Готові списки джерел за темами / Transcription mechanism

Добірка наукової літератури з теми "Transcription mechanism"

Автор: Grafiati
Опубліковано: 7 липня 2024
Оновлено: 7 липня 2024

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Зміст

  1. Статті в журналах
  2. Дисертації
  3. Книги
  4. Частини книг
  5. Тези доповідей конференцій
  6. Звіти організацій

Статті в журналах з теми "Transcription mechanism":

1

Sui, Zhiyuan, Yongjie Zhang, Zhishuai Zhang, Chenguang Wang, Xiaojun Li, Feng Xing, and Mingxing Chu. "Analysis of Lin28B Promoter Activity and Screening of Related Transcription Factors in Dolang Sheep." Genes 14, no. 5 (May 7, 2023): 1049. http://dx.doi.org/10.3390/genes14051049.

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The Lin28B gene is involved in the initiation of puberty, but its regulatory mechanisms remain unclear. Therefore, in this study, we aimed to study the regulatory mechanism of the Lin28B promoter by cloning the Lin28B proximal promoter for bioinformatic analysis. Next, a series of deletion vectors were constructed based on the bioinformatic analysis results for dual-fluorescein activity detection. The transcriptional regulation mechanism of the Lin28B promoter region was analyzed by detecting mutations in transcription factor-binding sites and overexpression of transcription factors. The dual-luciferase assay showed that the Lin28B promoter region −837 to −338 bp had the highest transcriptional activity, and the transcriptional activity of the Lin28B transcriptional regulatory region decreased significantly after Egr1 and SP1 mutations. Overexpression of the Egr1 transcription factor significantly enhanced the transcription of Lin28B, and the results indicated that Egr1 and SP1 play important roles in regulating Lin28B. These results provide a theoretical basis for further research on the transcriptional regulation of sheep Lin28B during puberty initiation.
2

HANDA, HIROSHI. "Mechanism of adenovirus transcription." Uirusu 37, no. 2 (1987): 229–40. http://dx.doi.org/10.2222/jsv.37.229.

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3

Basu, Urmimala, Alicia M. Bostwick, Kalyan Das, Kristin E. Dittenhafer-Reed, and Smita S. Patel. "Structure, mechanism, and regulation of mitochondrial DNA transcription initiation." Journal of Biological Chemistry 295, no. 52 (October 30, 2020): 18406–25. http://dx.doi.org/10.1074/jbc.rev120.011202.

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Mitochondria are specialized compartments that produce requisite ATP to fuel cellular functions and serve as centers of metabolite processing, cellular signaling, and apoptosis. To accomplish these roles, mitochondria rely on the genetic information in their small genome (mitochondrial DNA) and the nucleus. A growing appreciation for mitochondria's role in a myriad of human diseases, including inherited genetic disorders, degenerative diseases, inflammation, and cancer, has fueled the study of biochemical mechanisms that control mitochondrial function. The mitochondrial transcriptional machinery is different from nuclear machinery. The in vitro re-constituted transcriptional complexes of Saccharomyces cerevisiae (yeast) and humans, aided with high-resolution structures and biochemical characterizations, have provided a deeper understanding of the mechanism and regulation of mitochondrial DNA transcription. In this review, we will discuss recent advances in the structure and mechanism of mitochondrial transcription initiation. We will follow up with recent discoveries and formative findings regarding the regulatory events that control mitochondrial DNA transcription, focusing on those involved in cross-talk between the mitochondria and nucleus.
4

Xu, Jun, Jenny Chong, and Dong Wang. "Strand-specific effect of Rad26 and TFIIS in rescuing transcriptional arrest by CAG trinucleotide repeat slip-outs." Nucleic Acids Research 49, no. 13 (July 1, 2021): 7618–27. http://dx.doi.org/10.1093/nar/gkab573.

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Abstract Transcription induced CAG repeat instability is associated with fatal neurological disorders. Genetic approaches found transcription-coupled nucleotide excision repair (TC-NER) factor CSB protein and TFIIS play critical roles in modulating the repeat stability. Here, we took advantage of an in vitro reconstituted yeast transcription system to investigate the underlying mechanism of RNA polymerase II (Pol II) transcriptional pausing/stalling by CAG slip-out structures and the functions of TFIIS and Rad26, the yeast ortholog of CSB, in modulating transcriptional arrest. We identified length-dependent and strand-specific mechanisms that account for CAG slip-out induced transcriptional arrest. We found substantial R-loop formation for the distal transcriptional pausing induced by template strand (TS) slip-out, but not non-template strand (NTS) slip-out. In contrast, Pol II backtracking was observed at the proximal transcriptional pausing sites induced by both NTS and TS slip-out blockage. Strikingly, we revealed that Rad26 and TFIIS can stimulate bypass of NTS CAG slip-out, but not TS slip-out induced distal pausing. Our biochemical results provide new insights into understanding the mechanism of CAG slip-out induced transcriptional pausing and functions of transcription factors in modulating transcription-coupled CAG repeat instability, which may pave the way for developing potential strategies for the treatment of repeat sequence associated human diseases.
5

Wang, Yaolai, Jiaming Qi, Jie Shao, and Xu-Qing Tang. "Signaling Mechanism of Transcriptional Bursting: A Technical Resolution-Independent Study." Biology 9, no. 10 (October 19, 2020): 339. http://dx.doi.org/10.3390/biology9100339.

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Gene transcription has been uncovered to occur in sporadic bursts. However, due to technical difficulties in differentiating individual transcription initiation events, it remains debated as to whether the burst size, frequency, or both are subject to modulation by transcriptional activators. Here, to bypass technical constraints, we addressed this issue by introducing two independent theoretical methods including analytical research based on the classic two-model and information entropy research based on the architecture of transcription apparatus. Both methods connect the signaling mechanism of transcriptional bursting to the characteristics of transcriptional uncertainty (i.e., the differences in transcriptional levels of the same genes that are equally activated). By comparing the theoretical predictions with abundant experimental data collected from published papers, the results exclusively support frequency modulation. To further validate this conclusion, we showed that the data that appeared to support size modulation essentially supported frequency modulation taking into account the existence of burst clusters. This work provides a unified scheme that reconciles the debate on burst signaling.
6

Lopez, Alex B., Chuanping Wang, Charlie C. Huang, Ibrahim Yaman, Yi Li, Kaushik Chakravarty, Peter F. Johnson, et al. "A feedback transcriptional mechanism controls the level of the arginine/lysine transporter cat-1 during amino acid starvation." Biochemical Journal 402, no. 1 (January 25, 2007): 163–73. http://dx.doi.org/10.1042/bj20060941.

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The adaptive response to amino acid limitation in mammalian cells inhibits global protein synthesis and promotes the expression of proteins that protect cells from stress. The arginine/lysine transporter, cat-1, is induced during amino acid starvation by transcriptional and post-transcriptional mechanisms. It is shown in the present study that the transient induction of cat-1 transcription is regulated by the stress response pathway that involves phosphorylation of the translation initiation factor, eIF2 (eukaryotic initiation factor-2). This phosphorylation induces expression of the bZIP (basic leucine zipper protein) transcription factors C/EBP (CCAAT/enhancer-binding protein)-β and ATF (activating transcription factor) 4, which in turn induces ATF3. Transfection experiments in control and mutant cells, and chromatin immunoprecipitations showed that ATF4 activates, whereas ATF3 represses cat-1 transcription, via an AARE (amino acid response element), TGATGAAAC, in the first exon of the cat-1 gene, which functions both in the endogenous and in a heterologous promoter. ATF4 and C/EBPβ activated transcription when expressed in transfected cells and they bound as heterodimers to the AARE in vitro. The induction of transcription by ATF4 was inhibited by ATF3, which also bound to the AARE as a heterodimer with C/EBPβ. These results suggest that the transient increase in cat-1 transcription is due to transcriptional activation caused by ATF4 followed by transcriptional repression by ATF3 via a feedback mechanism.
7

Medina, Gerardo, Katy Juárez, Brenda Valderrama, and Gloria Soberón-Chávez. "Mechanism of Pseudomonas aeruginosa RhlR Transcriptional Regulation of the rhlAB Promoter." Journal of Bacteriology 185, no. 20 (October 15, 2003): 5976–83. http://dx.doi.org/10.1128/jb.185.20.5976-5983.2003.

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ABSTRACT Pseudomonas aeruginosa contains two transcription regulators (LasR and RhlR) that, when complexed with their specific autoinducers (3-oxo-dodecanoyl-homoserine lactone and butanoyl-homoserine lactone, respectively) activate transcription of different virulence-associated traits. We studied the RhlR-dependent transcriptional regulation of the rhlAB operon encoding rhamnosyltransferase 1, an enzyme involved in the synthesis of the surfactant monorhamnolipid, and showed that RhlR binds to a specific sequence in the rhlAB regulatory region, both in the presence and in the absence of its autoinducer. Our data suggest that in the former case it activates transcription, whereas in the latter it acts as a transcriptional repressor of this promoter. RhlR seems to repress the transcription of other quorum-sensing-regulated genes; thus, RhlR repressor activity might be of importance in the finely regulated expression of P. aeruginosa virulence-associated traits.
8

Jackson, Kelly A., Ruth A. Valentine, Lisa J. Coneyworth, John C. Mathers, and Dianne Ford. "Mechanisms of mammalian zinc-regulated gene expression." Biochemical Society Transactions 36, no. 6 (November 19, 2008): 1262–66. http://dx.doi.org/10.1042/bst0361262.

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Mechanisms through which gene expression is regulated by zinc are central to cellular zinc homoeostasis. In this context, evidence for the involvement of zinc dyshomoeostasis in the aetiology of diseases, including Type 2 diabetes, Alzheimer's disease and cancer, highlights the importance of zinc-regulated gene expression. Mechanisms elucidated in bacteria and yeast provide examples of different possible modes of zinc-sensitive gene regulation, involving the zinc-regulated binding of transcriptional activators and repressors to gene promoter regions. A mammalian transcriptional regulatory mechanism that mediates zinc-induced transcriptional up-regulation, involving the transcription factor MTF1 (metal-response element-binding transcription factor 1), has been studied extensively. Gene responses in the opposite direction (reduced mRNA levels in response to increased zinc availability) have been observed in mammalian cells, but a specific transcriptional regulatory process responsible for such a response has yet to be identified. Examples of single zinc-sensitive transcription factors regulating gene expression in opposite directions are emerging. Although zinc-induced transcriptional repression by MTF1 is a possible explanation in some specific instances, such a mechanism cannot account for repression by zinc of all mammalian genes that show this mode of regulation, indicating the existence of as yet uncharacterized mechanisms of zinc-regulated transcription in mammalian cells. In addition, recent findings reveal a role for effects of zinc on mRNA stability in the regulation of specific zinc transporters. Our studies on the regulation of the human gene SLC30A5 (solute carrier 30A5), which codes for the zinc transporter ZnT5, have revealed that this gene provides a model system by which to study both zinc-induced transcriptional down-regulation and zinc-regulated mRNA stabilization.
9

Lee, Sang C., Angeliki Magklara, and Catharine L. Smith. "HDAC Activity Is Required for Efficient Core Promoter Function at the Mouse Mammary Tumor Virus Promoter." Journal of Biomedicine and Biotechnology 2011 (2011): 1–14. http://dx.doi.org/10.1155/2011/416905.

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Histone deacetylases (HDACs) have been shown to be required for basal or inducible transcription at a variety of genes by poorly understood mechanisms. We demonstrated previously that HDAC inhibition rapidly repressed transcription from the mouse mammary tumor virus (MMTV) promoter by a mechanism that does not require the binding of upstream transcription factors. In the current study, we find that HDACs work through the core promoter sequences of MMTV as well as those of several cellular genes to facilitate transcriptional initiation through deacetylation of nonhistone proteins.
10

Nudler, E., A. Goldfarb, and M. Kashlev. "Discontinuous mechanism of transcription elongation." Science 265, no. 5173 (August 5, 1994): 793–96. http://dx.doi.org/10.1126/science.8047884.

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Також вас можуть зацікавити розширені добірки на тему "Transcription mechanism" для конкретних типів джерел:
Статті в журналах Дисертації Книги

Дисертації з теми "Transcription mechanism":

1

An, Sungwhan. "Mechanism of coronavirus transcription /." Digital version accessible at:, 1998. http://wwwlib.umi.com/cr/utexas/main.

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2

Ng, King Pan. "The mechanism of the transcription activation mediated by the Ewing sarcoma activation domain /." View abstract or full-text, 2008. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202008%20NG.

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3

Churcher, Mark Jonathan. "Studies on the mechanism of action of Tat." Thesis, Open University, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.359975.

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4

Ignatov, Michael E. "Cis-Acting Elements in Mechanism of HIV-1 Reverse Transcription." Case Western Reserve University School of Graduate Studies / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=case1149088883.

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5

Grably, Melanie R. "Revealing the mechanism of HSP104 transcription initiation in the yeast S.cerevisiae." E-thesis Full text, 2008. http://shemer.mslib.huji.ac.il/dissertations/W/JSL/001444203.pdf.

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6

Cocklin, Simon. "Investigation into the molecular mechanism of nitrogen metabolite repression." Thesis, University of Newcastle Upon Tyne, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327280.

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7

Hegde, Nagaratna Shridhar. "Investigating the molecular mechanism of thiostrepton inhibition of FOXM1 activity." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609983.

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8

Shakya, Arvind. "Mechanism of matrix metalloproteinase expression in atherosclerosis /." Free to MU Campus, others may purchase, 2003. http://wwwlib.umi.com/cr/mo/fullcit?p1418063.

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9

Mukherjee, Pooja. "Study of the co-translational assembly mechanism of transcription complexes in mammalian cells." Thesis, Strasbourg, 2019. http://www.theses.fr/2019STRAJ051.

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La majorité des processus biologiques sont réalisés par des complexes protéiques multisubunités dans les cellules et une quantité importante d'énergie est requise par les cellules pour construire ces énormes complexes. Contrairement aux bactéries, les gènes codant pour les protéines sont dispersés dans le génome des eucaryotes, ce qui complique la compréhension de l'assemblage des complexes protéiques. En utilisant l'immunoprécipitation d'ARN suivie par la détection des ARNm à l'échelle du génome par analyse par micropuce, ARN molécule unique, FISH, immunofluorescence, cellules souches embryonnaires knock-out de souris et approches de permutation de domaines, nous montrons que les complexes de transcription multisubunit de mammifère s'assemblent de manière co-traductionnelle. Nous démontrons que les domaines de dimérisation et leurs positions dans les sous-unités en interaction déterminent la voie d'assemblage de co-traduction (simultanée ou séquentielle). En outre, les expériences cytoplasmiques IF-smFISH et bicolores smFISH indiquent que l'assemblage de co-traduction décrit se produit clairement dans le cytoplasme de cellules humaines. Des résultats identiques dans les cellules de levure, de souris et humaine suggèrent que l'assemblage par co-traduction est un mécanisme général chez les eucaryotes, qui pourrait être nécessaire pour éviter les interactions non spécifiques et l'agrégation de protéines dans la cellule
Majority of the biological processes are carried out by multisubunit protein complexes in cells and a significant amount of energy is required by the cells to build these huge complexes. Unlike bacteria, genes encoding proteins are dispersed in the genome of eukaryotes and this makes the assembly of protein complexes more complicated to understand. By using RNA immunoprecipitation followed by genome-wide detection of mRNAs by microarray analysis, single molecule RNA FISH, immunofluoresence, mouse knock-out embryonic stem cells and domain swapping approaches, we show that the mammalian multisubunit transcription complexes assemble co-translationally. We demonstrate that the dimerization domains and their positions in the interacting subunits determine the co-translational assembly pathway (simultaneous or sequential). Furthermore, cytoplasmic IF-smFISH and two-colour smFISH experiments indicate that the described co-translational assembly is clearly occurring in the cytoplasm of human cells. Identical results in yeast, mouse and human cells suggests that co-translational assembly is a general mechanism in eukaryotes which might be necessary to avoid non-specific interactions and protein aggregation in the cell
10

Rowe-Magnus, Dean Allistair. "The mechanism of transcription activation by the Bacillus subtilis response regulator, Spo0A." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0022/NQ38968.pdf.

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Книги з теми "Transcription mechanism":

1

Tsai, Ming-Jer. Mechanism of steroid hormone regulation of gene transcription. Austin, Tex: R.G. Landes Co., 1994.

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2

Vitiello, Christal Lourdes. Mechanism of Transcription Arrest By The Nun Protein of Bacteriophage HK022. [New York, N.Y.?]: [publisher not identified], 2012.

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3

Landini, Paolo. Mechanism of transcription activation by the Ada protein of Escherichia coli. Birmingham: University of Birmingham, 1999.

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4

Bailey, Elizabeth Jean. The Mechanism of NusG-Mediated Transcription-Translation Coupling and The Role of RacR in Transcription Regulation in Escherichia coli. [New York, N.Y.?]: [publisher not identified], 2019.

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5

Berry, Andrew Edward. Towards a molecular mechanism for light induction of gene transcription in myxococcus xanthus. [s.l.]: typescript, 1997.

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6

de, Kloet E. R., Azmitia Efrain C, Landfield Philip W, and New York Academy of Sciences., eds. Brain corticosteroid receptors: Studies on the mechanism, function, and neurotoxicity of corticosteroid action. New York, N.Y: New York Academy of Sciences, 1994.

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7

Eckstein, Fritz, and David M. J. Lilley, eds. Mechanisms of Transcription. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60691-5.

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8

Cold Spring Harbor Symposia on Quantitative Biology (63nd 1998). Mechanisms of transcription. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory, 1998.

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9

1932-, Eckstein Fritz, and Lilley, David M. J. 1948-, eds. Mechanisms of transcription. Berlin: Springer, 1997.

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10

Courey, Albert J. Mechanisms in transcriptional regulation. Malden, MA: Blackwell Pub., 2008.

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Частини книг з теми "Transcription mechanism":

1

Thomm, Michael. "Transcription: Mechanism and Regulation." In Archaea, 139–57. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555815516.ch6.

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2

Sousa, R. "Fundamental Aspects of T7 RNA Polymerase Structure and Mechanism." In Mechanisms of Transcription, 1–14. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60691-5_1.

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3

Travers, Andrew. "The mechanism of eukaryotic transcription." In DNA-Protein Interactions, 130–57. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1480-6_6.

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4

Muskhelishvili, G., and A. Travers. "Stabilization of DNA Microloops by FIS — A Mechanism for Torsional Transmission in Transcription Activation and DNA Inversion." In Mechanisms of Transcription, 179–90. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60691-5_12.

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5

Orea-Soufi, Alba, David Dávila, María Salazar-Roa, María de Mar Lorente, and Guillermo Velasco. "Phosphorylation of FOXO Proteins as a Key Mechanism to Regulate Their Activity." In FOXO Transcription Factors, 51–59. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8900-3_5.

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6

Baric, Ralph S., Chien Kou Shieh, Stephen A. Stohlman, and Michael M. C. Lai. "Studies into the Mechanism of MHV Transcription." In Coronaviruses, 137–49. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-1280-2_16.

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7

van der Horst, Gijsbertus T. J., Harry van Steeg, Rob J. W. Berg, Kiyoji Tanaka, Errol Friedberg, Dirk Bootsma, and Jan H. J. Hoeijmakers. "Transcription-coupled Repair as a Biodefence Mechanism." In Biodefence Mechanisms Against Environmental Stress, 181–87. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-72082-6_19.

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8

Schaad, Mary C., Wan Chen, Sheila A. Peel, and Ralph S. Baric. "Studies into the Mechanism for MHV Transcription." In Coronaviruses, 85–90. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2996-5_14.

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9

Polosa, Paola Loguercio, Marina Roberti, and Palmiro Cantatore. "Mechanism and Regulation of Mitochondrial Transcription in Animal Cells." In Organelle Genetics, 271–95. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-22380-8_11.

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10

Santero, E., T. Hoover, and S. Kustu. "Mechanism of transcription from nif promoters: involvement of IHF." In Nitrogen Fixation, 459–66. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-6432-0_45.

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Тези доповідей конференцій з теми "Transcription mechanism":

1

Kim, Sehun, Tomoki Hayashi, and Tomoki Toda. "Note-level Automatic Guitar Transcription Using Attention Mechanism." In 2022 30th European Signal Processing Conference (EUSIPCO). IEEE, 2022. http://dx.doi.org/10.23919/eusipco55093.2022.9909659.

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2

Nishikimi, Ryo, Eita Nakamura, Masataka Goto, and Kazuyoshi Yoshii. "End-To-End Melody Note Transcription Based on a Beat-Synchronous Attention Mechanism." In 2019 IEEE Workshop on Applications of Signal Processing to Audio and Acoustics (WASPAA). IEEE, 2019. http://dx.doi.org/10.1109/waspaa.2019.8937207.

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3

Su, Ming, Roberto Mantovani, and Jaro Sodek. "MECHANISM OF NF-Y MEDIATED TRANSCRIPTION OF THE OSTEOPONTIN AND BONE SIALOPROTEIN GENES." In 3rd International Conference on Osteopontin and SIBLING (Small Integrin-Binding Ligand, N-linked Glycoprotein) Proteins, 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.262.

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4

Cheng, Jiandong, Mengdi Xu, Yirong Liu, and Wei Huang. "AttBind: Prediction of Transcription Factor Binding Sites Across Cell-types Based on Attention Mechanism." In 2022 7th International Conference on Computer and Communication Systems (ICCCS). IEEE, 2022. http://dx.doi.org/10.1109/icccs55155.2022.9846215.

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5

Soky, Kak, Sheng Li, Masato Mimura, Chenhui Chu, and Tatsuya Kawahara. "Leveraging Simultaneous Translation for Enhancing Transcription of Low-resource Language via Cross Attention Mechanism." In Interspeech 2022. ISCA: ISCA, 2022. http://dx.doi.org/10.21437/interspeech.2022-343.

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King, Elizabeth M., and Robert Newton. "Dexamethasone-Induced MKP-1 Inhibits MSK1 Phosphorylation: A Mechanism For Inhibition Of NF-?B-Dependent Transcription." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5762.

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7

Nishikimi, Ryo, Eita Nakamura, Satoru Fukayama, Masataka Goto, and Kazuyoshi Yoshii. "Automatic Singing Transcription Based on Encoder-decoder Recurrent Neural Networks with a Weakly-supervised Attention Mechanism." In ICASSP 2019 - 2019 IEEE International Conference on Acoustics, Speech and Signal Processing (ICASSP). IEEE, 2019. http://dx.doi.org/10.1109/icassp.2019.8683024.

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Hong, Samuel, and Xiaodong Cheng. "Abstract PR01: Structural mechanism of sequence-specific 5-methylcytosine (5mC) recognition by AP-1 transcription factors." In Abstracts: AACR Special Conference: Chromatin and Epigenetics in Cancer; September 24-27, 2015; Atlanta, GA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.chromepi15-pr01.

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Mantaj, Julia, Paul J. Jackson, David E. Thurston, and Khondaker Miraz Rahman. "Abstract 5242: Further evidence that the DNA-interactive Pyrrolobenzodiazepine (PBD) Dimer SJG-136 works through a transcription factor inhibition mechanism." 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.am2017-5242.

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Wei, Sung Jen, Thinh H. Nguyen, Dustin G. Mook, Monish R. Makena, Dattesh Verlekar, Ashly Hindle, Gloria Martinez, et al. "Abstract 1293: MYC transcription activation mediated by OCT4 as a mechanism of resistance to 13-cisRA-mediated differentiation in neuroblastoma." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-1293.

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Звіти організацій з теми "Transcription mechanism":

1

Pichersky, Eran, Alexander Vainstein, and Natalia Dudareva. Scent biosynthesis in petunia flowers under normal and adverse environmental conditions. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7699859.bard.

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The ability of flowering plants to prosper throughout evolution, and for many crop plants to set fruit, is strongly dependent on their ability to attract pollinators. To that end many plants synthesize a spectrum of volatile compounds in their flowers. Scent is a highly dynamic trait that is strongly influenced by the environment. However, with high temperature conditions becoming more common, the molecular interplay between this type of stress and scent biosynthesis need to be investigated. Using petunia as a model system, our project had three objectives: (1) Determine the expression patterns of genes encoding biosynthetic scent genes (BSGs) and of several genes previously identified as encoding transcription factors involved in scent regulation under normal and elevated temperature conditions. (2) Examine the function of petunia transcription factors and a heterologous transcription factor, PAPl, in regulating genes of the phenylpropanoid/benzenoid scent pathway. (3) Study the mechanism of transcriptional regulation by several petunia transcription factors and PAPl of scent genes under normal and elevated temperature conditions by examining the interactions between these transcription factors and the promoters of target genes. Our work accomplished the first two goals but was unable to complete the third goal because of lack of time and resources. Our general finding was that when plants grew at higher temperatures (28C day/22C night, vs. 22C/16C), their scent emission decreased in general, with the exception of a few volatiles such as vanillin. To understand why, we looked at gene transcription levels, and saw that generally there was a good correlation between levels of transcriptions of gene specifying enzymes for specific scent compounds and levels of emission of the corresponding scent compounds. Enzyme activity levels, however, showed little difference between plants growing at different temperature regimes. Plants expressing the heterologous gene PAPl showed general increase in scent emission in control temperature conditions but emission decreased at the higher temperature conditions, as seen for control plants. Finally, expression of several transcription factor genes decreased at high temperature, but expression of new transcription factor, EOB-V, increased, implicating it in the decrease of transcription of BSGs. The major conclusion of this work is that high temperature conditions negatively affect scent emission from plants, but that some genetic engineering approaches could ameliorate this problem.
2

Hirschberg, Joseph, and Gloria A. Moore. Molecular Analysis of Carotenoid Biosynthesis in Plants: Characterizing the Genes Psy, Pds and CrtL-e. United States Department of Agriculture, August 1993. http://dx.doi.org/10.32747/1993.7568744.bard.

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In this research we have studied the molecular biology of carotenoid biosynthesis in tomato. The investigations focused on the genes Pds and Psy, encoding desaturase and phytoene synthase, respectively, which are key enzymes in the biosynthetic pathway of lycopene and b-carotene. In addition, we have investigated the genes for lycopene cyclase. We have cloned from tomato and characterized the cDNA of CrtL-e, which encodes the lycopene e-cyclase, and analyzed its expression during fruit development. The results establish a paradigm for the regulation of carotenoid pigment biosynthesis during the ripening process of fruits. It is concluded that transcriptional regulation of genes that encode carotenoid-biosynthesis enzymes is the major mechanism that governs specific pigment accumulation. During the ripening of tomato fruits transcription of the genes encoding the enzymes phytoene synthase and phytoene desaturase is up-regulated, while the transcription of the genes for both lycopene cyclases decreases and thus the conversion of lycopene to subsequent carotenoids is inhibited. These findings support the working hypothesis of the molecular approach to manipulating carotenogenesis by altering gene expression in transgenic plants, and offer obvious strategies to future application in agriculture. The molecular and physiological knowledge on carotenogenesis gained in this project, suggest a concept for manipulating gene expression that will alter carotenoid composition in fruits and flowers.
3

Shaw, John, Arieh Rosner, Thomas Pirone, Benjamin Raccah, and Yehezkiel Antignus. The Role of Specific Viral Genes and Gene Products in Potyviral Pathogenicity, Host Range and Aphid Transmission. United States Department of Agriculture, August 1992. http://dx.doi.org/10.32747/1992.7561070.bard.

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In this research we have studied the molecular biology of carotenoid biosynthesis in tomato. The investigations focused on the genes Pds and Psy, encoding desaturase and phytoene synthase, respectively, which are key enzymes in the biosynthetic pathway of lycopene and b-carotene. In addition, we have investigated the genes for lycopene cyclase. We have cloned from tomato and characterized the cDNA of CrtL-e, which encodes the lycopene e-cyclase, and analyzed its expression during fruit development. The results establish a paradigm for the regulation of carotenoid pigment biosynthesis during the ripening process of fruits. It is concluded that transcriptional regulation of genes that encode carotenoid-biosynthesis enzymes is the major mechanism that governs specific pigment accumulation. During the ripening of tomato fruits transcription of the genes encoding the enzymes phytoene synthase and phytoene desaturase is up-regulated, while the transcription of the genes for both lycopene cyclases decreases and thus the conversion of lycopene to subsequent carotenoids is inhibited. These findings support the working hypothesis of the molecular approach to manipulating carotenogenesis by altering gene expression in transgenic plants, and offer obvious strategies to future application in agriculture. The molecular and physiological knowledge on carotenogenesis gained in this project, suggest a concept for manipulating gene expression that will alter carotenoid composition in fruits and flowers.
4

Fromm, Hillel, Paul Michael Hasegawa, and Aaron Fait. Calcium-regulated Transcription Factors Mediating Carbon Metabolism in Response to Drought. United States Department of Agriculture, June 2013. http://dx.doi.org/10.32747/2013.7699847.bard.

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Original objectives: The long-term goal of the proposed research is to elucidate the transcription factors, genes and metabolic networks involved in carbon metabolism and partitioning in response to water deficit. The proposed research focuses on the GTLcalcium/calmodulinbindingTFs and the gene and metabolic networks modulated by these TFs in Arabidopsis thaliana. The specific objectives are as follows. Objective-1 (USA): Physiological analyses of GTL1 loss- and gain-of-function plants under water sufficient and drought stress conditions Objective 2 (USA / Israel-TAU): Characterizion of GTL target genes and bioinformatic analysis of data to eulcidate gene-network topology. Objective-3 (Israel-TAU): Regulation of GTLmediated transcription by Ca²⁺/calmodulin: mechanism and biological significance. Objective-4 (Israel-BGU): Metabolic networks and carbon partitioning in response to drought. Additional direction: In the course of the project we added another direction, which was reported in the 2nd annual report, to elucidate genes controlling drought avoidance. The TAU team has isolated a few unhydrotropic (hyd) mutants and are in the process of mapping these mutations (of hyd13 and hyd15; see last year's report for a description of these mutants under salt stress) in the Arabidopsis genome by map-based cloning and deep sequencing. For this purpose, each hyd mutant was crossed with a wild type plant of the Landsberg ecotype, and at the F2 stage, 500-700 seedlings showing the unhydrotropic phenotype were collected separately and pooled DNA samples were subkected to the Illumina deep sequencing technology. Bioinformatics were used to identify the exact genomic positions of the mutations (based on a comparison of the genomic sequences of the two Arabidopsis thaliana ecotypes (Columbia and Landsberg). Background: To feed the 9 billion people or more, expected to live on Earth by the mid 21st century, the production of high-quality food must increase substantially. Based on a 2009 Declaration of the World Summit on Food Security, a target of 70% more global food production by the year 2050 was marked, an unprecedented food-production growth rate. Importantly, due to the larger areas of low-yielding land globally, low-yielding environments offer the greatest opportunity for substantial increases in global food production. Nowadays, 70% of the global available water is used by agriculture, and 40% of the world food is produced from irrigated soils. Therefore, much needs to be done towards improving the efficiency of water use by plants, accompanied by increased crop yield production under water-limiting conditions. Major conclusions, solutions and achievements: We established that AtGTL1 (Arabidopsis thaliana GT-2 LIKE1) is a focal determinant in water deficit (drought) signaling and tolerance, and water use efficiency (WUE). The GTL1 transcription factor is an upstream regulator of stomatal development as a transrepressor of AtSDD1, which encodes a subtilisin protease that activates a MAP kinase pathway that negatively regulates stomatal lineage and density. GTL1 binds to the core GT3 cis-element in the SDD1 promoter and transrepresses its expression under water-sufficient conditions. GTL1 loss-of-function mutants have reduced stomatal number and transpiration, and enhanced drought tolerance and WUE. In this case, higher WUE under water sufficient conditions occurs without reduction in absolute biomass accumulation or carbon assimilation, indicating that gtl1-mediated effects on stomatal conductance and transpiration do not substantially affect CO₂ uptake. These results are proof-of-concept that fine-tuned regulation of stomatal density can result in drought tolerance and higher WUE with maintenance of yield stability. Implications: Accomplishments during the IS-4243-09R project provide unique tools for continued discovery research to enhance plant drought tolerance and WUE.
5

Elroy-Stein, Orna, and Dmitry Belostotsky. Mechanism of Internal Initiation of Translation in Plants. United States Department of Agriculture, December 2010. http://dx.doi.org/10.32747/2010.7696518.bard.

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Original objectives Elucidation of PABP's role in crTMV148 IRES function in-vitro using wheat germ extract and krebs-2 cells extract. Fully achieved. Elucidation of PABP's role in crTMV148 IRES function in-vivo in Arabidopsis. Characterization of the physical interactions of PABP and other potential ITAFs with crTMV148 IRES. Partly achieved. To conduct search for additional ITAFs using different approaches and evaluate the candidates. Partly achieved. Background of the topic The power of internal translation via the activity of internal ribosomal entry site (IRES) elements allow coordinated synthesis of multiple gene products from a single transcription unit, and thereby enables to bypass the need for sequential transformation with multiple independent transgenes. The key goal of this project was to identify and analyze the IRES-trans-acting factors (ITAFs) that mediate the activity of a crucifer-infecting tobamovirus (crTMV148) IRES. The remarkable conservation of the IRES activity across the phylogenetic spectrum (yeast, plants and animals) strongly suggests that key ITAFs that mediate its activity are themselves highly conserved. Thus, crTMV148 IRES offers opportunity for elucidation of the fundamental mechanisms underlying internal translation in higher plants in order to enable its rational manipulation for the purpose of agricultural biotechnology. Major conclusions and achievements. - CrTMV IRES requires PABP for maximal activity. This conclusion was achieved by PABP depletion and reconstitution of wheat germ- and Krebs2-derived in-vitro translation assays using Arabidopsis-derived PABP2, 3, 5, 8 and yeast Pab1p. - Mutations in the internal polypurine tract of the IRES decrease the high-affinity binding of all phylogenetically divergent PABPs derived from Arabidopsis and yeast in electro mobility gel shift assays. - Mutations in the internal polypurine tract decrease IRES activity in-vivo. - The 3'-poly(A) tail enhances crTMV148 IRES activity more efficiently in the absence of 5'-methylated cap. - In-vivo assembled RNPs containing proteins specifically associated with the IRES were purified from HEK293 cells using the RNA Affinity in Tandem (RAT) approach followed by their identification by mass spectroscopy. - This study yielded a list of potential protein candidates that may serve as ITAFs of crTMV148 IRES activity, among them are a/b tubulin, a/g actin, GAPDH, enolase 1, ribonuclease/angiogenin inhibitor 1, 26S proteasome subunit p45, rpSA, eEF1Bδ, and proteasome b5 subunit. Implications, both scientific and agriculture. The fact that the 3'-poly(A) tail enhances crTMV148 IRES activity more efficiently in the absence of 5'-methylated cap suggests a potential joint interaction between PABP, the IRES sequence and the 3'-poly(A). This has an important scientific implication related to IRES function in general.
6

Lers, Amnon, and Gan Susheng. Study of the regulatory mechanism involved in dark-induced Postharvest leaf senescence. United States Department of Agriculture, January 2009. http://dx.doi.org/10.32747/2009.7591734.bard.

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Postharvest leaf senescence contributes to quality losses in flowers and leafy vegetables. The general goal of this research project was to investigate the regulatory mechanisms involved in dark-induced leaf senescence. The regulatory system involved in senescence induction and control is highly complex and possibly involves a network of senescence promoting pathways responsible for activation of the senescence-associated genes. Pathways involving different internal signals and environmental factors may have distinctive importance in different leaf senescence systems. Darkness is known to have a role in enhancement of postharvest leaf senescence and for getting an insight into its regulatory mechanism/s we have applied molecular genetics and functional genomics approaches. The original objectives were: 1. Identification of dark-induced SAGs in Arabidopsis using enhancer/promoter trap lines and microarray approaches; 2. Molecular and functional characterization of the identified genes by analyzing their expression and examining the phenotypes in related knockout mutant plants; 3. Initial studies of promoter sequences for selected early dark-induced SAGs. Since genomic studies of senescence, with emphasis on dark-induced senescence, were early-on published which included information on potential regulatory genes we decided to use this new information. This is instead of using the uncharacterized enhancer/promoter trap lines as originally planned. We have also focused on specific relevant genes identified in the two laboratories. Based on the available genomic analyses of leaf senescence 10 candidate genes hypothesized to have a regulatory role in dark-induced senescence were subjected to both expression as well as functional analyses. For most of these genes senescence-specific regulation was confirmed, however, functional analyses using knock-out mutants indicated no consequence to senescence progression. The transcription factor WARK75 was found to be specifically expressed during natural and dark-induced leaf senescence. Functional analysis demonstrated that in detached leaves senescence under darkness was significantly delayed while no phenotypic consequences could be observed on growth and development, including no effect on natural leaf senescence,. Thus, WARKY75 is suggested to have a role in dark-induced senescence, but not in natural senescence. Another regulatory gene identified to have a role in senescence is MKK9 encoding for a Mitogen-Activated Protein Kinase Kinase 9 which is upregulated during senescence in harvested leaves as well as in naturally senescing leaves. MKK9 can specifically phosphorylate another kinase, MPK6. Both knockouts of MKK9 and MPK6 displayed a significantly senescence delay in harvested leaves and possibly function as a phosphorelay that regulates senescence. To our knowledge, this is the first report that clearly demonstrates the involvement of a MAP kinase pathway in senescence. This research not only revealed a new signal transduction pathway, but more important provided significant insights into the regulatory mechanisms underlying senescence in harvested leaves. In an additional line of research we have employed the promoter of the senescence-induced BFN1 gene as a handle for identifying components of the regulatory mechanism. This gene was shown to be activated during darkinduced senescence of detached leaves, as well as natural senescence. This was shown by following protein accumulation and promoter activity which demonstrated that this promoter is activated during dark-induced senescence. Analysis of the promoter established that, at least some of the regulatory sequences reside in an 80 bps long fragment of the promoter. Overall, progress was made in identification of components with a role in dark-induced senescence in this project. Further studies should be done in order to better understand the function of these components and develop approaches for modulating the progress of senescence in crop plants for the benefit of agriculture.
7

Lapidot, Moshe, and Vitaly Citovsky. molecular mechanism for the Tomato yellow leaf curl virus resistance at the ty-5 locus. United States Department of Agriculture, January 2016. http://dx.doi.org/10.32747/2016.7604274.bard.

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Tomato yellow leaf curl virus (TYLCV) is a major pathogen of tomato that causes extensive crop loss worldwide, including the US and Israel. Genetic resistance in the host plant is considered highly effective in the defense against viral infection in the field. Thus, the best way to reduce yield losses due to TYLCV is by breeding tomatoes resistant or tolerant to the virus. To date, only six major TYLCV-resistance loci, termed Ty-1 to Ty-6, have been characterized and mapped to the tomato genome. Among tomato TYLCV-resistant lines containing these loci, we have identified a major recessive quantitative trait locus (QTL) that was mapped to chromosome 4 and designated ty-5. Recently, we identified the gene responsible for the TYLCV resistance at the ty-5 locus as the tomato homolog of the gene encoding messenger RNA surveillance factor Pelota (Pelo). A single amino acid change in the protein is responsible for the resistant phenotype. Pelo is known to participate in the ribosome-recycling phase of protein biosynthesis. Our hypothesis was that the resistant allele of Pelo is a “loss-of-function” mutant, and inhibits or slows-down ribosome recycling. This will negatively affect viral (as well as host-plant) protein synthesis, which may result in slower infection progression. Hence we have proposed the following research objectives: Aim 1: The effect of Pelota on translation of TYLCV proteins: The goal of this objective is to test the effect Pelota may or may not have upon translation of TYLCV proteins following infection of a resistant host. Aim 2: Identify and characterize Pelota cellular localization and interaction with TYLCV proteins: The goal of this objective is to characterize the cellular localization of both Pelota alleles, the TYLCV-resistant and the susceptible allele, to see whether this localization changes following TYLCV infection, and to find out which TYLCV protein interacts with Pelota. Our results demonstrate that upon TYLCV-infection the resistant allele of pelota has a negative effect on viral replication and RNA transcription. It is also shown that pelota interacts with the viral C1 protein, which is the only viral protein essential for TYLCV replication. Following subcellular localization of C1 and Pelota it was found that both protein localize to the same subcellular compartments. This research is innovative and potentially transformative because the role of Peloin plant virus resistance is novel, and understanding its mechanism will lay the foundation for designing new antiviral protection strategies that target translation of viral proteins. BARD Report - Project 4953 Page 2
8

Ohad, Nir, and Robert Fischer. Regulation of Fertilization-Independent Endosperm Development by Polycomb Proteins. United States Department of Agriculture, January 2004. http://dx.doi.org/10.32747/2004.7695869.bard.

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Arabidopsis mutants that we have isolated, encode for fertilization-independent endosperm (fie), fertilization-independent seed2 (fis2) and medea (mea) genes, act in the female gametophyte and allow endosperm to develop without fertilization when mutated. We cloned the FIE and MEA genes and showed that they encode WD and SET domain polycomb (Pc G) proteins, respectively. Homologous proteins of FIE and MEA in other organisms are known to regulate gene transcription by modulating chromatin structure. Based on our results, we proposed a model whereby both FIE and MEA interact to suppress transcription of regulatory genes. These genes are transcribed only at proper developmental stages, as in the central cell of the female gametophyte after fertilization, thus activating endosperm development. To test our model, the following questions were addressed: What is the Composition and Function of the Polycomb Complex? Molecular, biochemical, genetic and genomic approaches were offered to identify members of the complex, analyze their interactions, and understand their function. What is the Temporal and Spatial Pattern of Polycomb Proteins Accumulation? The use of transgenic plants expressing tagged FIE and MEA polypeptides as well as specific antibodies were proposed to localize the endogenous polycomb complex. How is Polycomb Protein Activity Controlled? To understand the molecular mechanism controlling the accumulation of FIE protein, transgenic plants as well as molecular approaches were proposed to determine whether FIE is regulated at the translational or posttranslational levels. The objectives of our research program have been accomplished and the results obtained exceeded our expectation. Our results reveal that fie and mea mutations cause parent-of-origin effects on seed development by distinct mechanisms (Publication 1). Moreover our data show that FIE has additional functions besides controlling the development of the female gametophyte. Using transgenic lines in which FIE was not expressed or the protein level was reduced during different developmental stages enabled us for the first time to explore FIE function during sporophyte development (Publication 2 and 3). Our results are consistent with the hypothesis that FIE, a single copy gene in the Arabidopsis genome, represses multiple developmental pathways (i.e., endosperm, embryogenesis, shot formation and flowering). Furthermore, we identified FIE target genes, including key transcription factors known to promote flowering (AG and LFY) as well as shoot and leaf formation (KNAT1) (Publication 2 and 3), thus demonstrating that in plants, as in mammals and insects, PcG proteins control expression of homeobox genes. Using the Yeast two hybrid system and pull-down assays we demonstrated that FIE protein interact with MEA via the N-terminal region (Publication 1). Moreover, CURLY LEAF protein, an additional member of the SET domain family interacts with FIE as well. The overlapping expression patterns of FIE, with ether MEA or CLF and their common mutant phenotypes, demonstrate the versatility of FIE function. FIE association with different SET domain polycomb proteins, results in differential regulation of gene expression throughout the plant life cycle (Publication 3). In vitro interaction assays we have recently performed demonstrated that FIE interacts with the cell cycle regulatory component Retinobalsoma protein (pRb) (Publication 4). These results illuminate the potential mechanism by which FIE may restrain embryo sac central cell division, at least partly, through interaction with, and suppression of pRb-regulated genes. The results of this program generated new information about the initiation of reproductive development and expanded our understanding of how PcG proteins regulate developmental programs along the plant life cycle. The tools and information obtained in this program will lead to novel strategies which will allow to mange crop plants and to increase crop production.
9

Barash, Itamar, and Robert Rhoads. Translational Mechanisms Governing Milk Protein Levels and Composition. United States Department of Agriculture, 2006. http://dx.doi.org/10.32747/2006.7696526.bard.

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Original objectives: The long-term goal of the research is to achieve higher protein content in the milk of ruminants by modulating the translational apparatus of the mammary gland genetically, nutritionally, or pharmacologically. The short-term objectives are to obtain a better understanding of 1) the role of amino acids (AA) as regulators of translation in bovine and mouse mammary epithelial cells and 2) the mechanism responsible for the synergistic enhancement of milk-protein mRNA polyadenylation by insulin and prolactin. Background of the topic: In many cell types and tissues, individual AA affect a signaling pathway which parallels the insulin pathway to modulate rates and levels of protein synthesis. Diverse nutritional and hormonal conditions are funneled to mTOR, a multidomain serine/threonine kinase that regulates a number of components in the initiation and elongation stages of translation. The mechanism by which AA signal mTOR is largely unknown. During the current grant period, we have studied the effect of essential AA on mechanisms involved in protein synthesis in differentiated mammary epithelial cells cultured under lactogenic conditions. We also studied lactogenic hormone regulation of milk protein synthesis in differentiated mammary epithelial cells. In the first BARD grant (2000-03), we discovered a novel mechanism for mRNA-specific hormone-regulated translation, namely, that the combination of insulin plus prolactin causes cytoplasmic polyadenylation of milk protein mRNAs, which leads to their efficient translation. In the current BARD grant, we have pursued the signaling pathways of this novel hormone action. Major conclusions/solutions/achievements: The positive and negative signaling from AA to the mTOR pathway, combined with modulation of insulin sensitization, mediates the synthesis rates of total and specific milk proteins in mammary epithelial cells. The current in vitro study revealed cryptic negative effects of Lys, His, and Thr on cellular mechanisms regulating translation initiation and protein synthesis in mammary epithelial cells that could not be detected by conventional in vivo analyses. We also showed that a signaling pathway involving Jak2 and Stat5, previously shown to lead from the prolactin receptor to transcription of milk protein genes, is also used for cytoplasmic polyadenylation of milk protein mRNAs, thereby stabilizing these mRNAs and activating them for translation. Implications: In vivo, plasma AA levels are affected by nutritional and hormonal effects as well as by conditions of exercise and stress. The amplitude in plasma AA levels resembles that applied in the current in vitro study. Thus, by changing plasma AA levels in the epithelial cell microenvironment or by sensitizing the mTOR pathway to their presence, it should be possible to modulate the rate of milk protein synthesis. Furthermore, knowledge that phosphorylation of Stat5 is required for enhanced milk protein synthesis in response to lactogenic opens the possibility for pharmacologic approaches to increase the phosphorylation of Stat5 and, thereby, milk protein production.
10

Monteiro, Alvaro. Regulatory Mechanisms in Transcriptional Activation by BRCA1. Fort Belvoir, VA: Defense Technical Information Center, May 2002. http://dx.doi.org/10.21236/ada405483.

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