetologia ◽  
2021 ◽  
Author(s):  
Yukina Takeichi ◽  
Takashi Miyazawa ◽  
Shohei Sakamoto ◽  
Yuki Hanada ◽  
Lixiang Wang ◽  
...  

Abstract Aims/hypothesis Mitochondria are highly dynamic organelles continuously undergoing fission and fusion, referred to as mitochondrial dynamics, to adapt to nutritional demands. Evidence suggests that impaired mitochondrial dynamics leads to metabolic abnormalities such as non-alcoholic steatohepatitis (NASH) phenotypes. However, how mitochondrial dynamics are involved in the development of NASH is poorly understood. This study aimed to elucidate the role of mitochondrial fission factor (MFF) in the development of NASH. Methods We created mice with hepatocyte-specific deletion of MFF (MffLiKO). MffLiKO mice fed normal chow diet (NCD) or high-fat diet (HFD) were evaluated for metabolic variables and their livers were examined by histological analysis. To elucidate the mechanism of development of NASH, we examined the expression of genes related to endoplasmic reticulum (ER) stress and lipid metabolism, and the secretion of triacylglycerol (TG) using the liver and primary hepatocytes isolated from MffLiKO and control mice. Results MffLiKO mice showed aberrant mitochondrial morphologies with no obvious NASH phenotypes during NCD, while they developed full-blown NASH phenotypes in response to HFD. Expression of genes related to ER stress was markedly upregulated in the liver from MffLiKO mice. In addition, expression of genes related to hepatic TG secretion was downregulated, with reduced hepatic TG secretion in MffLiKO mice in vivo and in primary cultures of MFF-deficient hepatocytes in vitro. Furthermore, thapsigargin-induced ER stress suppressed TG secretion in primary hepatocytes isolated from control mice. Conclusions/interpretation We demonstrated that ablation of MFF in liver provoked ER stress and reduced hepatic TG secretion in vivo and in vitro. Moreover, MffLiKO mice were more susceptible to HFD-induced NASH phenotype than control mice, partly because of ER stress-induced apoptosis of hepatocytes and suppression of TG secretion from hepatocytes. This study provides evidence for the role of mitochondrial fission in the development of NASH. Graphical abstract


2020 ◽  
Vol 21 (7) ◽  
pp. 2549 ◽  
Author(s):  
Asghar Ali ◽  
Mark Stenglein ◽  
Thomas Spencer ◽  
Gerrit Bouma ◽  
Russell Anthony ◽  
...  

LIN28 inhibits let-7 miRNA maturation which prevents cell differentiation and promotes proliferation. We hypothesized that the LIN28-let-7 axis regulates proliferation-associated genes in sheep trophectoderm in vivo. Day 9-hatched sheep blastocysts were incubated with lentiviral particles to deliver shRNA targeting LIN28 specifically to trophectoderm cells. At day 16, conceptus elongation was significantly reduced in LIN28A and LIN28B knockdowns. Let-7 miRNAs were significantly increased and IGF2BP1-3, HMGA1, ARID3B, and c-MYC were decreased in trophectoderm from knockdown conceptuses. Ovine trophoblast (OTR) cells derived from day 16 trophectoderm are a useful tool for in vitro experiments. Surprisingly, LIN28 was significantly reduced and let-7 miRNAs increased after only a few passages of OTR cells, suggesting these passaged cells represent a more differentiated phenotype. To create an OTR cell line more similar to day 16 trophectoderm we overexpressed LIN28A and LIN28B, which significantly decreased let-7 miRNAs and increased IGF2BP1-3, HMGA1, ARID3B, and c-MYC compared to control. This is the first study showing the role of the LIN28-let-7 axis in trophoblast proliferation and conceptus elongation in vivo. These results suggest that reduced LIN28 during early placental development can lead to reduced trophoblast proliferation and sheep conceptus elongation at a critical period for successful establishment of pregnancy.


2017 ◽  
Vol 43 (3) ◽  
pp. 1090-1099 ◽  
Author(s):  
Zhonghua Jiang ◽  
Tingting Yu ◽  
Zhining Fan ◽  
Hongmei Yang ◽  
Xin Lin

Background/Aims: Krüppel-like factor (KLF) 7 protein is a member of the KLF transcription factor family, which plays important roles in regulating the expression of genes involved in cell growth, proliferation, differentiation and metabolism. However, the role of KLF7 in gastric cancer (GC) is unknown. The aim of this study is to explore the role of KLF7 in GC and its correlation with clinicopathological characteristics and prognosis of GC patients. Methods: We first systematically evaluated dysregulation of the KLF family in The Cancer Genome Atlas (TCGA) GC database. Then, 252 patients who underwent surgery for GC were enrolled to validate the results from the TCGA. Functional studies were also used to explore the role of KLF7 in GC. Results: In the TCGA database, we found that KLF7 was an independent predictor for survival by both univariate and multivariate analysis (P<0.05). In a validation cohort, KLF7 expression was significantly increased in GC tissues compared with adjacent normal controls (P=0.013). High KLF7 expression correlated with inferior prognostic factors, such as T stage (P=0.022), N stage (P =0.005) and lymphovascular invasion (P=0.009). Furthermore, we observed a strong negative correlation between KLF7 expression and 5-year overall survival and disease-free survival in GC patients (P<0.05). Moreover, our in vitro studies showed a notable decrease in migration in KLF7 knockdown cells. Conclusion: KLF7 has an important role in GC progression, as it inhibits GC cell migration and may serve as a prognostic marker.


2011 ◽  
Vol 22 (17) ◽  
pp. 3263-3275 ◽  
Author(s):  
T. T. Giang Ho ◽  
Audrey Stultiens ◽  
Johanne Dubail ◽  
Charles M. Lapière ◽  
Betty V. Nusgens ◽  
...  

RhoGTPases are key signaling molecules regulating main cellular functions such as migration, proliferation, survival, and gene expression through interactions with various effectors. Within the RhoA-related subclass, RhoA and RhoC contribute to several steps of tumor growth, and the regulation of their expression affects cancer progression. Our aim is to investigate their respective contributions to the acquisition of an invasive phenotype by using models of reduced or forced expression. The silencing of RhoC, but not of RhoA, increased the expression of genes encoding tumor suppressors, such as nonsteroidal anti-inflammatory drug–activated gene 1 (NAG-1), and decreased migration and the anchorage-independent growth in vitro. In vivo, RhoC small interfering RNA (siRhoC) impaired tumor growth. Of interest, the simultaneous knockdown of RhoC and NAG-1 repressed most of the siRhoC-related effects, demonstrating the central role of NAG-1. In addition of being induced by RhoC silencing, NAG-1 was also largely up-regulated in cells overexpressing RhoA. The silencing of RhoGDP dissociation inhibitor α (RhoGDIα) and the overexpression of a RhoA mutant unable to bind RhoGDIα suggested that the effect of RhoC silencing is indirect and results from the up-regulation of the RhoA level through competition for RhoGDIα. This study demonstrates the dynamic balance inside the RhoGTPase network and illustrates its biological relevance in cancer progression.


2015 ◽  
Vol 54 (2) ◽  
pp. 125-135 ◽  
Author(s):  
Juan Zhang ◽  
Yunting Zhou ◽  
Cheng Chen ◽  
Feiyuan Yu ◽  
Yun Wang ◽  
...  

Hypothalamic glucose-sensing neurons regulate the expression of genes encoding feeding-related neuropetides POMC, AgRP, and NPY – the key components governing metabolic homeostasis. AMP-activated protein kinase (AMPK) is postulated to be the molecular mediator relaying glucose signals to regulate the expression of these neuropeptides. Whether other signaling mediator(s) plays a role is not clear. In this study, we investigated the role of ERK1/2 using primary hypothalamic neurons as the model system. The primary neurons were differentiated from hypothalamic progenitor cells. The differentiated neurons possessed the characteristic neuronal cell morphology and expressed neuronal post-mitotic markers as well as leptin-regulated orexigenic POMC and anorexigenic AgRP/NPY genes. Treatment of cells with glucose dose-dependently increased POMC and decreased AgRP/NPY expression with a concurrent suppression of AMPK phosphorylation. In addition, glucose treatment dose-dependently increased the ERK1/2 phosphorylation. Blockade of ERK1/2 activity with its specific inhibitor PD98059 partially (approximately 50%) abolished glucose-induced POMC expression, but had little effect on AgRP/NPY expression. Conversely, blockade of AMPK activity with its specific inhibitor produced a partial (approximately 50%) reversion of low-glucose-suppressed POMC expression, but almost completely blunted the low-glucose-induced AgRP/NPY expression. The results indicate that ERK1/2 mediated POMC but not AgRP/NPY expression. Confirming the in vitro findings, i.c.v. administration of PD98059 in rats similarly attenuated glucose-induced POMC expression in the hypothalamus, but again had little effect on AgRP/NPY expression. The results are indicative of a novel role of ERK1/2 in glucose-regulated POMC expression and offer new mechanistic insights into hypothalamic glucose sensing.


Reproduction ◽  
2018 ◽  
Vol 155 (5) ◽  
pp. 433-445 ◽  
Author(s):  
Stefania Muzzachi ◽  
Lorenzo Guerra ◽  
Nicola Antonio Martino ◽  
Maria Favia ◽  
Giuseppe Punzi ◽  
...  

Sperm motility, a feature essential forin vivofertilization, is influenced by intracellular pH (pHi) homeostasis. Several mechanisms are involved in pHiregulation, among which sodium–hydrogen exchangers (NHEs), a family of integral transmembrane proteins that catalyze the exchange of Na+for H+across lipid bilayers. A preliminary characterization of NHE activity and kinetic parameters, followed by analysis of the expression and localization of the protein in ram spermatozoa was performed. NHE activity showed an apparentKmfor external Na+of 17.61 mM. Immunoblotting revealed a molecular mass of 85 kDa. Immunolocalization pattern showed some species-specific aspects, such as positive labeling at the equatorial region of the sperm head. Cariporide, a selective NHE1 inhibitor, significantly reduced pHirecovery (85%). Similarly, exposure to cariporide significantly inhibited different motility parameters, including those related to sperm capacitation.In vitrofertilization (IVF) was not affected by cariporide, possibly due to the non-dramatic, although significant, drop in motility and velocity parameters or due to prolonged exposure during IVF, which may have caused progressive loss of its inhibitory effect. In conclusion, this is the first study documenting, in a large animal model (sheep) of well-known translational relevance, a direct functional role of NHE on sperm pHiand motility. The postulated specificity of cariporide toward isoform 1 of the Na+/H+exchanger seems to suggest that NHE1 may contribute to the observed effects on sperm cell functionality.


2008 ◽  
Vol 77 (1) ◽  
pp. 501-507 ◽  
Author(s):  
Tao Dong ◽  
Brian K. Coombes ◽  
Herb E. Schellhorn

ABSTRACT Citrobacter rodentium is a mouse enteropathogen that is closely related to Escherichia coli and causes severe colonic hyperplasia and bloody diarrhea. C. rodentium infection requires expression of genes of the locus of enterocyte effacement (LEE) pathogenicity island, which simulates infection by enteropathogenic E. coli and enterohemorrhagic E. coli in the human intestine, providing an effective model for studying enteropathogenesis. In this study we investigated the role of RpoS, the stationary phase sigma factor, in virulence in C. rodentium. Sequence analysis showed that the rpoS gene is highly conserved in C. rodentium and E. coli, exhibiting 92% identity. RpoS was critical for survival under heat shock conditions and during exposure to H2O2 and positively regulated the expression of catalase KatE (HPII). The development of the RDAR (red dry and rough) morphotype, an important virulence trait in E. coli, was also mediated by RpoS in C. rodentium. Unlike E. coli, C. rodentium grew well in the mouse colon, and the wild-type strain colonized significantly better than rpoS mutants. However, a mutation in rpoS conferred a competitive growth advantage over the wild type both in vitro in Luria-Bertani medium and in vivo in the mouse colon. Survival analysis showed that the virulence of an rpoS mutant was attenuated. The expression of genes on the LEE pathogenicity island, which are essential for colonization and virulence, was reduced in the rpoS mutant. In conclusion, RpoS is important for the stress response and is required for full virulence in C. rodentium.


Mutagenesis ◽  
2021 ◽  
Author(s):  
Peter Jenkinson

Abstract Since the mid-1970s, there have been many reports that purport to implicate aluminium in the aetiology of neurodegenerative disease. After several decades of research, the role of aluminium in such disease remains controversial and is not the subject of this review. However, if aluminium is implicated in such disease then it follows that there must be a toxicological mechanism or mode of action, and many researchers have investigated various potential mechanisms including the involvement of oxidative damage, cytotoxicity and genotoxicity. This paper reviews many of the publications of studies using various salts of aluminium and various genotoxicity end points, both in vitro and in vivo, with a focus on oxidative damage. The conclusion of this review is that the majority, if not all, of the publications that report positive results have serious technical flaws and/or implausible findings and consequently should contribute little or no weight to a weight of evidence (WoE) argument. There are many high-quality, Good Laboratory Practice (GLP)-compliant genotoxicity studies, that follow relevant OECD test guidelines and the European Chemicals Agency (ECHA) integrated mutagenicity testing strategy, on several salts of aluminium; all demonstrate clear negative results for both in vitro and in vivo genotoxicity. In addition, the claim for an oxidative mode of action for aluminium can be shown to be spurious. This review concludes that there are no reliable studies that demonstrate a potential for genotoxicity, or oxidative mode of action, for aluminium.


2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Haeri Jeong ◽  
Younhee Kim ◽  
Heung-Shick Lee

Abstract Background Corynebacterium glutamicum is used in the industrial production of amino acids and nucleotides. During the course of fermentation, C. glutamicum cells face various stresses and employ multiple regulatory genes to cope with the oxidative stress. The osnR gene plays a negative regulatory role in redox-dependent oxidative-stress responses, but the underlying mechanism is not known yet. Results Overexpression of the osnR gene in C. glutamicum affected the expression of genes involved in the mycothiol metabolism. ChIP-seq analysis revealed that OsnR binds to the promoter region of multiple genes, including osnR and cg0026, which seems to function in the membrane-associated redox metabolism. Studies on the role of the osnR gene involving in vitro assays employing purified OsnR proteins and in vivo physiological analyses have identified that OsnR inhibits the transcription of its own gene. Further, oxidant diamide stimulates OsnR-binding to the promoter region of the osnR gene. The genes affected by the overexpression of osnR have been found to be under the control of σH. In the osnR-overexpressing strain, the transcription of sigH is significantly decreased and the stimulation of sigH transcription by external stress is lost, suggesting that osnR and sigH form an intimate regulatory network. Conclusions Our study suggests that OsnR not only functions as a transcriptional repressor of its own gene and of those involved in redox-dependent stress responses but also participates in the global transcriptional regulation by controlling the transcription of other master regulators, such as sigH.


Blood ◽  
2021 ◽  
Author(s):  
Stefania Mazzi ◽  
Philippe Dessen ◽  
Mathieu Vieira ◽  
Virginie Dufour ◽  
Marie Cambot ◽  
...  

EZH2, the enzymatic component of PRC2, has been identified as a key factor in hematopoiesis. EZH2 loss of function mutations have been found in myeloproliferative neoplasms, more particularly in myelofibrosis, but the precise function of EZH2 in megakaryopoiesis is not fully delineated. Here, we show that EZH2 inhibition by small molecules and shRNA induces MK commitment by accelerating lineage marker acquisition without change in proliferation. Later in differentiation, EZH2 inhibition blocks proliferation, polyploidization and decreases proplatelet formation. EZH2 inhibitors similarly reduce MK polyploidization and proplatelet formation in vitro and platelet level in vivo in a JAK2V617F background. In transcriptome profiling, the defect in proplatelet formation was associated with an aberrant actin cytoskeleton regulation pathway, whereas polyploidization was associated with an inhibition of expression of genes involved in DNA replication and repair, and an upregulation of CDK inhibitors, more particularly CDKN1A and CDKN2D. The knockdown of CDKN1A and at a lesser extend of CDKN2D could partially rescue the percentage of polyploid MKs. Moreover, H3K27me3 and EZH2 ChIP assays revealed that only CDKN1A is a direct EZH2 target while CDKN2D expression is not directly regulated by EZH2 suggesting that EZH2 controls MK polyploidization directly through CDKN1A and indirectly through CDKN2D.


Sign in / Sign up

Export Citation Format

Share Document