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Добірка наукової літератури з теми "Cell metabolism Regulation"

Автор: Grafiati

Опубліковано: 4 червня 2021

Оновлено: 28 січня 2023

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Статті в журналах з теми "Cell metabolism Regulation"

GAO, Ping, and HaoRan WEI. "Regulation of cancer cell metabolism." SCIENTIA SINICA Vitae 47, no. 1 (January 1, 2017): 132–39. http://dx.doi.org/10.1360/n052016-00334.

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Hagel-Bradway, S., and R. Dziak. "Regulation of bone cell metabolism." Journal of Oral Pathology and Medicine 18, no. 6 (July 1989): 344–51. http://dx.doi.org/10.1111/j.1600-0714.1989.tb01564.x.

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Sun, Xinghui, and Mark W. Feinberg. "Regulation of Endothelial Cell Metabolism." Arteriosclerosis, Thrombosis, and Vascular Biology 35, no. 1 (January 2015): 13–15. http://dx.doi.org/10.1161/atvbaha.114.304869.

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Cairns, Rob A., Isaac S. Harris, and Tak W. Mak. "Regulation of cancer cell metabolism." Nature Reviews Cancer 11, no. 2 (January 24, 2011): 85–95. http://dx.doi.org/10.1038/nrc2981.

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Brynildsen, M. P., W. W. Wong, and J. C. Liao. "Transcriptional regulation and metabolism." Biochemical Society Transactions 33, no. 6 (October 26, 2005): 1423–26. http://dx.doi.org/10.1042/bst0331423.

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Understanding organisms from a systems perspective is essential for predicting cellular behaviour as well as designing gene-metabolic circuits for novel functions. The structure, dynamics and interactions of cellular networks are all vital components of systems biology. To facilitate investigation of these aspects, we have developed an integrative technique called network component analysis, which utilizes mRNA expression and transcriptional network connectivity to determine network component dynamics, functions and interactions. This approach has been applied to elucidate transcription factor dynamics in Saccharomyces cerevisiae cell-cycle regulation, detect cross-talks in Escherichia coli two-component signalling pathways, and characterize E. coli carbon source transition. An ultimate test of system-wide understanding is the ability to design and construct novel gene-metabolic circuits. To this end, artificial feedback regulation, cell–cell communication and oscillatory circuits have been constructed, which demonstrate the design principles of gene-metabolic regulation in the cell.

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Pokotylo, I. V. "Lipoxygenases and plant cell metabolism regulation." Ukrainian Biochemical Journal 87, no. 2 (April 27, 2015): 41–55. http://dx.doi.org/10.15407/ubj87.02.041.

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Spiegel, Sarah, and Alfred H. Merrill. "Sphingolipid metabolism and cell growth regulation." FASEB Journal 10, no. 12 (October 1996): 1388–97. http://dx.doi.org/10.1096/fasebj.10.12.8903509.

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Hough, Kenneth P., Danielle A. Chisolm, and Amy S. Weinmann. "Transcriptional regulation of T cell metabolism." Molecular Immunology 68, no. 2 (December 2015): 520–26. http://dx.doi.org/10.1016/j.molimm.2015.07.038.

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Wang, Yin-Hu, Anthony Y. Tao, Martin Vaeth, and Stefan Feske. "Calcium regulation of T cell metabolism." Current Opinion in Physiology 17 (October 2020): 207–23. http://dx.doi.org/10.1016/j.cophys.2020.07.016.

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Bailey, Shannon M., Uduak S. Udoh, and Martin E. Young. "Circadian regulation of metabolism." Journal of Endocrinology 222, no. 2 (June 13, 2014): R75—R96. http://dx.doi.org/10.1530/joe-14-0200.

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Анотація:

In association with sleep–wake and fasting–feeding cycles, organisms experience dramatic oscillations in energetic demands and nutrient supply. It is therefore not surprising that various metabolic parameters, ranging from the activity status of molecular energy sensors to circulating nutrient levels, oscillate in time-of-day-dependent manners. It has become increasingly clear that rhythms in metabolic processes are not simply in response to daily environmental/behavioral influences, but are driven in part by cell autonomous circadian clocks. By synchronizing the cell with its environment, clocks modulate a host of metabolic processes in a temporally appropriate manner. The purpose of this article is to review current understanding of the interplay between circadian clocks and metabolism, in addition to the pathophysiologic consequences of disruption of this molecular mechanism, in terms of cardiometabolic disease development.

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Дисертації з теми "Cell metabolism Regulation"

Tejedor, Vaquero Sonia 1988. "Influence of metabolism in the regulation of T cell differentiation." Doctoral thesis, Universitat Pompeu Fabra, 2018. http://hdl.handle.net/10803/664638.

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Glucose is a key nutrient for T cells. Despite that T cell activation is impaired when they are deprived of glucose, it has also been shown that T effector responses can be elicited in vivo in glucose-poor environments, such as the intratumoral niche, which raises the question of how these cells can maintain their function in nutrient-restricted sites. In this work, we analyzed the ability of T effector cells to be activated by pro-inflammatory polarizing conditions under limiting glucose availability, using an in vitro model in which effector Th0 cells were restimulated to secondary effector T cells in glucose deficiency (0.3 mM). We found that secondary effector T cells could express characteristic Th1 and Th17 cytokines such as IL-17A and IFNγ when exposed to low glucose, but they lost expression of IL-22. Secondary effector T cells adapted to low glucose by reducing their rate of glucose consumption and expression of glycolysis genes, although they still kept using glucose as the main fuel for ATP production. In addition, we found that glucose limitation caused a mild, progressive impairment on mTORC1 activity in these cells that explained in part the downregulation of IL-22, an mTORC1-dependent cytokine. Our results also showed that secondary effector T cells that had experienced glucose stress acquired a nutrient-trained phenotype, and when they were later restimulated under glucose sufficiency they induced an altered cytokine expression pattern with exacerbated production of IL-22 and reduced IFNγ production. Finally, we observed that effector CD4+ T cells generated in different activation contexts in vivo exhibited different patterns of glucose-sensitive genes upon restimulation ex vivo, which suggested that the context in which T effector cells are induced might be a relevant determinant in shaping different response patterns to glucose limitation upon further stimulation. Altogether, our results uncover a previously unappreciated robustness of T cells to maintain effector function under nutrient-restricted conditions, also revealing that a prior history of nutrient stress can influence future effector T cell responses.
La glucosa és un nutrient essencial per les cèl·lules T. Malgrat que l’activació T es veu disminuïda per la manca de glucosa, s’ha vist que respostes T efectores tenen lloc in vivo en entorns amb nivells baixos de glucosa, com són els tumors. Això planteja la incògnita de saber com aquestes cèl·lules poden mantenir les seves funcions en ambients pobres de nutrients. En aquest treball hem analitzat la capacitat de les cèl·lules T efectores (Th0) de ser activades en condicions pro-inflamatòries i nivells baixos de glucosa (0.3 mM). Hem vist que les cèl·lules T efectores secundàries poden induir citocines característiques de respostes Th1 i Th17 com la IL-17A i l’IFNγ en condicions de nivells baixos de glucosa, però perden la capacitat d’expressar la IL-22. Aquestes cèl·lules s’adapten a un entorn baix de glucosa reduint-ne el consum i reduint l’expressió de gens de la glicòlisi, malgrat tot, la glucosa segueix sent la seva principal font d’energia (ATP). A més a més, hem observat que nivells limitats de glucosa provoquen una lleu però progressiva deficiència en l’activitat d’mTORC1, necessària per la producció de la IL-22 i que explicaria en part la disminució dels nivells d’aquesta citocina. Els nostres resultats també mostren que les cèl·lules T efectores secundàries que han experimentat un estrès de glucosa adquireixen un fenotip de memòria que fa que responguin de manera alterada (producció exagerada de IL-22) a un segon estímul en presència de nivells normals de glucosa. Finalment, hem observat que les cèl·lules T CD4 efectores activades in vivo expressen diferencialment gens sensibles a glucosa quan són re-estimulades ex vivo. Això suggereix que el context d’activació d’una cèl·lula T és important per determinar la resposta d’aquestes cèl·lules a posteriors estimulacions en situació de baixa glucosa. En resum, els nostres resultats mostren que els limfòcits T son capaços de mantenir un ventall de funcions efectores en situacions de restricció de nutrients, però que el haver passat per una etapa d’estrès de nutrients pot condicionar els seus perfils d’expressió gènica en respostes efectores futures.

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Babić, Nikolina. "Regulation of energy metabolism of heart myoblasts /." Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/11563.

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Mathew, Jasmin. "Keratin 8/18 regulation of hepatic cell death and metabolism." Thesis, Université Laval, 2009. http://www.theses.ulaval.ca/2009/26554/26554.pdf.

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Szkolnicka, Dagmara Maria. "MicroRNA regulation of drug metabolism in stem cell-derived hepatocytes." Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/23421.

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Анотація:

The liver is a multi-functional and highly regenerative organ. While resilient, the liver is susceptible to organ damage and failure. In both the acute and chronic settings liver disease has dire consequences for health. A common cause of liver damage is adverse reactions to drugs which can lead to drug induced liver injury (DILI). This creates major problems for patients, clinicians, the pharmaceutical industry and regulatory authorities. In the context of drug overdose or serious adverse reactions, liver failure can be acute and life threatening, and in some cases require orthotopic liver transplantation. While transplantation is highly successful, such an approach has limitations and justifies basic science attempts to develop better human models to study liver injury and to develop scalable intervention strategies. With this in mind, we have studied the importance of microRNAs (miRs) in regulating human drug metabolism in pluripotent stem cell – derived hepatocytes and their potential to reduce liver toxicity in response to toxic levels of paracetamol. miRs are small non-coding RNAs that are approximately 20 - 24 nucleotides long and their major function is to fine tune gene expression of their target genes. Recently, it has been demonstrated that microRNAs play a role in regulating the first phase of drug metabolism however the second phase of drug metabolism, drug conjugation, has not been studied in detail. Drug conjugation is a crucial stage in human drug metabolism, and any alterations in this process can lead to changes in compound pharmacology, including therapeutic dose and clearance from the body. To test the importance of miRs in regulating phase II drug metabolism we opted to study the metabolism of a common used analgesic, paracetamol. When taken in the appropriate amounts paracetamol is modified by sulfotransferases (SULTs) and UDP - glucuronosyltransferases (UGTs) and removed from the body without organ damage. However, when paracetamol is taken above the recommended dose it is metabolised by phase I enzymes to generate a toxic intermediate N-acetyl-p-benzoquinone imine (NAPQI), which if untreated can lead to massive hepatocyte cell death and liver failure, placing the patient in a life threatening situation. In order to promote non-toxic drug metabolism, in the context of drug overdose, we employed candidate miRs to regulate different parts of the paracetamol metabolism pathway. In summary, we have focused on studying human drug metabolism in the major metabolic cell type of the liver, the hepatocyte. We have identified a novel microRNA (called miR-324-5p) which regulates phase II drug metabolism and reduces cell cytotoxicity. Additionally, a supportive role of anti-microRNA- 324 in response to fulminant plasma collected from paracetamol overdose patients is also observed. The findings of this project are novel, provide proof of concept and exemplify the power of stem cell based models to identify new approaches to treating human liver damage.

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Mukherjee, Abir. "ROLE OF LYSOPHOSPHATIDIC ACID IN REGULATION OF CANCER CELL METABOLISM." VCU Scholars Compass, 2012. http://scholarscompass.vcu.edu/etd/391.

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The simplest phospholipid, lysophosphatidic acid (LPA), is a heat stable component of serum known for its proliferative and migratory activities in cancer cells. Strong evidence suggests that LPA production and expression of its receptors are dysregulated in multiple human malignancies. The mechanism behind LPA-mediated tumor cell growth and oncogenesis remains poorly understood. In this thesis project I used ovarian and other cancer cells as a model system to examine the hypothesis that LPA present in the tumor microenvironment is a pathophysiological determinant of hyperactive de novo lipogenesis and aerobic glycolysis, two hallmarks of cancer cells. We demonstrated that LPA induced proteolytic activation of sterol regulatory element binding proteins (SREBPs) in a cancer specific manner, leading to activation of the SREBP-FAS (fatty acid synthase) lipogenic pathway. Treatment of cancer cell lines with LPA also led to dephosphorylation and inhibition of AMP-activated kinase (AMPK), thereby activating acetyl CoA carboxylase (ACC). Moreover, these effects of LPA were mediated by LPA2, a receptor subtype overexpressed in multiple cancers, providing an explanation for the cancer specific regulation of FAS and ACC by LPA. Downstream of the LPA2 receptor, we identified the Gα12-Rho-Rock pathway to activate SREBPs and the Gαq-PLC (phospholipase C) pathway to inactivate AMPK. Consistent with LPA mediated activation of the key lipogenic enzymes FAS and ACC, LPA stimulated de novo lipid synthesis via LPA2, leading to accumulation of intracellular triacylglycerol and phospholipids. Pharmacological and molecular inhibition of LPA2, FAS or ACC attenuated LPA-dependent cell proliferation, indicating that upregulation of lipid synthesis is an integral component of the proliferative response to LPA. In further support of this, downregulation of LPA2 expression led to dramatic inhibition of anchorage-dependent and –independent growth of ovarian cancer cells. To support increased biomass generation, rapidly proliferating cancer cells enhance carbon influx by activating glycolysis. In the next part of the study, we investigated if LPA signaling was also involved in activating aerobic glycolysis in cancer cells. LPA indeed activated glycolysis in ovarian and other cancer cells but failed to elicit this response in non-transformed cells, suggesting a cancer specific role of LPA in regulation of glucose metabolism. While LPA had no effect on glucose uptake, we found that LPA altered expression of multiple genes involved in glucose metabolism. The most significant observation was that LPA treatment dramatically upregulated expression of HK-2, one of the rate-limiting glycolytic enzymes. We explored the underlying mechanism and found that LPA activates HK-2 transcription through LPA2-mediated activation of SREBP-1. Two sterol regulator elements (SREs) on the human HK-2 promoter were identified to be responsible for LPA activation of the promoter. DNA pulldown and chromatin immunoprecipitation assays confirmed that SREBP-1 bound to these SREs in LPA-treated cells. Although in ovarian cancer cells, LPA treatment also stabilized Hif-1α protein, an established activator of HK-2 and glycolysis, LPA-regulated HK-2 expression and glycolysis was largely independent of Hif-1α. These results established that LPA stimulates glycolysis via the LPA2-SREBP-HK-2 cascade in neoplastic cells. Taken together, this dissertation provides the first evidence for regulation of cancer cell metabolism by LPA. The results indicate that LPA signaling is causally linked to lipogenic and glycolytic phenotypes of cancer cells. Therefore, targeting the key LPA2 receptor could offer a novel and innovative approach to blocking tumor-specific metabolism.

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Syal, Charvi. "Epigenetic Regulation of Lipid Metabolism in Neural Stem Cell Fate Decision." Thesis, Université d'Ottawa / University of Ottawa, 2019. http://hdl.handle.net/10393/38706.

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Bioactive lipids have emerged as prominent regulators of neural stem and progenitor cell (NPC) function under both physiological and pathological conditions. However, how lipid metabolism is regulated, and its role in modulation of NPC function remains unknown. In this regard, my study defines a novel epigenetic pathway that regulates lipid metabolism to determine NPC proliferation versus differentiation. Specifically, I show that activation of an atypical protein kinase C (aPKC)-mediated Ser436 phosphorylation of CREB binding protein (CBP) by aging, metformin stimulation and continued passaging in vitro, represses expression of monoacylglycerol lipase (Mgll) to promote neuronal differentiation of adult NPCs. Mgll, a lipase that hydrolyzes the endocannabinoid 2-arachidonoyl glycerol (2-AG) to produce arachidonic acid (ARA), is thus a key regulator of two critical bioactive lipid signaling pathways in the brain and a potential modulator of NPC function. I observed elevated Mgll levels, concomitant with neuronal differentiation deficits in both the lateral ventricle sub-ventricular zone (SVZ) and the hippocampal subgranular zone (SGZ) NPCs of phospho-null CBPS436A mice, that lack a functional aPKC-CBP pathway. Genetic knockdown of Mgll or inhibition of Mgll activity rescued these neuronal differentiation deficits. In addition, I found that CBPS436A SVZ NPCs exhibit enhanced proliferation at the expense of differentiation as an outcome of increased Mgll levels in culture. Interestingly, I also observed that SVZ NPCs from an Alzheimer’s disease (AD) model, the 3xTg mice, closely resemble CBPS436A NPC behaviour in culture. 3xTg NPCs exhibit attenuation of the aPKC-CBP pathway, which is associated with elevated Mgll expression and increased NPC proliferation at the expense of neuronal differentiation. Reactivation of the aPKC-CBP mediated-Mgll repression in 3xTg AD NPCs mitigates their differentiation deficits. These findings implicate Mgll as a critical switch that regulates NPC function by altering bioactive lipid signaling (2-AG versus ARA). They demonstrate that the aPKC-CBP mediated Mgll repression is essential for normal NPC function, and that when perturbed in AD, it causes impaired NPC function to generate fewer neurons, contributing to AD predisposition.

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Ng, Shyh Chang. "Regulation of Stem Cell Metabolism by the Lin28/let-7 Axis." Thesis, Harvard University, 2013. http://dissertations.umi.com/gsas.harvard:11217.

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My PhD thesis is focused on two fundamental aspects of stem cell metabolism: (1) the role of Lin28 in programming stem cell metabolism, and (2) how metabolism in turn fuels and governs pluripotency. Our studies led us to discover that the stem cell factor Lin28a promotes gigantism by enhancing glucose metabolism in mice, coinciding with discoveries that LIN28B polymorphisms influence height variation in human GWAS. Subsequently, we discovered that the Lin28/let-7 pathway controls glucose metabolism by orchestrating the upregulation of multiple insulin-PI3K-mTOR components, particularly in skeletal muscle progenitors. Since let-7 accumulates with aging, our discoveries suggest that let-7 could represent a new drug target for treating insulin resistance and type 2 diabetes during aging. During these studies, we also observed that Lin28a enhances tissue regeneration in adulthood. Regeneration capacity has long been known to decline with aging, but why juvenile organisms show enhanced tissue repair had remained unexplained. We found that Lin28a reactivation improved the regrowth of skin, hair, cartilage, bone and mesenchyme after injuries. Let-7 repression was necessary but insufficient to explain these phenotypes. In parallel, Lin28a bound to and enhanced the translation of mRNAs for several oxidative enzymes, thereby increasing OxPhos. Lin28a-mediated tissue repair was negated by OxPhos inhibition, whereas a pharmacologically-induced increase in OxPhos promoted wound repair. Thus, Lin28a enhanced tissue regeneration in adults by reprogramming cellular bioenergetics. My interest in the central principles of stem cell metabolism also led us to map the metabolic pathways associated with pluripotency during iPS reprogramming and Lin28/let-7 perturbation. Surprisingly, we found that Thr-Gly-S-adenosylmethionine (SAM) metabolism consistently showed the best correlation with pluripotency. 13Carbon isotope metabolomics further revealed that Thr was catabolized to generate Gly and acetyl-CoA, and ultimately SAM - essential for all methylation reactions. Thr is required for SAM and histone H3K4 methylation in mouse ESCs, thus regulating the open euchromatin and pluripotency of ESCs. Our study shed light on a novel amino acid pathway in stem cells, and demonstrated that metabolic conditions can direct cell fate. In summary, my work has helped us to understand how we can reprogram and manipulate metabolic networks to regulate stem cell homeostasis.

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Mofarrahi, Mahroo. "Regulation of skeletal muscle satellite cell proliferation by NADPH oxidase." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111521.

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Skeletal satellite cells are adult stem cells located among muscle fibers. Proliferation, migration and subsequent differentiation of these cells are critical steps in the repair of muscle injury. We document in this study the roles and mechanisms through which the NAPDH oxidase complex regulates skeletal satellite cell proliferation. The NADPH oxidase subunits Nox2, Nox4, p22phox, p47phox and p67 phox were detected in primary human and murine skeletal muscle satellite cells. In human satellite cells, NADPH oxidase-fusion proteins were localized in the cytosolic and membrane compartments of the cell, except for p47 phox, which was detected in the nucleus. In proliferating subconfluent satellite cells, both Nox2 and Nox4 contributed to O2- production. However, Nox4 expression was significantly attenuated in confluent cells and in differentiated myotubes. Proliferation of satellite cells was significantly reduced by antioxidants (N-acetylcysteine and apocynin), inhibition of p22phox expression using siRNA oligonucleotides, and reduction of Nox4 and p47phox activities with dominant-negative vectors resulted in attenuation of activities of the Erk1/2, PI-3 kinase/AKT and NFkappaB pathways and significant reduction in cyclin D1 levels. We conclude that NADPH oxidase is expressed in skeletal satellite cells and that its activity plays an important role in promoting proliferation of these cells.

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Aitchison, Robert E. D. "Mammary cell cyclic AMP : regulation of breakdown and influence on protein phosphorylation." Thesis, University of Glasgow, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.303363.

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Beauchamp, Pascal. "The functional role of the RNA-binding protein HuR in the regulation of muscle cell differentiation /." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111586.

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Muscle tissue development (myogenesis) involves the formation of specific fibers (myotubes) from muscle cells (myoblasts). For this to occur, the sequential expression of Myogenic Regulatory Factors (MRFs), such as MyoD and myogenin, is required. The expression of these MRFs is regulated posttranscriptionally by the RNA-binding protein HuR, whereby HuR associates with the 3'-untranslated regions of MyoD and myogenin mRNA, leading to a significant increase in their half-lives. Here we show that the cleavage of HuR by caspases at the aspartate (D) 226 residue is one of the main regulators of its pro-myogenic function. This proteolytic activity generates two cleavage products (CPs), HuR-CP1 and HuR-CP2, that differentially affect the myogenic process. Myoblasts overexpressing HuR-CP1 or the non-cleavable mutant of HuR, HuRD226A, are not able to engage myogenesis, while overexpressing HuR-CP2 enhances myotube formation. HuR-CP2 but not -CP1 promotes myogenesis by stabilizing the MyoD and myogenin mRNAs to the same levels as wt-HuR. Conversely, the inhibitory effects of HuR-CP1 and HuRD226A depend on their abilities to associate during myogenesis with the HuR import receptor, Trn2, leading to HuR accumulation in the cytoplasm. Therefore, we propose a model whereby the caspase-mediated cleavage of HuR generates two CPs that collaborate to regulate myogenesis; HuR-CP1 by interfering with the Trn2-mediated import of HuR and HuR-CP2 by participating in the stabilization of mRNAs encoding key MRFs.

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Книги з теми "Cell metabolism Regulation"

INSERM European Symposium on Hormones and Cell Regulation (15e 1990 Sainte-Odile, France). Hormones and cell regulation. Paris: INSERM, 1990.

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Inserm European Symposium on Hormones and Cell Regulation (13th 1988 Sainte-Odile, France). Hormones and cell regulation. London: Paris : INSERM, 1989.

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G, Thurman Ronald, Kauffman Frederick C, and Jungermann Kurt, eds. Regulation of hepatic metabolism: Intra- and intercellular compartmentation. New York: Plenum Press, 1986.

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Severin, E. S. Izbiratelʹnai͡a︡ reguli͡a︡t͡s︡ii͡a︡ kletochnogo metabolizma: Dolozheno na sorok pi͡a︡tom ezhegodnom Bakhovskom chtenii 17 marta 1989 g. Moskva: "Nauka", 1991.

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Felix, Bronner, ed. Intracellular calcium regulation. New York: Wiley-Liss, 1990.

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J, Clemens Michael, ed. Protein phosphorylation in cell growth regulation. Australia: Harwood Academic Publishers, 1996.

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Regulation of vitamin A homeostasis by the stellate cell (vitamin A-storing cell) system. New York: Nova Biomedical Books, 2011.

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Heinrich, Reinhart. The regulation of cellular systems. New York: Chapman & Hall, 1996.

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1931-, Dumont Jacques E., Nunez J, and Institut national de la santé et de la recherche médicale (France), eds. Hormones and cell regulation =: Hormones et Regulation Cellulaire: Proceedings of the 14th INSERM European Symposium on Hormones and Cell Regulation, held at Mont Sainte-Odile (France), September 25-28, 1989. London: Libbey, 1989.

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Inserm, European Symposium on Hormones and Cell Regulation (11th 1986 Sainte Odile France). Hormones and cell regulation =: Hormones et Regulation Cellulaire: Proceedings of the 11th INSERM European Symposium on Hormones and Cell Regulation, held at Sainte-Odile (France), 29 September-2 October, 1986. Paris: INSERM, 1987.

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Частини книг з теми "Cell metabolism Regulation"

Gouw, Arvin M., Annie L. Hsieh, Zachary E. Stine, and Chi V. Dang. "MYC Regulation of Metabolism and Cancer." In Tumor Cell Metabolism, 101–22. Vienna: Springer Vienna, 2015. http://dx.doi.org/10.1007/978-3-7091-1824-5_5.

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Blackmore, Peter F., Christopher J. Lynch, Stephen B. Bocckino, and John H. Exton. "Regulation of Hepatic Glycogenolysis by Calcium-Mobilizing Hormones." In Cell Calcium Metabolism, 179–85. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5598-4_19.

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Corkey, Barbara E., Keith Tornheim, Jude T. Deeney, M. Clay Glennon, Janice C. Parker, Franz M. Matschinsky, Neil B. Ruderman, and Marc Prentki. "Metabolic Regulation of Ca2+ Handling in Permeabilized Insulinoma Cells." In Cell Calcium Metabolism, 369–77. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5598-4_40.

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Vonakis, Becky M., and Jack Y. Vanderhoek. "Role of Calcium in the Regulation of Mammalian Lipoxygenases." In Cell Calcium Metabolism, 387–96. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5598-4_42.

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Morgan, James I., and Tom Curran. "Regulation of c-fos Expression by Voltage-Dependent Calcium Channels." In Cell Calcium Metabolism, 305–12. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5598-4_33.

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Trump, Benjamin F., and Irene K. Berezesky. "Role of Ion Regulation in Cell Injury, Cell Death, and Carcinogenesis." In Cell Calcium Metabolism, 441–49. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5598-4_46.

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Lindros, Kai O., Gunnar Bengtsson, Mikko Salaspuro, and Hannu Väänänen. "Separation of Functionally Different Liver Cell Types." In Regulation of Hepatic Metabolism, 137–58. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5041-5_6.

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Hansford, Richard G., Rafael Moreno-Sánchez, and James M. Staddon. "Regulation of Pyruvate Dehydrogenase in Isolated Cardiac Myocytes and Hepatocytes by Cytosolic Calcium." In Cell Calcium Metabolism, 331–41. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5598-4_36.

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Paro, Renato, Ueli Grossniklaus, Raffaella Santoro, and Anton Wutz. "Epigenetics and Metabolism." In Introduction to Epigenetics, 179–201. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-68670-3_9.

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AbstractMost chromatin-modifying enzymes use metabolites as cofactors. Consequently, the cellular metabolism can influence the capacity of the cell to write or erase chromatin marks. This points to an intimate relationship between metabolic and epigenetic regulation. In this chapter, we describe the biosynthetic pathways of cofactors that are implicated in epigenetic and chromatin regulation and provide examples of how metabolic pathways can influence chromatin and epigenetic processes as well as their interplay in developmental and cancer biology.

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Kersten, Sander. "Regulation of Nutrient Metabolism and Inflammation." In Results and Problems in Cell Differentiation, 13–25. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-14426-4_2.

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Тези доповідей конференцій з теми "Cell metabolism Regulation"

Kasbawati, A. Y. Gunawan, R. Hertadi, and K. A. Sidarto. "Metabolic regulation and maximal reaction optimization in the central metabolism of a yeast cell." In SYMPOSIUM ON BIOMATHEMATICS (SYMOMATH 2014). AIP Publishing LLC, 2015. http://dx.doi.org/10.1063/1.4914436.

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Amitrano, Andrea, Brandon Walling, Kyun Do Kim, Brandon Berry, Adam Trewin, Andrew Wojtovich, and Minsoo Kim. "Abstract A73: Optogenetic regulation of T cell metabolism in the tumor microenvironment." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; October 1-4, 2017; Boston, MA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/2326-6074.tumimm17-a73.

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Blenis, John, Gina Lee, Jamie Dempsey, and Christina England. "Abstract IA03: mTORC1/S6K1: Regulation of RNA biogenesis, protein synthesis, and cell metabolism." In Abstracts: AACR Special Conference on Translational Control of Cancer: A New Frontier in Cancer Biology and Therapy; October 27-30, 2016; San Francisco, CA. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.transcontrol16-ia03.

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Golovatskaya, I. F., M. V. Nechaeva, and E. V. Boiko. "20E-dependent regulation of growth and secondary metabolism of cell culture Lychnis chalcedonica L." In IX Congress of society physiologists of plants of Russia "Plant physiology is the basis for creating plants of the future". Kazan University Press, 2019. http://dx.doi.org/10.26907/978-5-00130-204-9-2019-124.

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Audet-Walsh, Étienne, David Papadopoli, Julie St-Pierre, and Vincent Giguère. "Abstract 2436: Regulation of breast cancer cell metabolism by the AMPK/ERR/PGC pathway." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2436.

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Burkhart, Richard, Danielle Pineda, Joseph Cozzitorto, Charles Yeo, Jonathan Brody, and Jordan Winter. "Abstract 5144: RNA-binding protein HuR supports post-transcriptional regulation of pancreatic cancer cell metabolism." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-5144.

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Vilyanen, D. V., E. Yu Garnik, V. I. Tarasenko, and Yu M. Konstantinov. "STUDY OF CHLOROPHYLL METABOLISM IN A DOUBLE ARABIDOPSIS THALIANA MUTANT GDH1GDH2 DURING A LONG-TERM EXPOSITION OF PLANTS IN THE DARK." In The Second All-Russian Scientific Conference with international participation "Regulation Mechanisms of Eukariotic Cell Organelle Functions". SIPPB SB RAS, 2018. http://dx.doi.org/10.31255/978-5-94797-318-1-22-24.

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Carroll, Patrick A., Daniel Diolaiti, Pei-Feng Cheng, Haiwei Gu, Danijel Djukovic, Daniel Raftery, Donald E. Ayer, Charles H. Muller, and Robert N. Eisenman. "Abstract PR12: Transcriptional regulation of metabolism by MLX and its binding partners is essential for tumor cell survival and spermatogenesis." In Abstracts: AACR Special Conference: Metabolism and Cancer; June 7-10, 2015; Bellevue, WA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3125.metca15-pr12.

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Iwata, Shigeru, Mingzeng Zhang, Maiko Hajime, Naoaki Ohkubo, Hiroko Miyata, Yasuyuki Todoroki, Shingo Nakayamada, and Yoshiya Tanaka. "OP0196 IMBALANCE BETWEEN MEMORY TH1 AND TH1-TREG CELLS DEPENDS ON DIFFERENTIAL REGULATION OF CELL METABOLISM IN PATIENTS WITH SLE." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.3409.

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Schnepp, Patricia M., Dennis D. Lee, Ian H. Guldner, Treasa O'Tighearnaigh, Bhavana Palakurthi, Kaitlyn E. Eckert, Tiffany A. Toni, Brandon L. Ashfeld, and Siyuan Zhang. "Abstract 4934: Brain metastatic microenvironment reshapes cancer cell metabolism through epigenetic up-regulation of glutamate decarboxylase 1." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4934.

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Звіти організацій з теми "Cell metabolism Regulation"

Granot, David, and Richard Amasino. Regulation of Senescence by Sugar Metabolism. United States Department of Agriculture, January 2003. http://dx.doi.org/10.32747/2003.7585189.bard.

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Research objectives a. Analyze transgenic plants that undergo rapid senescence due to increased expression of hexokinase. b. Determine if hexokinase-induced senescence accelerates natural senescence using senescence specific promoters that drive expression of a reporter gene (GUS) and a cytokinin producing gene (IPT - isopentyl transferase). c. Isolate and analyze plant genes that suppress sugar-induced cell death (SICD) in yeast, genes that potentially are involved in programmed cell death and senescence in plants. Background to the topic Leaf senescence is a regulated process of programmed cell death (PCD) in which metabolites are recycled to other active parts of the plant. Senescence associated genes (SAGs) are expressed throughout leaf senescence. Sugar flux and metabolism is thought to playa fundamental regulatory role in senescence. We found that transgenic tomato plants with high hexokinase activity, the initial enzymatic step of sugar (hexose) metabolism, undergo rapid leaf senescence, directly correlated with hexokinase activity. These plants provide a unique opportunity to analyze the regulatory role of sugar metabolism in senescence, and its relation to cytokinin, a senescence-inhibiting hormone. In addition, we found that sugar induces programmed cells death of yeast cells in direct correlation to hexokinase activity. We proposed to use the sugar induced cell death (SICD) to isolate Arabidopsis genes that suppress SICD. Such genes could potentially be involved in senescence induced PCD in plants. Major conclusions The promoters of Arabidopsis senescence-associated genes, SAG12 and SAGI3, are expressed in senescing tomato leaves similar to their expression in Arabidopsis leaves, indicating that these promoters are good senescence markers for tomato plants. Increased hexokinase activity accelerated senescence and induced expression of pSAG12 and pSAG13 promoters in tomato plants, suggesting that sugar regulate natural senescence via hexokinase. Expression of IPT, a cytokinin producing gene, under pSAG12 and pSAG13 promoters, delayed senescence of tomato leaves. Yet, senescence accelerated by hexokinase was epistatic over cytokinin, indicating that sugar regulation of senescence is dominant over the senescence-inhibiting hormone. A gene designated SFP1, which is similar to the major super family monosaccharide transporters, is induced during leaf senescence in Arabidopsis and may be involved in sugar transport during senescence. Accordingly, adult leaves accumulate sugars that may accelerate hexokinase activity. Light status of the entire plant affects the senescence of individual leaves. When individual leaves are darkened, senescence is induced in the covered leaves. However, whole adult plant placed in darkness show delayed senescence. In a search for Arabidopsis genes that suppress SICD we isolated 8 cDNA clones which confer partial resistance to SICD. One of the clones encodes a vesicle associated membrane protein - VAMP. This is the first evidence that vesicle trafficking might be involved in cell death. Implications Increased hexokinase activity accelerates senescence. We hypothesized that, reduced hexokinase activity may delay senescence. Preliminary experiments using a hexokinase inhibitor support this possible implication. Currently we are analyzing various practical approaches to delay leaf senescence via hexokinase inhibition. .

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Ben-Arie, Ruth, John M. Labavitch, and Amos Blumenfeld. Hormonal Regulation of Cell Wall Metabolism During Fruit Ripening. United States Department of Agriculture, August 1987. http://dx.doi.org/10.32747/1987.7568074.bard.

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Meidan, Rina, and Robert Milvae. Regulation of Bovine Corpus Luteum Function. United States Department of Agriculture, March 1995. http://dx.doi.org/10.32747/1995.7604935.bard.

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The main goal of this research plan was to elucidate regulatory mechanisms controlling the development, function of the bovine corpus luteum (CL). The CL contains two different sterodigenic cell types and therefore it was necessary to obtain pure cell population. A system was developed in which granulosa and theca interna cells, isolated from a preovulatory follicle, acquired characteristics typical of large (LL) and small (SL) luteal cells, respectively, as judged by several biochemical and morphological criteria. Experiments were conducted to determine the effects of granulosa cells removal on subsequent CL function, the results obtained support the concept that granulosa cells make a substaintial contribution to the output of progesterone by the cyclic CL but may have a limited role in determining the functional lifespan of the CL. This experimental model was also used to better understand the contribution of follicular granulosa cells to subsequent luteal SCC mRNA expression. The mitochondrial cytochrome side-chain cleavage enzyme (SCC), which converts cholesterol to pregnenolone, is the first and rate-limiting enzyme of the steroidogenic pathway. Experiments were conducted to characterize the gene expression of P450scc in bovine CL. Levels of P450scc mRNA were higher during mid-luteal phase than in either the early or late luteal phases. PGF 2a injection decreased luteal P450scc mRNA in a time-dependent manner; levels were significantly reduced by 2h after treatment. CLs obtained from heifers on day 8 of the estrous cycle which had granulosa cells removed had a 45% reduction in the levels of mRNA for SCC enzymes as well as a 78% reduction in the numbers of LL cells. To characterize SCC expression in each steroidogenic cell type we utilized pure cell populations. Upon luteinization, LL expressed 2-3 fold higher amounts of both SCC enzymes mRNAs than SL. Moreover, eight days after stimulant removal, LL retained their P4 production capacity, expressed P450scc mRNA and contained this protein. In our attempts to establish the in vitro luteinization model, we had to select the prevulatory and pre-gonadotropin surge follicles. The ratio of estradiol:P4 which is often used was unreliable since P4 levels are high in atretic follicles and also in preovulatory post-gonadotropin follicles. We have therefore examined whether oxytocin (OT) levels in follicular fluids could enhance our ability to correctly and easily define follicular status. Based on E2 and OT concentrations in follicular fluids we could more accurately identify follicles that are preovulatory and post gonadotropin surge. Next we studied OT biosynthesis in granulosa cells, cells which were incubated with forskolin contained stores of the precursor indicating that forskolin (which mimics gonadotropin action) is an effective stimulator of OT biosynthesis and release. While studying in vitro luteinization, we noticed that IGF-I induced effects were not identical to those induced by insulin despite the fact that megadoses of insulin were used. This was the first indication that the cells may secrete IGF binding protein(s) which regonize IGFs and not insulin. In a detailed study involving several techniques, we characterized the species of IGF binding proteins secreted by luteal cells. The effects of exogenous polyunsaturated fatty acids and arachidonic acid on the production of P4 and prostanoids by dispersed bovine luteal cells was examined. The addition of eicosapentaenoic acid and arachidonic acid resulted in a dose-dependent reduction in basal and LH-stimulated biosynthesis of P4 and PGI2 and an increase in production of PGF 2a and 5-HETE production. Indomethacin, an inhibitor of arachidonic acid metabolism via the production of 5-HETE was unaffected. Results of these experiments suggest that the inhibitory effect of arachidonic acid on the biosynthesis of luteal P4 is due to either a direct action of arachidonic acid, or its conversion to 5-HETE via the lipoxgenase pathway of metabolism. The detailed and important information gained by the two labs elucidated the mode of action of factors crucially important to the function of the bovine CL. The data indicate that follicular granulosa cells make a major contribution to numbers of large luteal cells, OT and basal P4 production, as well as the content of cytochrome P450 scc. Granulosa-derived large luteal cells have distinct features: when luteinized, the cell no longer possesses LH receptors, its cAMP response is diminished yet P4 synthesis is sustained. This may imply that maintenance of P4 (even in the absence of a Luteotropic signal) during critical periods such as pregnancy recognition, is dependent on the proper luteinization and function of the large luteal cell.

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Blumwald, Eduardo, and Avi Sadka. Citric acid metabolism and mobilization in citrus fruit. United States Department of Agriculture, October 2007. http://dx.doi.org/10.32747/2007.7587732.bard.

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Accumulation of citric acid is a major determinant of maturity and fruit quality in citrus. Many citrus varieties accumulate citric acid in concentrations that exceed market desires, reducing grower income and consumer satisfaction. Citrate is accumulated in the vacuole of the juice sac cell, a process that requires both metabolic changes and transport across cellular membranes, in particular, the mitochondrial and the vacuolar (tonoplast) membranes. Although the accumulation of citrate in the vacuoles of juice cells has been clearly demonstrated, the mechanisms for vacuolar citrate homeostasis and the components controlling citrate metabolism and transport are still unknown. Previous results in the PIs’ laboratories have indicated that the expression of a large number of a large number of proteins is enhanced during fruit development, and that the regulation of sugar and acid content in fruits is correlated with the differential expression of a large number of proteins that could play significant roles in fruit acid accumulation and/or regulation of acid content. The objectives of this proposal are: i) the characterization of transporters that mediate the transport of citrate and determine their role in uptake/retrieval in juice sac cells; ii) the study of citric acid metabolism, in particular the effect of arsenical compounds affecting citric acid levels and mobilization; and iii) the development of a citrus fruit proteomics platform to identify and characterize key processes associated with fruit development in general and sugar and acid accumulation in particular. The understanding of the cellular processes that determine the citrate content in citrus fruits will contribute to the development of tools aimed at the enhancement of citrus fruit quality. Our efforts resulted in the identification, cloning and characterization of CsCit1 (Citrus sinensis citrate transporter 1) from Navel oranges (Citrus sinesins cv Washington). Higher levels of CsCit1 transcripts were detected at later stages of fruit development that coincided with the decrease in the juice cell citrate concentrations (Shimada et al., 2006). Our functional analysis revealed that CsCit1 mediates the vacuolar efflux of citrate and that the CsCit1 operates as an electroneutral 1CitrateH2-/2H+ symporter. Our results supported the notion that it is the low permeable citrateH2 - the anion that establishes the buffer capacity of the fruit and determines its overall acidity. On the other hand, it is the more permeable form, CitrateH2-, which is being exported into the cytosol during maturation and controls the citrate catabolism in the juice cells. Our Mass-Spectrometry-based proteomics efforts (using MALDI-TOF-TOF and LC2- MS-MS) identified a large number of fruit juice sac cell proteins and established comparisons of protein synthesis patterns during fruit development. So far, we have identified over 1,500 fruit specific proteins that play roles in sugar metabolism, citric acid cycle, signaling, transport, processing, etc., and organized these proteins into 84 known biosynthetic pathways (Katz et al. 2007). This data is now being integrated in a public database and will serve as a valuable tool for the scientific community in general and fruit scientists in particular. Using molecular, biochemical and physiological approaches we have identified factors affecting the activity of aconitase, which catalyze the first step of citrate catabolism (Shlizerman et al., 2007). Iron limitation specifically reduced the activity of the cytosolic, but not the mitochondrial, aconitase, increasing the acid level in the fruit. Citramalate (a natural compound in the juice) also inhibits the activity of aconitase, and it plays a major role in acid accumulation during the first half of fruit development. On the other hand, arsenite induced increased levels of aconitase, decreasing fruit acidity. We have initiated studies aimed at the identification of the citramalate biosynthetic pathway and the role(s) of isopropylmalate synthase in this pathway. These studies, especially those involved aconitase inhibition by citramalate, are aimed at the development of tools to control fruit acidity, particularly in those cases where acid level declines below the desired threshold. Our work has significant implications both scientifically and practically and is directly aimed at the improvement of fruit quality through the improvement of existing pre- and post-harvest fruit treatments.

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Pell, Eva J., Sarah M. Assmann, Amnon Schwartz, and Hava Steinberger. Ozone Altered Stomatal/Guard Cell Function: Whole Plant and Single Cell Analysis. United States Department of Agriculture, December 2000. http://dx.doi.org/10.32747/2000.7573082.bard.

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Original objectives (revisions from original proposal are highlighted) 1. Elucidate the direct effects O3 and H2O2 on guard cell function, utilizing assays of stomatal response in isolated epidermal peels and whole cell gas exchange. 2. Determine the mechanistic basis of O3 and H2O2 effects on the plasma membrane through application of the electrophysiological technique of patch clamping to isolated guard cells. 3. Determine the relative sensitivity of Israeli cultivars of economically important crops to O3 and determine whether differential leaf conductance responses to O3 can explain relative sensitivity to the air pollutant: transfer of technological expertise to Israel. Background to the topic For a long time O3 has been known to reduce gas exchange in plants; it has however been unclear if O3 can affect the stomatal complex directly. Ion channels are essential in stomatal regulation, but O3 has never before been shown to affect these directly. Major conclusions, solution, achievements 1. Ozone inhibits light-induced stomatal opening in epidermal peels isolated from Vicia faba, Arabidopsis thaliana and Nicotiana tabacum in V. faba plants this leads to reduced assimilation without a direct effect on the photosynthetic apparatus. Stomatal opening is more sensitive to O3 than stomatal closure. 2. Ozone causes inhibition of inward K+ channels (involved in stomatal opening) while no detectable effect is observed o the outward K+ channels (stomatal closure). 3. Hydrogen peroxide inhibits stomatal opening and induces stomatal closure in epidermal peels isolated from Vicia faba. 4. Hydrogen peroxide enhances stomatal closure by increasing K+ efflux from guard cells via outward rectifying K+ channels. 5. Based on epidermal peel experiments we have indirectly shown that Ca2+ may play a role in the guard cell response to O3. However, direct measurement of the guard cell [Ca2+]cyt did not show a response to O3. 6. Three Israeli cultivars of zucchini, Clarita, Yarden and Bareqet, were shown to be relatively sensitive to O3 (0.12 ml1-1 ). 7. Two environmentally important Israeli pine species are adversely affected by O3, even at 0.050 ml1-1 , a level frequently exceeded under local tropospheric conditions. P. brutia may be better equipped than P. halepensis to tolerate O3 stress. 8. Ozone directly affects pigment biosynthesis in pine seedlings, as well as the metabolism of O5 precursors, thus affecting the allocation of resources among various metabolic pathways. 9. Ozone induces activity of antioxidant enzymes, and of ascorbate content i the mesophyll and epidermis cells of Commelina communis L. Implications, both scientific and agricultural We have improved the understanding of how O3 and H2O2 do affect guard cell and stomatal function. We have shown that economical important Israeli species like zucchini and pine are relatively sensitive to O3.

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Schuster, Gadi, and David Stern. Integration of phosphorus and chloroplast mRNA metabolism through regulated ribonucleases. United States Department of Agriculture, August 2008. http://dx.doi.org/10.32747/2008.7695859.bard.

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New potential for engineering chloroplasts to express novel traits has stimulated research into relevant techniques and genetic processes, including plastid transformation and gene regulation. This proposal continued our long time BARD-funded collaboration research into mechanisms that influence chloroplast RNA accumulation, and thus gene expression. Previous work on cpRNA catabolism has elucidated a pathway initiated by endonucleolytic cleavage, followed by polyadenylation and exonucleolytic degradation. A major player in this process is the nucleus-encoded exoribonuclease/polymerasepolynucleotidephoshorylase (PNPase). Biochemical characterization of PNPase has revealed a modular structure that controls its RNA synthesis and degradation activities, which in turn are responsive to the phosphate (P) concentration. However, the in vivo roles and regulation of these opposing activities are poorly understood. The objectives of this project were to define how PNPase is controlled by P and nucleotides, using in vitro assays; To make use of both null and site-directed mutations in the PNPgene to study why PNPase appears to be required for photosynthesis; and to analyze plants defective in P sensing for effects on chloroplast gene expression, to address one aspect of how adaptation is integrated throughout the organism. Our new data show that P deprivation reduces cpRNA decay rates in vivo in a PNPasedependent manner, suggesting that PNPase is part of an organismal P limitation response chain that includes the chloroplast. As an essential component of macromolecules, P availability often limits plant growth, and particularly impacts photosynthesis. Although plants have evolved sophisticated scavenging mechanisms these have yet to be exploited, hence P is the most important fertilizer input for crop plants. cpRNA metabolism was found to be regulated by P concentrations through a global sensing pathway in which PNPase is a central player. In addition several additional discoveries were revealed during the course of this research program. The human mitochondria PNPase was explored and a possible role in maintaining mitochondria homeostasis was outlined. As polyadenylation was found to be a common mechanism that is present in almost all organisms, the few examples of organisms that metabolize RNA with no polyadenylation were analyzed and described. Our experiment shaded new insights into how nutrient stress signals affect yield by influencing photosynthesis and other chloroplast processes, suggesting strategies for improving agriculturally-important plants or plants with novel introduced traits. Our studies illuminated the poorly understood linkage of chloroplast gene expression to environmental influences other than light quality and quantity. Finely, our finding significantly advanced the knowledge about polyadenylation of RNA, the evolution of this process and its function in different organisms including bacteria, archaea, chloroplasts, mitochondria and the eukaryotic cell. These new insights into chloroplast gene regulation will ultimately support plant improvement for agriculture

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Blumwald, Eduardo, and Avi Sadka. Sugar and Acid Homeostasis in Citrus Fruit. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7697109.bard.

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Citrus fruit quality standards have been determined empirically, depending on species and on the particular growing regions. In general, the TSS (total soluble solids) to total acidity (TA) ratio determines whether citrus fruit can be marketed. Soluble sugars account for most of the TSS during harvest while TA is determined almost solely by the citric acid content, which reaches levels of 1-5% by weight in many cultivated varieties. Acid and sugar homeostasis in the fruit is critical for the management of existing cultivars, the development of new cultivars, the improvement of pre- and post-harvest strategies and the control of fruit quality and disorders. The current proposal (a continuation of a previous proposal) aimed at: (1) completing the citrus fruit proteome and metabolome, and establish a citrus fruit functional database, (2) further characterization of the control of fruit acidity by studying the regulation of key steps affecting citrate metabolism, and determine the fate of citrate during acid decline stage, and (3) Studying acid and sugar homeostasis in citrus fruits by characterizing transport mechanisms across membranes. These aims were completed as the following: (1) Our initial efforts were aimed at the characterization and identification of citric acid transporters in citrus juice cells. The identification of citrate transporters at the vacuole of the citrus juice cell indicated that the steady-state citrate cytosolic concentration and the action of the cytosolic aconitase were key elements in establishing the pH homeostat in the cell that regulates the metabolic shift towards carbon usage in the fruit during the later stages of fruit development. We focused on the action of aconitase, the enzyme mediating the metabolic use of citric acid in the cells, and identified processes that control carbon fluxes in developing citrus fruits that control the fruit acid load; (2) The regulation of aconitase, catalyzing a key step in citrate metabolism, was further characterized by using two inhibitors, citramalte and oxalomalte. These compounds significantly increased citrate content and reduced the enzyme’s activity. Metabolite profiling and changes of amino-acid metabolizing enzymes in oxalomalate- treated cells suggested that the increase in citrate, caused by aconitase inhibition, induces amino acid synthesis and the GABA shunt, in accordance with the suggested fate of citrate during the acid decline stage in citrus fruit. (3) We have placed a considerable amount of time on the development of a citrus fruit proteome that will serve to identify all of the proteins in the juice cells and will also serve as an aid to the genomics efforts of the citrus research community (validating the annotation of the fruit genes and the different ESTs). Initially, we identified more than 2,500 specific fruit proteins and were able to assign a function to more than 2,100 proteins (Katz et al., 2007). We have now developed a novel Differential Quantitative LC-MS/MS Proteomics Methodology for the identification and quantitation of key biochemical pathways in fruits (Katz et al., 2010) and applied this methodology to identify determinants of key traits for fruit quality (Katz et al., 2011). We built “biosynthesis maps” that will aid in defining key pathways associated with the development of key fruit quality traits. In addition, we constructed iCitrus (http://wiki.bioinformatics.ucdavis.edu/index.php/ICitrus), a “functional database” that is essentially a web interface to a look-up table that allows users to use functional annotations in the web to identify poorly annotated citrus proteins. This resource will serve as a tool for growers and field extension specialists.

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Kornbluth, Sally. Metabolic Regulation of Ovarian Cancer Cell Death. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada570124.

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Kornbluth, Sally. Metabolic Regulation of Ovarian Cancer Cell Death. Fort Belvoir, VA: Defense Technical Information Center, July 2013. http://dx.doi.org/10.21236/ada597625.

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Lers, Amnon, E. Lomaniec, S. Burd, A. Khalchitski, L. Canetti, and Pamela J. Green. Analysis of Senescence Inducible Ribonuclease in Tomato: Gene Regulation and Function. United States Department of Agriculture, February 2000. http://dx.doi.org/10.32747/2000.7570563.bard.

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Natural leaf senescence has a negative influence on yield. Postharvest induced senescence contributes to the losses of quality in flowers, foliage, and vegetables. Strategies designed to control the senescence process in crop plants could therefore have great applied significance. Senescence is regulated by differential gene expression yet, functional characterization of the genes specifically induced and study of their expression control, is still in its infancy. Study of senescence-specific genes is required to allow identification of regulatory elements participating in senescence-induced expression and thus provide insights into the genetic regulation of senescence. A main feature of senescence is the hydrolysis of macromolecules by hydrolases of various types such as RNases and proteases. This study was aimed a analysis of senescence-inducible RNases in tomato with the following objectives: Isolation of senescence-inducible RNase cDNA clones; Expression analyses of RNase genes during senescence; Identification of sequences required for senescence-induced gene expression; Functional analyses of senescence-inducible RNases. We narrowed our aims somewhat to focus on the first three objectives because the budget we were awarded was reduced from that requested. We have expanded our research for identification senescence-related RNase/nuclease activities as we thought it will direct us to new RNase/nuclease genes. We have also carried out research in Arabidopsis and parsley, which enabled us to draw mire general conclusions. We completed the first and second objectives and have made considerable progress on the remaining two. We have defined growth conditions suitable for this research and defined the physiological and biochemical parameters characteristic to the advance of leaf senescence. In tomato and arabidopsis we have focused on natural leaf senescence. Parsley was used mainly for study of postharvest senescence in detached leaves. We have identified a 41-kD a tomato nuclease, LeNUCI, specifically induced during senescence which can degrade both RNA and DNA. This activity could be induced by ethylene in young leaves and was subjected to detailed analysis, which enabled its classification as Nuclease I enzyme. LeNUCI may be involved in nucleic acid metabolism during tomato leaf senescence. In parsley senescing leaves we identified 2 main senescence-related nuclease activities of 41 and 39-kDa. These activities were induced in both naturally or artificially senescing leaves, could degrade both DNA and RNA and were very similar in their characteristics to the LeNUCI. Two senescence-induced RNase cDNAs were cloned from tomato. One RNase cDNA was identical to the tomato LX RNase while the second corresponded to the LE RNase. Both were demonstrated before to be induced following phosphate starvation of tomato cell culture but nothing was known about their expression or function in plants. LX gene expression was much more senescence specific and ethylene could activate it in detached young leaves. LE gene expression, which could be transiently induced by wounding, appeared to be activated by abscisic acid. We suggest that the LX RNase has a role in RNA catabolism in the final stage of senescence, and LE may be a defense-related protein. Transgenic plants were generated for altering LX gene expression. No major visible alterations in the phenotype were observed so far. Detailed analysis of senescence in these plants is performed currently. The LX promoter was cloned and its analysis is performed currently for identification of senescence-specific regulatory elements. In Arabidopsis we have identified and characterized a senescence-associated nuclease 1 gene, BFN1, which is highly expressed during leaf and stem senescence. BFN1, is the first example of a senescence- associated gene encoding a nuclease I enzyme as well as the first nuclease I cloned and characterized from Arabidopsis. Our progress should provide excellent tools for the continued analysis of regulation and function of senescence-inducible ribonucleases and nucleases in plants. The cloned genes can be used in reverse genetic approaches, already initiated, which can yield a more direct evidence for the function of these enzymes. Another contribution of this research will be in respect to the molecular mechanism, which controls senescence. We had already initiated in this project and will continue to identify and characterize regulatory elements involved in senescence-specific expression of the genes isolated in this work.

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