Relevant bibliographies by topics / RNA metabolism

Academic literature on the topic 'RNA metabolism'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 July 2024

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Journal articles on the topic "RNA metabolism"

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Stern, David B., Michel Goldschmidt-Clermont, and Maureen R. Hanson. "Chloroplast RNA Metabolism." Annual Review of Plant Biology 61, no. 1 (June 2, 2010): 125–55. http://dx.doi.org/10.1146/annurev-arplant-042809-112242.

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Riddihough, Guy. "RNA Methylation and Metabolism." Science 339, no. 6119 (January 31, 2013): 490.4–491. http://dx.doi.org/10.1126/science.339.6119.490-d.

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Volkening, Kathryn, and Michael J. Strong. "RNA Metabolism in Neurodegenerative Disease." Current Chemical Biology 5, no. 2 (May 1, 2011): 90–98. http://dx.doi.org/10.2174/2212796811105020090.

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Liu, Elaine Y., Christopher P. Cali, and Edward B. Lee. "RNA metabolism in neurodegenerative disease." Disease Models & Mechanisms 10, no. 5 (May 1, 2017): 509–18. http://dx.doi.org/10.1242/dmm.028613.

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Mao, Steve. "RNA modification meets immune metabolism." Science 365, no. 6458 (September 12, 2019): 1131.15–1133. http://dx.doi.org/10.1126/science.365.6458.1131-o.

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Hammani, Kamel, and Philippe Giegé. "RNA metabolism in plant mitochondria." Trends in Plant Science 19, no. 6 (June 2014): 380–89. http://dx.doi.org/10.1016/j.tplants.2013.12.008.

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Ramachandran, Vanitharani, and Xuemei Chen. "Small RNA metabolism in Arabidopsis." Trends in Plant Science 13, no. 7 (July 2008): 368–74. http://dx.doi.org/10.1016/j.tplants.2008.03.008.

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Gao, Fen-Biao, and J. Paul Taylor. "RNA metabolism in neurological disease." Brain Research 1584 (October 2014): 1–2. http://dx.doi.org/10.1016/j.brainres.2014.09.011.

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Houston, Stephanie. "lnc(RNA)-ing myeloid metabolism." Nature Immunology 24, no. 9 (August 21, 2023): 1396. http://dx.doi.org/10.1038/s41590-023-01615-w.

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Chatterjee, Biswanath, Che-Kun James Shen, and Pritha Majumder. "RNA Modifications and RNA Metabolism in Neurological Disease Pathogenesis." International Journal of Molecular Sciences 22, no. 21 (November 1, 2021): 11870. http://dx.doi.org/10.3390/ijms222111870.

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The intrinsic cellular heterogeneity and molecular complexity of the mammalian nervous system relies substantially on the dynamic nature and spatiotemporal patterning of gene expression. These features of gene expression are achieved in part through mechanisms involving various epigenetic processes such as DNA methylation, post-translational histone modifications, and non-coding RNA activity, amongst others. In concert, another regulatory layer by which RNA bases and sugar residues are chemically modified enhances neuronal transcriptome complexity. Similar RNA modifications in other systems collectively constitute the cellular epitranscriptome that integrates and impacts various physiological processes. The epitranscriptome is dynamic and is reshaped constantly to regulate vital processes such as development, differentiation and stress responses. Perturbations of the epitranscriptome can lead to various pathogenic conditions, including cancer, cardiovascular abnormalities and neurological diseases. Recent advances in next-generation sequencing technologies have enabled us to identify and locate modified bases/sugars on different RNA species. These RNA modifications modulate the stability, transport and, most importantly, translation of RNA. In this review, we discuss the formation and functions of some frequently observed RNA modifications—including methylations of adenine and cytosine bases, and isomerization of uridine to pseudouridine—at various layers of RNA metabolism, together with their contributions to abnormal physiological conditions that can lead to various neurodevelopmental and neurological disorders.
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Dissertations / Theses on the topic "RNA metabolism"

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Stoppel, Rhea. "Chloroplast RNA metabolism." Diss., lmu, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-152718.

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Conrad, Heather Miller. "Nuclear and mitochondrial mutations affecting mitochondrial RNA metabolism." Connect to resource, 1987. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1230739011.

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Waters, Margaret Fiona. "Enzymes of RNA metabolism in Nostoc sp. MAC." Thesis, University of Liverpool, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.329409.

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LOFFREDA, ALESSIA. "RNA Metabolism alteration in amyotrophic lateral sclerosis models." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2014. http://hdl.handle.net/10281/81488.

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Project1: Unraveling the impact of microRNA on Amyotrophic Lateral Sclerosis pathogenesis. Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease that specifically affects upper and lower motor neurons leading to progressive paralysis and death. There is currently no effective treatment. Thus, identification of the signaling pathways and cellular mediators of ALS remains a major challenge in the search for novel therapeutics. Recent studies have shown that microRNA have a significant impact on normal CNS development and onset and progression of neurological disorders. Based on this evidence, in this study we test the hypothesis that misregulation of miRNA expression play a role in the pathogenesis of ALS. Hence, we exploited human neuroblastoma cell lines expressing SOD(G93A) mutation as tools to investigate the role of miRNAs in familiar ALS. To this end, we initially checked the key molecules involved in miRNAs biogenesis and processing on these cells and we found a different protein expression pattern. Subsequently, we performed a genome-wide scale miRNA expression, using whole-genome small RNA deep-sequencing followed by quantitative real time validation (qPCR). This strategy allowed us to find a small group of up and down regulated miRNA, which are predicted to play a role in the motorneurons physiology and pathology. We measured this group of misregulated miRNA by qPCR on cDNA derived from (G93A) mice at different stage of disease and furthermore on cDNA derived from lymphocytes from a group of sporadic ALS patients. We found that mir-129-5p was up-regulated in cells, mice and in patients and we validated that HuD as mir129-5p target. It has been reported that ELAVL4/HuD plays a role in neuronal plasticity, in recovery from axonal injury and multiple neurological diseases. Furthermore, we generated stable cell line overespressing mir129-5p and we found a reduction in neurite outgrowth and in the expression of differentiation markers in compare to control cells. Taken together these data strongly suggest that microRNAs play a role in ALS pathogenesis and in particular that mir129-5p can affect neuronal plasticity by modulating ELAVL4/HuD level. Project 2: FUS/TLS depletion leads an impairment of cell proliferation and DNA Damage Response. FUS/TLS (fused in sarcoma/translocated in liposarcoma) protein, a ubiquitously expressed RNA-binding protein, has been linked to a variety of cellular processes, such as RNA metabolism, microRNA biogenesis and DNA repair. However, the precise role of FUS protein remains unclear. Recently, FUS has been linked to Amyotrophic Lateral Sclerosis (ALS), a neurodegenerative disorder characterized by the dysfunction and death of motor neurons. Based on the observation that some mutations in the FUS gene induce cytoplasmic accumulation of FUS aggregates, we decided to explore a loss-of-function hypothesis (i.e. inhibition of FUS’ nuclear function) to unravel the role of this protein. To this purpose, we generated a SH-SY5Y human neuroblastoma cell line which expresses a doxycycline induced shRNA targeting FUS and that specifically depletes the protein. In order to characterize this cell line we performed growth proliferation and survival assays. From these experiments emerged that FUS-depleted cells display alterations in cell proliferation. In order to explain this observation, we tested different hypothesis (e.g. apoptosis, senescence or slow-down growth). We observed that FUS-depleted cells growth slower than control cells. Based on the notion that FUS interacts with the miRNA processing proteins (Morlando et al. 2012), to explain this phenotype, we looked at miRNAs expression and we found an up-regulation of mir-7. Interestingly, this up-regulation is also observed in cells that express the ALS-linked FUS R521C mutation. Finally, since an increasing number of work correlated FUS with DNA damage and repair we explored the effects of DNA damage in FUS-depleted cells by monitoring important components of DNA Damage Response (DDR). We found that FUS depletion had an effect on the initial level of DNA damage by inducing the phosphorylation of H2AX in basal condition and that it delayed DSB repair when acute DNA damage occurs. Interestingly, genotoxic treatment resulted in changes in the subcellular localization of FUS in normal cells. We are currently exploring on one hand the mechanism by which FUS depletion leads to DNA damage, and on the other the functional significance of FUS relocalization after genotoxic stress. Taken together, these studies may contribute to the knowledge of the role of FUS in these cellular processes and will allow us to draw a clearer picture of mechanisms of neurodegenerative diseases.
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Miller, Harvey. "The metabolism of tRNAAspargine in the friend erthroleukemia cell /." Thesis, McGill University, 1992. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=60725.

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I have measured the metabolism of tRNA$ sp{ rm Asn}$ in Friend cells undergoing erythroid differentiation, using an assay exploiting the tRNA$ sp{ rm Asn}$ gene's ability to specifically hybridize tRNA$ sp{ rm Asn}$. The concentrations of tRNA$ sp{ rm Asn}$ measured as a proportion of the total tRNA population (relative concentration) decreased until day 3 post-induction, and then increased on day 4. The relative concentrations of tRNA$ sp{ rm Asn}$ are influenced by tRNA$ sp{ rm Asn}$ having lower turnover rate in comparison to the total tRNA population, and by the relative rate that labelled, newly synthesized tRNA$ sp{ rm Asn}$ accumulates in vivo. The rate of tRNA$ sp{ rm Asn}$ synthesis in nuclei isolated from Friend cells at different times during differentiation also fluctuates. This fluctuation may reflect changes in RNA polymerase III activity in these isolated nuclei.
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Bird, Gregory A. "Exploring the roles of the RNA Polymerase II CTD in pre-MRNA metabolism /." Connect to full text at ProQuest Digital Dissertations. IP filtered, 2005.

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Thesis (Ph.D. in Molecular Biology) -- University of Colorado at Denver and Health Sciences Center, 2005.
Typescript. Includes bibliographical references (leaves 130-152). Free to UCDHSC affiliates. Online version available via ProQuest Digital Dissertations;
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Goulet, Isabelle. "New Roles for Arginine Methylation in RNA Metabolism and Cancer." Thèse, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/20293.

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Because it can expand the range of a protein’s interactions or modulate its activity, post-translational methylation of arginine residues in proteins must be duly coordinated and ‘decoded’ to ensure appropriate cellular interpretation of this biological cue. This can be achieved through modulation of the enzymatic activity/specificity of the protein arginine methyltransferases (PRMTs) and proper recognition of the methylation ‘mark’ by a subset of proteins containing ‘methyl-sensing’ protein modules known as ‘Tudor’ domains. In order to gain a better understanding of these regulatory mechanisms, we undertook a detailed biochemical characterization of the predominant member of the PRMT family, PRMT1, and of the novel Tudor domain-containing protein 3 (TDRD3). First, we found that PRMT1 function can be modulated by 1) the expression of up to seven PRMT1 isoforms (v1-7), each with a unique N-terminal region that confers distinct substrate specificity, and by 2) differential subcellular localization, as revealed by the presence of a nuclear export sequence unique to PRMT1v2. Second, our findings suggest that TDRD3 is recruited to cytoplasmic stress granules (SGs) in response to environmental stress potentially by engaging in methyl-dependent protein-protein interactions with proteins involved in the control of gene expression. We also found that arginine methylation may serve as a general regulator of overall SG dynamics. Finally, we uncovered that alteration of PRMT1, TDRD3, and global arginine methylation levels in breast cancer cells may be closely associated with disease progression and poor prognosis. Therefore, further studies into the pathophysiological consequences ensuing from misregulation of arginine methylation will likely lead to the development of novel strategies for the prevention and treatment of breast cancer.
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Hong, Lingzi. "Act1-Mediated RNA Metabolism in IL-17-Driven Inflammatory Diseases." Case Western Reserve University School of Graduate Studies / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=case162673878106271.

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Smith, Richard Wilson. "RNA metabolism and the control of protein synthesis in fish." Thesis, University of Aberdeen, 1996. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU089891.

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This thesis examines the regulation of protein synthesis by pre - translational events; with particular reference to the means by which RNA is able to reduce the energetic cost of protein synthesis. Protein synthesis was measured by the application of a "flooding dose" of 3H-phenylalnine. Protein synthesis rates are then calculated from the "free intracellular" and "protein bound" specific radioactivity (dpm nmole-1 phenylalanine). A similar approach was used to investigate RNA synthesis: i.e. a flooding dose of 3H-uridine. As with protein synthesis RNA synthesis rates was assessed by the relating precursor and product (uridine nucleotide and RNA) radioactivity. Oxygen consumption was measured by monitoring the decline in partial pressure in calibrated respirometery chambers. In fish cells protein synthesis was regulated in terms of the amount (ie the "capacity" for protein synthesis) and the translational efficiency of the RNA. Translationally efficient RNA equated to RNA with an increased turnover. In order to minimise RNA production costs, rapidly synthesised RNA places more reliance on the salvage of exogenous nucleosides, as opposed to the relatively expensive alternative of intracellular synthesis. During yolk sac larval development of the African wels (Clarius gariepinus) protein synthesis rates decline whilst oxygen consumption and the amount of RNA (relative to protein) remains constant. Thus the increasing protein synthesis costs resulted from a reduction in RNA translational efficiency. This was mirrored by a declining RNA synthesis rate. Larval fish growth is primarily due to the repartitioning of yolk sac proteins since early life history stages are thought unable to sustain rapid rates of protein turnover. This pre - translational strategy optimises growth and regulates protein synthesis; whilst, at the same time maintaining the capacity for protein synthesis in anticipation of exogenous feeding.
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Benbahouche, Nour el Houda. "Investigating the role of extended CBC complexes in RNA metabolism." Thesis, Montpellier, 2015. http://www.theses.fr/2015MONTS002.

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Le CBC intervient dans de nombreuses étapes du métabolisme des ARN, telle que l’épissage, la maturation de l’extrémité 3’, la dégradation, l’export et la traduction. Ainsi, le CBC constitue un complexe majeur qui peut orchestrer les différentes étapes de maturation des ARN. Récemment, nous avons identifié le complexe CBCAP, composé de CBC, ARS2 et PHAX. Nous avons montré que la protéine ARS2 stimule la formation des extrémités 3’ de plusieurs familles d’ARN dont les snARN. De plus, ARS2 stimule le recrutement de PHAX sur le CBC. Ainsi, nous proposons un modèle où CBC-ARS2 stimule la formation de l’extrémité 3’ des pré-snARN et recrute PHAX pour favoriser leur export. Une autre étude a identifié un autre complexe le CBCN, constitué de CBC, Ars2, et de ZC3H18-NEXT au lieu de PHAX. CBCN recrute l’exosome et stimule la dégradation de certains ARN, comme les PROMPTS et les transcrits «read-through » des snARN et des ARNm d’histone. Ainsi, PHAX et ZC3H18 destinent leur ARN cibles vers l’export ou la dégradation. Il a été montré que PHAX reconnait et lie spécialement les ARN de petite taille. D’une manière remarquable, nos données de CLIP-Seq et de RIP suivie par des analyses avec des puces « All genes » montrent que PHAX lie aussi d’autres familles d’ARN. En effet, PHAX lie les ARNm ainsi que des ARN non-codant avec une légère préférence pour les snARN (en comparaison avec ZC3H18). Afin de mieux comprendre le rôle de PHAX et ZC3H18, j’ai tout d’abord démontré si les deux protéines se lient simultanément au CBC. Pour ce faire, J’ai réalisé des tests de compétitions entre PHAX et ZC3H18, in vivo, et j’ai montré que la surexpression de ZC3H18 déplace PHAX du CBC et vice versa. Puis en utilisant la technique de « Tethering Assays » j’ai pu montrer que PHAX et ZC3H18 ont des effets opposés sur la biogénèse des ARNm. De plus PHAX semble avoir un effet positif sur la maturation des ARNm et ce, en empêchant ZC3H18 et l’exosome d’être recruter. Nous avons aussi montré que la déplétion de PHAX et ZC3H18 a des conséquences fonctionnelles sur le taux des formes matures des snARN. Dans le but de caractériser la protéine ZC3H18, j’ai réalisé un crible double-hybride et j’ai montré que ZC3H18 interagit avec plusieurs facteurs d’épissage. J’ai aussi identifié les domaines de ZC3H18 impliqués dans ses différentes interactions. D’une manière intéressante, l’interaction de ZC3H18 avec certains facteurs d’épissage peut être exclusive à son interaction avec NEXT. De plus, des expériences de protéomique réalisés sur un des facteurs d’épissage trouvé dans le crible, montrent qu’il co-purifie au sein d’un complexe qui pourrait faire le lien entre la coiffe et la machinerie d’épissage. En accord avec ces résultats, nos données de RNA-seq montrent que la déplétion de ZC3H18 engendre un défaut d’épissage pour des introns qui sont proches de la coiffe et ceci pour un nombre restreint de gènes. Ainsi, notre travail décode davantage le rôle de la coiffe dans les différentes étapes de maturation des ARN et suggère un modèle où la séquence des transcrits naissant stimule la formation d’un complexe spécifique à cet ARN parmi plusieurs autres
The cap binding complex (CBC) plays a key role in a number of gene expression pathways and has been proposed to participate in the discrimination of RNA families. It also enhances many RNA processing steps, including transcription, splicing, 3’end formation, degradation, export and translation.Recently, we identified the CBCAP complex, composed of CBC, Ars2 and PHAX. We showed that Ars2 stimulates snRNA 3'-end processing as well as PHAX binding to the CBC, hence coupling snRNA maturation with their export. Other studies showed that the CBC and ARS2 can form another complex that contains ZC3H18-NEXT instead of PHAX. This complex, named CBCN, is a cofactor of the RNA exosome and is involved in the degradation of cryptic RNAs such as PROMPTs and read-through transcripts at histone and snRNA genes. Thus, PHAX and ZC3H18 target specific families of capped RNA toward either export or degradation. Previous studies proposed that PHAX binds specifically to small RNAs and discriminates them over other RNA species. Surprisingly, our CLIP-Seq and RIP-microarrays data showed that in contrast to expectations, PHAX was not specific for snRNAs. It also binds mRNAs as well as other non-coding RNAs and has a weak preference for snRNAs comparing to ZC3H18. To better understand the role of PHAX and ZC3H18, Ifirst determined whether PHAX and ZC3H18 can bind simultaneously to the CBC. Competitive LUMIER IPs indicated that binding of these proteins is mutually exclusive. I then used tethering assays and could show that PHAX and ZC3H18 have opposite effect on mRNA biogenesis. These data go against a model where binding of PHAX or ZC3H18 discriminate RNA families, and instead suggest promiscuous binding for these proteins. In addition, PHAX may exert a positive effect on mRNA processing by preventing binding of ZC3H18 and recruitment of the RNA exosome. Last but not least, our RT-QPCR data show that PHAX and ZC3H18 depletions have functional consequences on the level of mature snRNA, and this is due to a competition between both proteins which occur on those snRNA read-through transcripts.To further explore the role of ZC3H18, I performed a two-hybrid screen and identified several splicing factors. I could validate these interactions, identify the domains involved and show that binding of some of these factors is exclusive with that of NEXT. Importantly, proteomic experiments with one of these factors identified a complex that makes the link between the cap and the splicing machinery. In agreement, RNA-Seq analysis of ZC3H18 knock-down cells showed alterations in splicing of cap-proximal introns, for a small set of genes.Altogether, this work reveals how the multiple roles of the RNA cap are achieved at the biochemical level, and suggests that the nascent RNA sequence triggers formation of one among several mutually exclusive complexes
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Books on the topic "RNA metabolism"

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Cruz-Reyes, Jorge, and Michael W. Gray, eds. RNA Metabolism in Mitochondria. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-78190-7.

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Bindereif, Albrecht, ed. RNA Metabolism in Trypanosomes. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-28687-2.

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Sattler, Rita, and Christopher J. Donnelly, eds. RNA Metabolism in Neurodegenerative Diseases. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-89689-2.

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B, Harford Joe, and Morris David R. 1939-, eds. mRNA metabolism & post-transcriptional gene regulation. New York: Wiley-Liss, 1997.

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Rabinovich, Peter M. Synthetic messenger RNA and cell metabolism modulation: Methods and protocols. New York: Humana Press, 2013.

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service), SpringerLink (Online, ed. RNA Exosome. New York, NY: Landes Bioscience and Springer Science+Business Media, LLC, 2010.

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Rabinovich, Peter M., ed. Synthetic Messenger RNA and Cell Metabolism Modulation. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-260-5.

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Clouet-d'Orval, Béatrice, ed. RNA Metabolism and Gene Expression in Archaea. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-65795-0.

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Malik, Saiqa Balagh. Investigations into RNA metabolism in critical illness. Roehampton: University of Surrey Roehampton, 2002.

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R, Schoenberg Daniel, ed. mRNA processing and metabolism: Methods and protocols. Totowa, N.J: Humana Press, 2004.

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Book chapters on the topic "RNA metabolism"

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Chen, Xuemei. "MicroRNA Metabolism in Plants." In RNA Interference, 117–36. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-75157-1_6.

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Saavedra, Francisco, Ekaterina Boyarchuk, Francisca Alvarez, Geneviève Almouzni, and Alejandra Loyola. "Metabolic Deregulations Affecting Chromatin Architecture: One-Carbon Metabolism and Krebs Cycle Impact Histone Methylation." In RNA Technologies, 573–606. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-14792-1_23.

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Drakulic, Srdja, Jorge Cuellar, and Rui Sousa. "The Mitochondrial Transcription Machinery." In RNA Metabolism in Mitochondria, 1–15. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-78190-7_1.

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Freyer, Christoph, Paula Clemente, and Anna Wredenberg. "Mitochondrial RNA Turnover in Metazoa." In RNA Metabolism in Mitochondria, 17–46. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-78190-7_2.

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Saoji, Maithili, and Rachel T. Cox. "Mitochondrial RNase P Complex in Animals: Mitochondrial tRNA Processing and Links to Disease." In RNA Metabolism in Mitochondria, 47–71. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-78190-7_3.

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Weber-Lotfi, Frédérique, and André Dietrich. "Intercompartment RNA Trafficking in Mitochondrial Function and Communication." In RNA Metabolism in Mitochondria, 73–123. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-78190-7_4.

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Cruz-Reyes, Jorge, Blaine H. M. Mooers, Vikas Kumar, Pawan K. Doharey, Joshua Meehan, and Luenn Chaparro. "Control Mechanisms of the Holo-Editosome in Trypanosomes." In RNA Metabolism in Mitochondria, 125–44. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-78190-7_5.

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Faktorová, Drahomíra, Matus Valach, Binnypreet Kaur, Gertraud Burger, and Julius Lukeš. "Mitochondrial RNA Editing and Processing in Diplonemid Protists." In RNA Metabolism in Mitochondria, 145–76. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-78190-7_6.

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Dodbele, Samantha, Jane E. Jackman, and Michael W. Gray. "Mechanisms and Evolution of tRNA 5′-Editing in Mitochondria." In RNA Metabolism in Mitochondria, 177–98. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-78190-7_7.

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Houtz, Jillian, Nicole Cremona, and Jonatha M. Gott. "Editing of Mitochondrial RNAs in Physarum polycephalum." In RNA Metabolism in Mitochondria, 199–222. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-78190-7_8.

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Conference papers on the topic "RNA metabolism"

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Daleffi, Natalia Soriani, Marcella Pecora Milazzotto, and Fernanda Nascimento Almeida. "Modeling and Implementation of a Web Database for RNA-Seq of Bovine Embryonic Cells." In Brazilian e-Science Workshop. Sociedade Brasileira de Computação - SBC, 2023. http://dx.doi.org/10.5753/bresci.2023.234243.

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This paper aims to develop a dedicated RNA-Seq database for bovine embryos, generated to gain insights into reproductive metabolism. The data is categorized into three groups, each obtained from distinct experiments. The primary objective is to streamline data analysis through a platform, named TranscriptomicsSeqDB, which standardizes and organizes RNA-Seq information from the Laboratory of Embryonic Metabolism and Epigenetics at UFABC, São Paulo, Brazil. Apart from data storage and management, TranscriptomicsSeqDB provides a user-friendly search interface with predefined queries to facilitate gene-specific indicator analysis.
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El-fadl, Rihab, Nasser Rizk, Amena Fadel, and Abdelrahman El Gamal. "The Profile of Hepatic Gene Expression of Glucose Metabolism in Mice on High Fat Diet." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0213.

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Obesity is a growing problem worldwide, and recent data indicated that 20% of the populations would be obese. Obesity arises as a multifactorial disease caused by inherited traits that interact with lifestyle factors such as diet and physical activity. The liver plays an essential role in the gluco-regulation via regulating glucose, lipid and protein metabolism. The process of glucose metabolism is controlled by a range of molecular mechanisms and genes which affect the metabolism of the liver during intake of high fat diet (HFD). The objective of this research is to investigate the profile of hepatic gene expression of glucose metabolism in mice on HFD treated with leptin (5 mg/kg BW Ip injection). Ten wild type CD1 mice fed on HFD is used for this study, where groups are control (vehicle - leptin) and test group (vehicle + leptin). Body weight (BW) was measured, and blood chemistry, insulin and leptin were measured at the end of the experiments. Total RNA was isolated from the liver tissue, and RTPCR profiler array technology was used to evaluate the mRNA expression of 84 essential genes of hepatic glucose metabolism. The data of the BW and blood chemistry are not significantly different between the two groups. Leptin treatment enhanced the metabolic pathways and the candidate genes of the different metabolic pathway; glycogen metabolism such as Gys1, Gys2 and Pygm, pentose phosphate shunt such as Rpia and suppressed the glycolysis such as Aldob, and TCA cycle such as Mdh1b. In conclusion, this study has shown that leptin could affect the profile of the hepatic mouse genes of glucose metabolism in the early stages of HFD to induce obesity
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3

Cetin-Atalay, R., K. W. D. Shin, T. Cho, A. Y. Meliton, J. Szafran, P. S. Woods, K. Sun, O. R. Shamaa, G. M. Mutlu, and R. B. Hamanaka. "Mitochondrial one Carbon Metabolism Regulates RNA Methylation in Human Lung Fibroblasts." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a2610.

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Blanco, Fernando F., Mahsa Zarei, Jonathan R. Brody, Laszlo G. Boros, and Jordan M. Winter. "Abstract 1191: The RNA binding protein, HuR, regulates pancreatic cancer cell metabolism." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1191.

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5

Redis, Roxana S., Cristina Ivan, Luz Vela, Weiqin Lu, Cristian Rodriguez-Aguayo, Andre LB Ambrosio, Sandra M. Gomes Dias, Ioana Berindan-Neagoe, and George A. Calin. "Abstract 2871: Allele-specific modulation of cancer metabolism by a long noncoding RNA." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2871.

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Lu, Y., E. Zhang, M. Guo, X. Zhao, M. Adam, N. Gupta, E. J. A. Kopras, et al. "Single Cell RNA Sequencing Identifies Aberrant Sphingolipid Metabolism and Actions in Pulmonary Lymphangioleiomyomatosis." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1214.

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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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Wang, Qian (Kevin), Michelle van Geldermalsen, Angel Pang, Blake Zhang, and Jeff Holst. "Abstract A036: Blocking DNA and RNA synthesis by targeting glutamine metabolism in prostate cancer." In Abstracts: AACR Special Conference: Prostate Cancer: Advances in Basic, Translational, and Clinical Research; December 2-5, 2017; Orlando, Florida. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.prca2017-a036.

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Wang, Ling-Yu, Chiu-Lien Hung, Yen-Ling Yu, Hongwu Chen, Shiv Srivastava, Gyorgy Petrovics, and Hsing-Jien Kung. "Abstract B16: A novel long non-coding RNA connects c-Myc to tumor metabolism." In Abstracts: AACR Special Conference on Myc: From Biology to Therapy; January 7-10, 2015; La Jolla, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3125.myc15-b16.

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Singatulina, A. S., M. V. Sukhanova, and O. I. Lavrik. "FACTOR HPF1 REGULATES THE ACTIVITY OF POLY(ADP-RIBOSE)POLYMERASES 1 AND 2 AND THE FORMATION OF POLY(ADP-RIBOSE)-CONTAINING COMPARTMENTS WITH THE PARTICIPATION OF THE RNA-BINDING PROTEIN FUS." In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-281.

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Poly(ADP-ribose) polymerases 1 and 2 (PARP1/2) synthesize poly(ADP-ribose) (PAR) by covalently modifying a number of proteins involved in DNA/RNA metabolism, including themselves. PARP1/2 are key regulators of DNA repair via autopoly(ADP-ribosyl)ation at the site of DNA damage. The study of factors that modulate PARP1/2 activity in response to genotoxic stress is an important task in modern biology.
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Reports on the topic "RNA metabolism"

1

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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Stern, David, and Gadi Schuster. Manipulating Chloroplast Gene Expression: A Genetic and Mechanistic Analysis of Processes that Control RNA Stability. United States Department of Agriculture, June 2004. http://dx.doi.org/10.32747/2004.7586541.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 BARD-funded research dealt with the 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 exoribo-nuclease/polymerase polynucleotide phosphorylase (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. During the funding period, new insights emerged into the molecular mechanism of RNA metabolism in the chloroplast and cyanobacteria, suggesting strategies for improving agriculturally-important plants or plants with novel introduced traits.
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Whitham, Steven A., Amit Gal-On, and Tzahi Arazi. Functional analysis of virus and host components that mediate potyvirus-induced diseases. United States Department of Agriculture, March 2008. http://dx.doi.org/10.32747/2008.7591732.bard.

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The mechanisms underlying the development of symptoms in response to virus infection remain to be discovered in plants. Insight into symptoms induced by potyviruses comes from evidence implicating the potyviral HC-Pro protein in symptom development. In particular, recent studies link the development of symptoms in infected plants to HC-Pro's ability to interfere with small RNA metabolism and function in plant hosts. Moreover, mutation of the highly conserved FRNK amino acid motif to FINK in the HC-Pro of Zucchini yellow mosaic virus (ZYMV) converts a severe strain into an asymptomatic strain, but does not affect virus accumulation in cucurbit hosts. The ability of this FINK mutation to uncouple symptoms from virus accumulation creates a unique opportunity to study symptom etiology, which is usually confounded by simultaneous attenuation of both symptoms and virus accumulation. Our goal was to determine how mutations in the conserved FRNK motif affect host responses to potyvirus infection in cucurbits and Arabidopsis thaliana. Our first objective was to define those amino acids in the FRNK motif that are required for symptoms by mutating the FRNK motif in ZYMV and Turnip mosaic virus (TuMV). Symptom expression and accumulation of resulting mutant viruses in cucurbits and Arabidopsis was determined. Our second objective was to identify plant genes associated with virus disease symptoms by profiling gene expression in cucurbits and Arabidopsis in response to mutant and wild type ZYMV and TuMV, respectively. Genes from the two host species that are differentially expressed led us to focus on a subset of genes that are expected to be involved in symptom expression. Our third objective was to determine the functions of small RNA species in response to mutant and wild type HC-Pro protein expression by monitoring the accumulation of small RNAs and their targets in Arabidopsis and cucurbit plants infected with wild type and mutant TuMV and ZYMV, respectively. We have found that the maintenance of the charge of the amino acids in the FRNK motif of HC-Pro is required for symptom expression. Reduced charge (FRNA, FRNL) lessen virus symptoms, and maintain the suppression of RNA silencing. The FRNK motif is involved in binding of small RNA species including microRNAs (miRNA) and short interfering RNAs (siRNA). This binding activity mediated by the FRNK motif has a role in protecting the viral genome from degradation by the host RNA silencing system. However, it also provides a mechanism by which the FRNK motif participates in inducing the symptoms of viral infection. Small RNA species, such as miRNA and siRNA, can regulate the functions of plant genes that affect plant growth and development. Thus, this binding activity suggests a mechanism by which ZYMVHC-Pro can interfere with plant development resulting in disease symptoms. Because the host genes regulated by small RNAs are known, we have identified candidate host genes that are expected to play a role in symptoms when their regulation is disrupted during viral infections. As a result of this work, we have a better understanding of the FRNK amino acid motif of HC-Pro and its contribution to the functions of HC-Pro, and we have identified plant genes that potentially contribute to symptoms of virus infected plants when their expression becomes misregulated during potyviral infections. The results set the stage to establish the roles of specific host genes in viral pathogenicity. The potential benefits include the development of novel strategies for controlling diseases caused by viruses, methods to ensure stable expression of transgenes in genetically improved crops, and improved potyvirus vectors for expression of proteins or peptides in plants.
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Sionov, Edward, Nancy Keller, and Shiri Barad-Kotler. Mechanisms governing the global regulation of mycotoxin production and pathogenicity by Penicillium expansum in postharvest fruits. United States Department of Agriculture, January 2017. http://dx.doi.org/10.32747/2017.7604292.bard.

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The original objectives of the study, as defined in the approved proposal, are: To characterize the relationship of CreA and LaeA in regulation of P T production To understand how PacC modulates P. expansumpathogenicity on apples To examine if other secondary metabolites are involved in virulence or P. expansumfitness To identify the signaling pathways leading to PAT synthesis Penicilliumexpansum, the causal agent of blue mould rot, is a critical health concern because of the production of the mycotoxinpatulin (PAT) in colonized apple fruit tissue. Although PAT is produced by many Penicilliumspecies, the factors activating its biosynthesis were not clear. This research focused on host and fungal mechanisms of activation of LaeA (the global regulator of secondary metabolism), PacC (the global pH modulator) and CreA (the global carbon catabolite regulator) on PAT synthesis with intention to establish P. expansumas the model system for understanding mycotoxin synthesis in fruits. The overall goal of this proposal is to identify critical host and pathogen factors that mechanistically modulate P. expansumgenes and pathways to control activation of PAT production and virulence in host. Several fungal factors have been correlated with disease development in apples, including the production of PAT, acidification of apple tissue by the fungus, sugar content and the global regulator of secondary metabolism and development, LaeA. An increase in sucrose molarity in the culture medium from 15 to 175 mM negatively regulated laeAexpression and PAT accumulation, but, conversely, increased creAexpression, leading to the hypothesis that CreA could be involved in P. expansumPAT biosynthesis and virulence, possibly through the negative regulation of LaeA. We found evidence for CreAtranscriptional regulation of laeA, but this was not correlated with PAT production either in vitro or in vivo, thus suggesting that CreA regulation of PAT is independent of LaeA. Our finding that sucrose, a key ingredient of apple fruit, regulates PAT synthesis, probably through suppression of laeAexpression, suggests a potential interaction between CreA and LaeA, which may offer control therapies for future study. We have also identified that in addition to PAT gene cluster, CreA regulates other secondary metabolite clusters, including citrinin, andrastin, roquefortine and communesins, during pathogenesis or during normal fungal growth. Following creation of P. expansumpacCknockout strain, we investigated the involvement of the global pH regulator PacC in fungal pathogenicity. We demonstrated that disruption of the pH signaling transcription factor PacC significantly decreased the virulence of P. expansumon deciduous fruits. This phenotype is associated with an impairment in fungal growth, decreased accumulation of gluconic acid and reduced synthesis of pectolytic enzymes. We showed that glucose oxidase- encoding gene, which is essential for gluconic acid production and acidification during fruit colonization, was significantly down regulated in the ΔPepacCmutant, suggesting that gox is PacC- responsive gene. We have provided evidence that deletion of goxgene in P. expansumled to a reduction in virulence toward apple fruits, further indicating that GOX is a virulence factor of P. expansum, and its expression is regulated by PacC. It is also clear from the present data that PacC in P. expansumis a key factor for the biosynthesis of secondary metabolites, such as PAT. On the basis of RNA-sequencing (RNA-seq) analysis and physiological experimentation, the P. expansumΔlaeA, ΔcreAand ΔpacCmutants were unable to successfully colonize apples for a multitude of potential mechanisms including, on the pathogen side, a decreased ability to produce proteolytic enzymes and to acidify the environment and impaired carbon/nitrogen metabolism and, on the host side, an increase in the oxidative defence pathways. Our study defines these global regulatory factors and their downstream signalling pathways as promising targets for the development of strategies to fight against this post-harvest pathogen.
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Porat, Ron, Gregory T. McCollum, Amnon Lers, and Charles L. Guy. Identification and characterization of genes involved in the acquisition of chilling tolerance in citrus fruit. United States Department of Agriculture, December 2007. http://dx.doi.org/10.32747/2007.7587727.bard.

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Citrus, like many other tropical and subtropical fruit are sensitive to chilling temperatures. However, application of a pre-storage temperature conditioning (CD) treatment at 16°C for 7 d or of a hot water brushing (HWB) treatment at 60°C for 20 sec remarkably enhances chilling tolerance and reduces the development of chilling injuries (CI) upon storage at 5°C. In the current research, we proposed to identify and characterize grapefruit genes that are induced by CD, and may contribute to the acquisition of fruit chilling tolerance, by two different molecular approaches: cDNA array analysis and PCR cDNA subtraction. In addition, following the recent development and commercialization of the new Affymetrix Citrus Genome Array, we further performed genome-wide transcript profiling analysis following exposure to CD and chilling treatments. To conduct the cDNA array analysis, we constructed cDNA libraries from the peel tissue of CD- and HWB-treated grapefruit, and performed an EST sequencing project including sequencing of 3,456 cDNAs from each library. Based on the obtained sequence information, we chose 70 stress-responsive and chilling-related genes and spotted them on nylon membranes. Following hybridization the constructed cDNA arrays with RNA probes from control and CD-treated fruit and detailed confirmations by RT-PCR analysis, we found that six genes: lipid-transfer protein, metallothionein-like protein, catalase, GTP-binding protein, Lea5, and stress-responsive zinc finger protein, showed higher transcript levels in flavedo of conditioned than in non-conditioned fruit stored at 5 ᵒC. The transcript levels of another four genes: galactinol synthase, ACC oxidase, temperature-induced lipocalin, and chilling-inducible oxygenase, increased only in control untreated fruit but not in chilling-tolerant CD-treated fruit. By PCR cDNA subtraction analysis we identified 17 new chilling-responsive and HWB- and CD-induced genes. Overall, characterization of the expression patterns of these genes as well as of 11 more stress-related genes by RNA gel blot hybridizations revealed that the HWB treatment activated mainly the expression of stress-related genes(HSP19-I, HSP19-II, dehydrin, universal stress protein, EIN2, 1,3;4-β-D-glucanase, and SOD), whereas the CD treatment activated mainly the expression of lipid modification enzymes, including fatty acid disaturase2 (FAD2) and lipid transfer protein (LTP). Genome wide transcriptional profiling analysis using the newly developed Affymetrix Citrus GeneChip® microarray (including 30,171 citrus probe sets) revealed the identification of three different chilling-related regulons: 1,345 probe sets were significantly affected by chilling in both control and CD-treated fruits (chilling-response regulon), 509 probe sets were unique to the CD-treated fruits (chilling tolerance regulon), and 417 probe sets were unique to the chilling-sensitive control fruits (chilling stress regulon). Overall, exposure to chilling led to expression governed arrest of general cellular metabolic activity, including concretive down-regulation of cell wall, pathogen defense, photosynthesis, respiration, and protein, nucleic acid and secondary metabolism. On the other hand, chilling enhanced various adaptation processes, such as changes in the expression levels of transcripts related to membranes, lipid, sterol and carbohydrate metabolism, stress stimuli, hormone biosynthesis, and modifications in DNA binding and transcription factors.
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6

Wolf, Shmuel, and William J. Lucas. Involvement of the TMV-MP in the Control of Carbon Metabolism and Partitioning in Transgenic Plants. United States Department of Agriculture, October 1999. http://dx.doi.org/10.32747/1999.7570560.bard.

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The function of the 30-kilodalton movement protein (MP) of tobacco mosaic virus (TMV) is to facilitate cell-to-cell movement of viral progeny in infected plants. Our earlier findings have indicated that this protein has a direct effect on plasmodesmal function. In addition, these studies demonstrated that constitutive expression of the TMV MP gene (under the control of the CaMV 35S promoter) in transgenic tobacco plants significantly affects carbon metabolism in source leaves and alters the biomass distribution between the various plant organs. The long-term goal of the proposed research was to better understand the factors controlling carbon translocation in plants. The specific objectives were: A) To introduce into tobacco and potato plants a virally-encoded (TMV-MP) gene that affects plasmodesmal functioning and photosynthate partitioning under tissue-specific promoters. B) To introduce into tobacco and potato plants the TMV-MP gene under the control of promoters which are tightly repressed by the Tn10-encoded Tet repressor, to enable the expression of the protein by external application of tetracycline. C) To explore the mechanism by which the TMV-MP interacts with the endogenous control o~ carbon allocation. Data obtained in our previous project together with the results of this current study established that the TMV-MP has pleiotropic effects when expressed in transgenic tobacco plants. In addition to its ability to increase the plasmodesmal size exclusion limit, it alters carbohydrate metabolism in source leaves and dry matter partitioning between the various plant organs, Expression of the TMV-MP in various tissues of transgenic potato plants indicated that sugars and starch levels in source leaves are reduced below those of control plants when the TMV-MP is expressed in green tissue only. However, when the TMV-MP was expressed predominantly in PP and CC, sugar and starch levels were raised above those of control plants. Perhaps the most significant result obtained from experiments performed on transgenic potato plants was the discovery that the influence of the TMV-MP on carbohydrate allocation within source leaves was under developmental control and was exerted only during tuber development. The complexity of the mode by which the TMV-MP exerts its effect on the process of carbohydrate allocation was further demonstrated when transgenic tobacco plants were subjected to environmental stresses such as drought stress and nutrients deficiencies, Collectively, these studies indicated that the influence of the TMV-MP on carbon allocation L the result of protein-protein interaction within the source tissue. Based on these results, together with the findings that plasmodesmata potentiate the cell-to-cell trafficking of viral and endogenous proteins and nucleoproteins complexes, we developed the theme that at the whole plant level, the phloem serves as an information superhighway. Such a long-distance communication system may utilize a new class of signaling molecules (proteins and/or RNA) to co-ordinate photosynthesis and carbon/nitrogen metabolism in source leaves with the complex growth requirements of the plant under the prevailing environmental conditions. The discovery that expression of viral MP in plants can induce precise changes in carbon metabolism and photoassimilate allocation, now provide a conceptual foundation for future studies aimed at elucidating the communication network responsible for integrating photosynthetic productivity with resource allocation at the whole-plant level. Such information will surely provide an understanding of how plants coordinate the essential physiological functions performed by distantly-separated organs. Identification of the proteins involved in mediating and controlling cell-to-cell transport, especially at the companion cell-sieve element boundary, will provide an important first step towards achieving this goal.
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7

Dudareva, Natalia, Alexander Vainstein, Eran Pichersky, and David Weiss. Integrating biochemical and genomic approaches to elucidate C6-C2 volatile production: improvement of floral scent and fruit aroma. United States Department of Agriculture, September 2007. http://dx.doi.org/10.32747/2007.7696514.bard.

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The specific objectives of approved proposal include to: 1. Elucidate the C6-C2 biochemical pathways leading to the biosynthesis of phenylacetaldehyde, phenylethyl alcohol and phenylethyl acetate in floral tissues of ornamentally important plants, pefunia and roses. 2. Isolate and characterrze genes responsible for the production of these C6-C2 compounds and those involved in the regulation of the pathway using genomic and transcriptomic tools. 3. Determine whether altering the expression of key genes of this pathway can result in changing the aroma characteristics of flowers. Aldehydes are intermediates in a variety of biochemical pathways including those involved in the metabolism of carbohydrates, vitamins, steroids, amino acids, benzylisoquinoline alkaloids, hormones, and lipids. In plants they are also synthesized in response to environmental stresses such as salinity, cold, and heat shock or as flavors and aromas in fruits and flowers. Phenylacetaldehyde along with 2-phenylethanol and its acetate ester, are important scent compounds in numerous flowers, including petunias and roses. However, little is known about the biosynthesis of these volatile compounds in plants. We have shown that the formation PHA and 2-phenylethanol from Phe does not occur via trans-cinnamic acid and instead competes with the key enzyme of phenypropanoid metabolism Pheammonia-lyase (PAL) for Phe utilization. Using functional genomic approach and comparative gene expression profiling, we have isolated and characterized a novel enzyme from petunia and rose flowers that catalyzes the formation of the Ca-Czcompound phenylacetaldehyde (PHA) from L-phenylalanine (Phe) by the removal of both the carboxyl and amino groups. This enzyme, designated as phenylacetaldehyde synthases (PAAS), is a bifunctional enzyme that catalyzes the unprecedented efficient coupling of phenylalanine decarboxylation to oxidation, generating phenylacetaldehyde, CO2, ammonia, and hydrogen peroxide in stoichiometric amounts. Down-regulation of PAAS expression via RNA interference-based (RNAi) technology in petunia resulted in no PHA emission when compared with controls. These plants also produced no 2-phenylethanol, supporting our conclusion that PHA is a precursor of 2-phenylethanol. To understand the regulation of scent formation in plants we have also generated transgenic petunia and tobacco plants expressing the rose alcohol acetyltransferase (RhAAT) gene under the control of a CaMV-35S promoter. Although the preferred substrate of RhAAT in vitro is geraniol, in transgenic petunia flowers, it used phenylethyl alcohol and benzyl alcohol to produce the corresponding acetate esters, not generated by control flowers. These results strongly point to the dependence of volatile production on substrate availability. Analysis of the diurnal regulation of scent production in rose flowers revealed that although the daily emission of most scent compounds is synchronized, various independently evolved mechanisms control the production, accumulation and release of different volatiles. This research resulted in a fundamental discovery of biochemical pathway, enzymes and genes involved in biosynthesis of C6-C2s compounds, and provided the knowledge for future engineering plants for improved scent quality.
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Or, Etti, David Galbraith, and Anne Fennell. Exploring mechanisms involved in grape bud dormancy: Large-scale analysis of expression reprogramming following controlled dormancy induction and dormancy release. United States Department of Agriculture, December 2002. http://dx.doi.org/10.32747/2002.7587232.bard.

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The timing of dormancy induction and release is very important to the economic production of table grape. Advances in manipulation of dormancy induction and dormancy release are dependent on the establishment of a comprehensive understanding of biological mechanisms involved in bud dormancy. To gain insight into these mechanisms we initiated the research that had two main objectives: A. Analyzing the expression profiles of large subsets of genes, following controlled dormancy induction and dormancy release, and assessing the role of known metabolic pathways, known regulatory genes and novel sequences involved in these processes B. Comparing expression profiles following the perception of various artificial as well as natural signals known to induce dormancy release, and searching for gene showing similar expression patterns, as candidates for further study of pathways having potential to play a central role in dormancy release. We first created targeted EST collections from V. vinifera and V. riparia mature buds. Clones were randomly selected from cDNA libraries prepared following controlled dormancy release and controlled dormancy induction and from respective controls. The entire collection (7920 vinifera and 1194 riparia clones) was sequenced and subjected to bioinformatics analysis, including clustering, annotations and GO classifications. PCR products from the entire collection were used for printing of cDNA microarrays. Bud tissue in general, and the dormant bud in particular, are under-represented within the grape EST database. Accordingly, 59% of the our vinifera EST collection, composed of 5516 unigenes, are not included within the current Vitis TIGR collection and about 22% of these transcripts bear no resemblance to any known plant transcript, corroborating the current need for our targeted EST collection and the bud specific cDNA array. Analysis of the V. riparia sequences yielded 814 unigenes, of which 140 are unique (keilin et al., manuscript, Appendix B). Results from computational expression profiling of the vinifera collection suggest that oxidative stress, calcium signaling, intracellular vesicle trafficking and anaerobic mode of carbohydrate metabolism play a role in the regulation and execution of grape-bud dormancy release. A comprehensive analysis confirmed the induction of transcription from several calcium–signaling related genes following HC treatment, and detected an inhibiting effect of calcium channel blocker and calcium chelator on HC-induced and chilling-induced bud break. It also detected the existence of HC-induced and calcium dependent protein phosphorylation activity. These data suggest, for the first time, that calcium signaling is involved in the mechanism of dormancy release (Pang et al., in preparation). We compared the effects of heat shock (HS) to those detected in buds following HC application and found that HS lead to earlier and higher bud break. We also demonstrated similar temporary reduction in catalase expression and temporary induction of ascorbate peroxidase, glutathione reductase, thioredoxin and glutathione S transferase expression following both treatments. These findings further support the assumption that temporary oxidative stress is part of the mechanism leading to bud break. The temporary induction of sucrose syntase, pyruvate decarboxylase and alcohol dehydrogenase indicate that temporary respiratory stress is developed and suggest that mitochondrial function may be of central importance for that mechanism. These finding, suggesting triggering of identical mechanisms by HS and HC, justified the comparison of expression profiles of HC and HS treated buds, as a tool for the identification of pathways with a central role in dormancy release (Halaly et al., in preparation). RNA samples from buds treated with HS, HC and water were hybridized with the cDNA arrays in an interconnected loop design. Differentially expressed genes from the were selected using R-language package from Bioconductor project called LIMMA and clones showing a significant change following both HS and HC treatments, compared to control, were selected for further analysis. A total of 1541 clones show significant induction, of which 37% have no hit or unknown function and the rest represent 661 genes with identified function. Similarly, out of 1452 clones showing significant reduction, only 53% of the clones have identified function and they represent 573 genes. The 661 induced genes are involved in 445 different molecular functions. About 90% of those functions were classified to 20 categories based on careful survey of the literature. Among other things, it appears that carbohydrate metabolism and mitochondrial function may be of central importance in the mechanism of dormancy release and studies in this direction are ongoing. Analysis of the reduced function is ongoing (Appendix A). A second set of hybridizations was carried out with RNA samples from buds exposed to short photoperiod, leading to induction of bud dormancy, and long photoperiod treatment, as control. Analysis indicated that 42 genes were significant difference between LD and SD and 11 of these were unique.
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Meagher, Richard B. Mechanisms and Determinants of RNA Turnover: Plant IRESs and Polycistrons for Metabolic Engineering. Office of Scientific and Technical Information (OSTI), August 2002. http://dx.doi.org/10.2172/835024.

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Ostersetzer-Biran, Oren, and Alice Barkan. Nuclear Encoded RNA Splicing Factors in Plant Mitochondria. United States Department of Agriculture, February 2009. http://dx.doi.org/10.32747/2009.7592111.bard.

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Mitochondria are the site of respiration and numerous other metabolic processes required for plant growth and development. Increased demands for metabolic energy are observed during different stages in the plants life cycle, but are particularly ample during germination and reproductive organ development. These activities are dependent upon the tight regulation of the expression and accumulation of various organellar proteins. Plant mitochondria contain their own genomes (mtDNA), which encode for a small number of genes required in organellar genome expression and respiration. Yet, the vast majority of the organellar proteins are encoded by nuclear genes, thus necessitating complex mechanisms to coordinate the expression and accumulation of proteins encoded by the two remote genomes. Many organellar genes are interrupted by intervening sequences (introns), which are removed from the primary presequences via splicing. According to conserved features of their sequences these introns are all classified as “group-II”. Their splicing is necessary for organellar activity and is dependent upon nuclear-encoded RNA-binding cofactors. However, to-date, only a tiny fraction of the proteins expected to be involved in these activities have been identified. Accordingly, this project aimed to identify nuclear-encoded proteins required for mitochondrial RNA splicing in plants, and to analyze their specific roles in the splicing of group-II intron RNAs. In non-plant systems, group-II intron splicing is mediated by proteins encoded within the introns themselves, known as maturases, which act specifically in the splicing of the introns in which they are encoded. Only one mitochondrial intron in plants has retained its maturaseORF (matR), but its roles in organellar intron splicing are unknown. Clues to other proteins required for organellar intron splicing are scarce, but these are likely encoded in the nucleus as there are no other obvious candidates among the remaining ORFs within the mtDNA. Through genetic screens in maize, the Barkan lab identified numerous nuclear genes that are required for the splicing of many of the introns within the plastid genome. Several of these genes are related to one another (i.e. crs1, caf1, caf2, and cfm2) in that they share a previously uncharacterized domain of archaeal origin, the CRM domain. The Arabidopsis genome contains 16 CRM-related genes, which contain between one and four repeats of the domain. Several of these are predicted to the mitochondria and are thus postulated to act in the splicing of group-II introns in the organelle(s) to which they are localized. In addition, plant genomes also harbor several genes that are closely related to group-II intron-encoded maturases (nMats), which exist in the nucleus as 'self-standing' ORFs, out of the context of their cognate "host" group-II introns and are predicted to reside within the mitochondria. The similarity with known group-II intron splicing factors identified in other systems and their predicted localization to mitochondria in plants suggest that nuclear-encoded CRM and nMat related proteins may function in the splicing of mitochondrial-encoded introns. In this proposal we proposed to (i) establish the intracellular locations of several CRM and nMat proteins; (ii) to test whether mutations in their genes impairs the splicing of mitochondrial introns; and to (iii) determine whether these proteins are bound to the mitochondrial introns in vivo.
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