Academic literature on the topic 'Conflicts between DNA replication and transcription'
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Journal articles on the topic "Conflicts between DNA replication and transcription"
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Saponaro, Marco. "Transcription–Replication Coordination." Life 12, no. 1 (January 13, 2022): 108. http://dx.doi.org/10.3390/life12010108.
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Transcription and replication are the two most essential processes that a cell does with its DNA: they allow cells to express the genomic content that is required for their functions and to create a perfect copy of this genomic information to pass on to the daughter cells. Nevertheless, these two processes are in a constant ambivalent relationship. When transcription and replication occupy the same regions, there is the possibility of conflicts between transcription and replication as transcription can impair DNA replication progression leading to increased DNA damage. Nevertheless, DNA replication origins are preferentially located in open chromatin next to actively transcribed regions, meaning that the possibility of conflicts is potentially an accepted incident for cells. Data in the literature point both towards the existence or not of coordination between these two processes to avoid the danger of collisions. Several reviews have been published on transcription–replication conflicts, but we focus here on the most recent findings that relate to how these two processes are coordinated in eukaryotes, considering advantages and disadvantages from coordination, how likely conflicts are at any given time, and which are their potential hotspots in the genome.
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Million-Weaver, Samuel, Ariana Nakta Samadpour, and Houra Merrikh. "Replication Restart after Replication-Transcription Conflicts Requires RecA in Bacillus subtilis." Journal of Bacteriology 197, no. 14 (May 4, 2015): 2374–82. http://dx.doi.org/10.1128/jb.00237-15.
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ABSTRACTEfficient duplication of genomes depends on reactivation of replication forks outside the origin. Replication restart can be facilitated by recombination proteins, especially if single- or double-strand breaks form in the DNA. Each type of DNA break is processed by a distinct pathway, though both depend on the RecA protein. One common obstacle that can stall forks, potentially leading to breaks in the DNA, is transcription. Though replication stalling by transcription is prevalent, the nature of DNA breaks and the prerequisites for replication restart in response to these encounters remain unknown. Here, we used an engineered site-specific replication-transcription conflict to identify and dissect the pathways required for the resolution and restart of replication forks stalled by transcription inBacillus subtilis. We found that RecA, its loader proteins RecO and AddAB, and the Holliday junction resolvase RecU are required for efficient survival and replication restart after conflicts with transcription. Genetic analyses showed that RecO and AddAB act in parallel to facilitate RecA loading at the site of the conflict but that they can each partially compensate for the other's absence. Finally, we found that RecA and either RecO or AddAB are required for the replication restart and helicase loader protein, DnaD, to associate with the engineered conflict region. These results suggest that conflicts can lead to both single-strand gaps and double-strand breaks in the DNA and that RecA loading and Holliday junction resolution are required for replication restart at regions of replication-transcription conflicts.IMPORTANCEHead-on conflicts between replication and transcription occur when a gene is expressed from the lagging strand. These encounters stall the replisome and potentially break the DNA. We investigated the necessary mechanisms forBacillus subtiliscells to overcome a site-specific engineered conflict with transcription of a protein-coding gene. We found that the recombination proteins RecO and AddAB both load RecA onto the DNA in response to the head-on conflict. Additionally, RecA loading by one of the two pathways was required for both replication restart and efficient survival of the collision. Our findings suggest that both single-strand gaps and double-strand DNA breaks occur at head-on conflict regions and demonstrate a requirement for recombination to restart replication after collisions with transcription.
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RUDOLPH, C., P. DHILLON, T. MOORE, and R. LLOYD. "Avoiding and resolving conflicts between DNA replication and transcription." DNA Repair 6, no. 7 (July 1, 2007): 981–93. http://dx.doi.org/10.1016/j.dnarep.2007.02.017.
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Urban, Vaclav, Jana Dobrovolna, Daniela Hühn, Jana Fryzelkova, Jiri Bartek, and Pavel Janscak. "RECQ5 helicase promotes resolution of conflicts between replication and transcription in human cells." Journal of Cell Biology 214, no. 4 (August 8, 2016): 401–15. http://dx.doi.org/10.1083/jcb.201507099.
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Collisions between replication and transcription machineries represent a significant source of genomic instability. RECQ5 DNA helicase binds to RNA-polymerase (RNAP) II during transcription elongation and suppresses transcription-associated genomic instability. Here, we show that RECQ5 also associates with RNAPI and enforces the stability of ribosomal DNA arrays. We demonstrate that RECQ5 associates with transcription complexes in DNA replication foci and counteracts replication fork stalling in RNAPI- and RNAPII-transcribed genes, suggesting that RECQ5 exerts its genome-stabilizing effect by acting at sites of replication-transcription collisions. Moreover, RECQ5-deficient cells accumulate RAD18 foci and BRCA1-dependent RAD51 foci that are both formed at sites of interference between replication and transcription and likely represent unresolved replication intermediates. Finally, we provide evidence for a novel mechanism of resolution of replication-transcription collisions wherein the interaction between RECQ5 and proliferating cell nuclear antigen (PCNA) promotes RAD18-dependent PCNA ubiquitination and the helicase activity of RECQ5 promotes the processing of replication intermediates.
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Lang, Kevin S., and Houra Merrikh. "The Clash of Macromolecular Titans: Replication-Transcription Conflicts in Bacteria." Annual Review of Microbiology 72, no. 1 (September 8, 2018): 71–88. http://dx.doi.org/10.1146/annurev-micro-090817-062514.
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Within the last decade, it has become clear that DNA replication and transcription are routinely in conflict with each other in growing cells. Much of the seminal work on this topic has been carried out in bacteria, specifically, Escherichia coli and Bacillus subtilis; therefore, studies of conflicts in these species deserve special attention. Collectively, the recent findings on conflicts have fundamentally changed the way we think about DNA replication in vivo. Furthermore, new insights on this topic have revealed that the conflicts between replication and transcription significantly influence many key parameters of cellular function, including genome organization, mutagenesis, and evolution of stress response and virulence genes. In this review, we discuss the consequences of replication-transcription conflicts on the life of bacteria and describe some key strategies cells use to resolve them. We put special emphasis on two critical aspects of these encounters: ( a) the consequences of conflicts on replisome stability and dynamics, and ( b) the resulting increase in spontaneous mutagenesis.
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Tehranchi, Ashley K., Matthew D. Blankschien, Yan Zhang, Jennifer A. Halliday, Anjana Srivatsan, Jia Peng, Christophe Herman, and Jue D. Wang. "The Transcription Factor DksA Prevents Conflicts between DNA Replication and Transcription Machinery." Cell 141, no. 4 (May 2010): 595–605. http://dx.doi.org/10.1016/j.cell.2010.03.036.
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McGlynn, Peter, Nigel J. Savery, and Mark S. Dillingham. "The conflict between DNA replication and transcription." Molecular Microbiology 85, no. 1 (May 31, 2012): 12–20. http://dx.doi.org/10.1111/j.1365-2958.2012.08102.x.
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St Germain, Commodore P., Hongchang Zhao, Vrishti Sinha, Lionel A. Sanz, Frédéric Chédin, and Jacqueline H. Barlow. "Genomic patterns of transcription–replication interactions in mouse primary B cells." Nucleic Acids Research 50, no. 4 (January 31, 2022): 2051–73. http://dx.doi.org/10.1093/nar/gkac035.
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Abstract Conflicts between transcription and replication machinery are a potent source of replication stress and genome instability; however, no technique currently exists to identify endogenous genomic locations prone to transcription–replication interactions. Here, we report a novel method to identify genomic loci prone to transcription–replication interactions termed transcription–replication immunoprecipitation on nascent DNA sequencing, TRIPn-Seq. TRIPn-Seq employs the sequential immunoprecipitation of RNA polymerase 2 phosphorylated at serine 5 (RNAP2s5) followed by enrichment of nascent DNA previously labeled with bromodeoxyuridine. Using TRIPn-Seq, we mapped 1009 unique transcription–replication interactions (TRIs) in mouse primary B cells characterized by a bimodal pattern of RNAP2s5, bidirectional transcription, an enrichment of RNA:DNA hybrids, and a high probability of forming G-quadruplexes. TRIs are highly enriched at transcription start sites and map to early replicating regions. TRIs exhibit enhanced Replication Protein A association and TRI-associated genes exhibit higher replication fork termination than control transcription start sites, two marks of replication stress. TRIs colocalize with double-strand DNA breaks, are enriched for deletions, and accumulate mutations in tumors. We propose that replication stress at TRIs induces mutations potentially contributing to age-related disease, as well as tumor formation and development.
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Trautinger, Brigitte W., Razieh P. Jaktaji, Ekaterina Rusakova, and Robert G. Lloyd. "RNA Polymerase Modulators and DNA Repair Activities Resolve Conflicts between DNA Replication and Transcription." Molecular Cell 19, no. 2 (July 2005): 247–58. http://dx.doi.org/10.1016/j.molcel.2005.06.004.
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Stevenson-Jones, Flint, Jason Woodgate, Daniel Castro-Roa, and Nikolay Zenkin. "Ribosome reactivates transcription by physically pushing RNA polymerase out of transcription arrest." Proceedings of the National Academy of Sciences 117, no. 15 (April 1, 2020): 8462–67. http://dx.doi.org/10.1073/pnas.1919985117.
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In bacteria, the first two steps of gene expression—transcription and translation—are spatially and temporally coupled. Uncoupling may lead to the arrest of transcription through RNA polymerase backtracking, which interferes with replication forks, leading to DNA double-stranded breaks and genomic instability. How transcription–translation coupling mitigates these conflicts is unknown. Here we show that, unlike replication, translation is not inhibited by arrested transcription elongation complexes. Instead, the translating ribosome actively pushes RNA polymerase out of the backtracked state, thereby reactivating transcription. We show that the distance between the two machineries upon their contact on mRNA is smaller than previously thought, suggesting intimate interactions between them. However, this does not lead to the formation of a stable functional complex between the enzymes, as was once proposed. Our results reveal an active, energy-driven mechanism that reactivates backtracked elongation complexes and thus helps suppress their interference with replication.
Dissertations / Theses on the topic "Conflicts between DNA replication and transcription"
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Trautinger, Brigitte W. "Interplay between DNA replication, transcription and repair." Thesis, University of Nottingham, 2002. http://eprints.nottingham.ac.uk/14281/.
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The Ruv ABC and RecBCD protein complexes together can collapse and repair arrested replication forks. With their help a fork structure can be re-established on which replication can be restarted. ruv and recB mutants are therefore quite sensitive to UV light. Their survival is greatly decreased in the absence of the signalling molecules (p)ppGpp and increased when excess (p)ppGpp is present. (p)ppGpp are the effector molecules of the stringent response, regulating adaptation to starvation and other stressful environmental changes. Absence of (p)ppGpp can be compensated for by mutations in RNA polymerase that are called stringent mutations. Some of those, called rpo *, also - like excess (p)ppGpp - increase the survival of UV irradiated ruv and recB cells. A model proposed by McGlynn and Lloyd (Cell, Vol. 101, pp35-45, March 31, 2000) suggests that this is achieved by modulation of RNA polymerase, which decreases the incidence of replication fork blocks. In this work twenty-seven rpo * mutants were isolated, sequenced and mapped on the 3D structure of Thermus aquatic us RNA polymerase. I have found mutants in the ~ and ~' subunits of RNA polymerase. They lie mostly on the inner surface of the protein, well placed to make contact with the DNA substrate or the RNA product. A large number of rifampicin resistant mutations among rpo* mutations is explained by an overlap between the so-called Rif pocket and the "rpo* pocket". rpo * mutations, like stringent mutations, lead to a decrease in cell size, suppress filamentation and increase viability. For in vitro studies I purified wild type and two mutant RNA polymerases with help of a his-tagged a subunit. The experiments confirmed that rpo* mutant RNA polymerases form less stable open complexes than wild type, just like previously investigated stringent RNA polymerases. In addition I have shown here that (p)ppGpp leads to the destabilisation of RNA polymerase complexes stalled by nucleotide starvation or UV-induced lesions, though there is as yet no indication that rpo * mutations act in the same way.
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Dzionek, Karol Wiktor. "The relationship between mitochondrial DNA transcription and replication." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648311.
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Cahn, Alice. "Fonction et régulation de l’ADN polymérase spécialisée eta dans la stabilité des régions intrinsèquement difficiles à répliquer." Electronic Thesis or Diss., université Paris-Saclay, 2020. http://www.theses.fr/2020UPASL061.
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La réplication complète et fidèle de l’ADN est cruciale pour transmettre l’information génétique de manière correcte aux cellules filles. Divers obstacles peuvent interférer avec la progression de la machinerie de réplication, et donc menacer l’intégrité du génome. Des ADN polymérases spécialisées, dites translésionnelles (polymérases TLS), assistent les ADN polymérases réplicatives pour la poursuite de la réplication malgré ces lésions. Elles peuvent répliquer de manière fidèle ou non ces entraves, mais sont mutagènes sur des séquences d’ADN non-endommagées. Au cours de ma thèse, j’ai pu caractériser davantage la contribution de l’ADN polymérase TLS eta (polη) au cours de la réplication non-perturbée. Cette polymérase permet principalement de prévenir la mutagénèse induite par les UV. Mais il a également été montré qu’elle promeut la stabilité des sites fragiles communs, et est associée au réplisome durant la phase S non-perturbée. Cependant, la nature des obstacles nécessitant polη et les conséquences de son absence pour la réplication de ces régions restaient à déterminer. Mes résultats montrent que polη est recrutée au niveau d’une fraction des fourches de réplication tout au long de la phase S et que l’absence de pol eta conduit à une modification du timing de réplication de régions génomiques riches en grands gènes transcrits, où les conflits entre réplication et transcription sont potentiellement plus fréquents. Plus généralement, je montre que le recrutement de pol eta à la fourche de réplication dépend de la transcription et qu’elle joue un rôle dans la prise en charge des conflits entre réplication et transcription. Ces résultats mettent en évidence un nouveau rôle de protection de la stabilité du génome pour cette ADN polymérase mutagèneComplete and accurate DNA replication is crucial to transfer correct genetic information to the daughter cells. Various obstacles can interfere with the progression of the replication machinery, threatening genome integrity. Specialized error-prone translesion DNA polymerases (TLS polymerases) assist the replicative polymerases to replicate across DNA lesions. During my PhD I characterized the contribution of TLS pol eta (polη), best known for its role in preventing UV-induced mutagenesis, during unperturbed replication. Polη was shown to promote the stability of the common fragile sites and associates with the replisome in unchallenged S phase. However, the kind of replication barriers requiring pol eta and the consequences of its absence on the replication of these regions were unclear. My results show that polη is recruited at a subset of replication forks all along the S phase and that polη defect modifies the replication timing of genomic regions enriched in large transcribed genes, where transcription-replication conflicts (TRCs) are more likely to occur. Overall, I show that polη recruitment at the replication fork is transcription-dependent, and that pol eta plays a role in the coping with TRCs. Altogether, these results highlight a new role for an error-prone DNA polymerase in protecting the genome stability
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Fryzelková, Jana. "Úloha helikázy RECQ5 při stabilizaci a opravě replikačních vidlic po jejich kolizi s transkripčním komplexem." Master's thesis, 2017. http://www.nusl.cz/ntk/nusl-355971.
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The progression of replication forks can be slowed down or paused by various external and internal factors during DNA replication. This phenomenon is referred to as replication stress and substantially contributes to genomic instability that is a hallmark of cancer. Transcription complex belongs to the internal replication-interfering factors and represents a barrier for progression of the replication complex. The replication forks are slowed down or paused while passing through the transcriptionally active regions of the genome that can lead to subsequent collapse of stalled forks and formation of DNA double-strand breaks, especially under conditions of increased replication stress. DNA helicase RECQ5 is significantly involved in maintenance of genomic stability during replication stress, but the mechanisms of its action are not clear. In this diploma theses, we have shown that RECQ5 helicase, in collaboration with BRCA1 protein, participates in the resolution of collisions between replication and transcription complexes. BRCA1 protein is a key factor in the homologous recombination process, which is essential for the restart of stalled replication forks. Furthermore, we have shown that RECQ5 helicase is involved in ubiquitination of PCNA protein at stalled replication forks. Key words DNA...
Book chapters on the topic "Conflicts between DNA replication and transcription"
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Stewart-Morgan, Kathleen R., and Anja Groth. "Profiling Chromatin Accessibility on Replicated DNA with repli-ATAC-Seq." In Chromatin Accessibility, 71–84. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2899-7_6.
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AbstractOpen or accessible chromatin typifies euchromatic regions and helps define cell type-specific transcription programs. DNA replication massively disorders chromatin composition and structure, and how accessible regions are affected by and recover from this disruption has been unclear. Here, we present repli-ATAC-seq, a protocol to profile accessible chromatin genome-wide on replicated DNA starting from 100,000 cells. In this method, replicated DNA is labeled with a short 5-ethynyl-2′-deoxyuridine (EdU) pulse in cultured cells and isolated from a population of tagmented fragments for amplification and next-generation sequencing. Repli-ATAC-seq provides high-resolution information on chromatin dynamics after DNA replication and reveals new insights into the interplay between DNA replication, transcription, and the chromatin landscape.
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Castro-Roa, Daniel, and Nikolay Zenki. "Relations Between Replication and Transcription." In Fundamental Aspects of DNA Replication. InTech, 2011. http://dx.doi.org/10.5772/20880.
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Bean, Daniel W., and Steven W. Matson. "Identification and characterization of DNA helicases." In Eukaryotic DNA Replication, 93–118. Oxford University PressOxford, 1999. http://dx.doi.org/10.1093/oso/9780199636815.003.0004.
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Abstract DNA helicases catalyse disruption of the hydrogen bonds between the two strands of duplex DNA to generate single-stranded DNA (ssDNA) products (1, 2). This reaction is generally referred to as an unwinding reaction. The ssDNA product(s) of the unwinding reaction is then available for use as a template for DNA replication or repair, or as a substrate in recombination. Enzymes that catalyse the unwinding of duplex RNA, RNA secondary structure, and DNA:RNA hybrids have also been described (3-7). These enzymes have important roles in mRNA biogenesis, transcription, and translation. Thus, helicase catalysed unwinding is not confined to the unwinding of duplex DNA. In fact, there are examples of enzymes that catalyse the un winding of more than one of these substrates (8-10). The well characterized T-antigen, for example, unwinds both duplex DNA and RNA:DNA hybrids (9). Presumably these substrate preferences are related to the biological function of the protein, although these relationships are not always immediately obvious. None the less, it is clear that all transactions involving either DNA or RNA require the (transient) existence of a single-stranded intermediate, and thus helicases play key roles in all aspects of nucleic acid metabolism (11).
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Almouzni, Genevieve. "Assembly of chromatin and nuclear structures in Xenopus egg extracts." In Chromatin, 195–218. Oxford University PressOxford, 1998. http://dx.doi.org/10.1093/oso/9780199635993.003.0010.
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Abstract The structural organization of DNA within the eukaryotic nucleus is tightly defined to accommodate the functional properties of a given cell type. Nuclear functions such as replication and transcription operate in a highly regulated fashion using chromatin as a template. During every cell cycle, each nucleus has to replicate itself, requiring duplication not only of DNA but also of the individual chromosomes together with all their structural and regulatory features. Chromatin organization is known to influence gene expression ( 1 ) and its remodelling during replication and cell cycling can affect the transcription process. To study the relationship between the structural organization of DNA and macromolecular events such as replication and transcription, an adequate system is required, accurately reproducing both structural and functional features of the eukaryotic cell.
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Foste!, Jennifer, and Linus L. Shen. "DNA Topoisomerases." In Pre-Equilibrium Nuclear Reactions, 564–624. Oxford University PressOxford, 1992. http://dx.doi.org/10.1093/oso/9780198517344.003.0011.
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Abstract DNA topoisomerases are a class of enzymes that modulate the topo logical structure of DNA. Since the discovery of the first topoisomerase 20 years ago (Wang 1971), many of the properties of this class of enzymes have been elucidated and this progress has been the subject of many reviews (Cozzarelli 1980; Gellert 1981; Liu 1983; Drlica 1984; Wang 1985, 1987b; Maxwell and Gellert 1986; Yanagida and Wang 1987; Osheroff 1989a; Austin and Fisher 1990, Champoux 1990; Hsieh 1990;.Osheroff et al. 1991). In purified systems, topoisomerases relax supercoiled DNA, and can tie and untie DNA knots, and link and unlink catenated DNA circles. In eukaryotic cells, type I topoisomerases are associated with elongating transcription and replication forks, while type II topoisomerases are essential for segregating daughter chromosomes after DNA replication is complete (Yanagida and Wang 1987). Topoisomerases are also the target of a number of antineoplastic and antibacterial agents whose cytotoxic effects appear to arise from the stabilization of a complex between the topoisomerase and DNA (Ross 1985; Glisson and Ross 1987; Drlica and Franco 1988; Liu 1989; Smith 1990).
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"Genes." In Examining the Causal Relationship Between Genes, Epigenetics, and Human Health, 162–85. IGI Global, 2019. http://dx.doi.org/10.4018/978-1-5225-8066-9.ch008.
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Genes are regions on DNA that contain the instructions for making specific proteins. In humans, genes vary in size from hundreds of DNA bases to over 3 million base pairs. From DNA to proteins, two steps are involved. Transcription is accessing the gene and reading the instructions therein in the nucleus producing as a single strand of RNA called messenger RNA (mRNA). Translation is reading the instructions on mRNA to assemble the specified proteins on the surface of ribosomes. Genetic mutations are heritable, small-scale alterations in one or more base pairs that damage DNA. Although new mutations introduce new variation, these are constantly removed from populations. Mutations can arise naturally during DNA replication or can be caused by environmental factors like chemicals or radiation. They can be harmful, neutral, or beneficial to the organism and are generally of five types: point mutations, frameshift mutations, transposons, transitions, and transversions. This chapter explores this aspect of genes.
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Wang, Qiuyu, Chris Smith, and Emma Davis. "The nucleus." In Thrive in Cell Biology. Oxford University Press, 2013. http://dx.doi.org/10.1093/hesc/9780199697328.003.0006.
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This chapter describes the size and shape of the nucleus which is maintained by a nuclear skeleton composed of fibrous proteins, which also provides an organizing frame to which the chromatin fibres are attached. The chapter explains replication as the process by which cellular DNA is copied to form two complete daughter strands of DNA, which occurs during interphase when the cell produces two copies of its chromosomal DNA before cell division begins. The chapter also talks about eukaryotic promoters that can be upstream or downstream of the transcription start, and vary between the various RNA polymerase types. The chapter shows how eukaryotic premRNA is formed by RNA polymerase II and notes that it requires modification following its transcription. It examines nucleoli as prominent structures that are present in nuclei.
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Dhavan, Gauri M., Mark R. Chance, and Michael Brenowitz. "Kinetics analysis of DNA-protein interactions by time-resolved synchrotron X-ray footprinting." In Kinetic Analysis of Macromolecules, 75–86. Oxford University PressOxford, 2003. http://dx.doi.org/10.1093/oso/9780198524946.003.0004.
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Abstract The binding of proteins to specific sequences of DNA is often the first step in the regulation of cellular events essential to cell function and growth such as transcription, DNA replication, site-specific recombination, and other processes that require DNA binding. The rates at which these protein-DNA complexes assemble is dependent upon the kinetics of each individual binding event as well as additional cooperative interactions between two or more protein molecules required for biological function. The study of the kinetics of association and dissociation of site-specific DNA contact events provides insight into the mechanism by which the complexes are formed and the role of each player in a larger nucleo-protein assembly.
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Brazma, Alvis. "Informed Self-organization." In Living Computers, 55–86. Oxford University PressOxford, 2023. http://dx.doi.org/10.1093/oso/9780192871947.003.0004.
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Abstract This chapter is a brief, non-orthodox introduction into molecular biology. As the Nobel Laureate Sidney Brenner wrote: ‘Biology is essentially (very low energy) physics with computations’. The chapter shows how molecular self-assembly and self-organization, combined with inherited information, form the basis of all known processes of life. In particular, the chapter discusses proteins and protein folding, self-assembly of protein complexes, DNA, RNA, Crick’s central dogma, and gene transcription and translation. In the end of this chapter, the analogy between von Neumann’s theory of self-replication and Francis Crick’s central dogma of molecular biology are discussed.
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Nabel, Gary J. "The role of cellular transcription factors in the regulation of human immunodeficiency virus gene expression." In Human Retroviruses, 49–74. Oxford University PressOxford, 1993. http://dx.doi.org/10.1093/oso/9780199633821.003.0003.
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Abstract The human immunodeficiency virus (HIV) is dependent on its host cell for the synthesis and processing of viral RNA. Steady-state levels of viral RNA can be regulated by several mechanisms, including the rate of transcriptional initiation, elongation, processing, export, and packaging. Diverse regulatory mechanisms have, therefore, evolved to control viral RNA during HIV replication. These events play a critical role in the regulation of viral replication. Relative to the human genome, the genomic complexity of HIV is relatively small, <0.001% in size. To regulate viral gene expression specifically, the virus has evolved its own regulatory gene products. These viral trans-activators are also dependent upon cellular factors that interact with viral proteins and cis-acting DNA and RNA regulatory elements to further modulate HIV gene expression. These mechanisms of regulation are diverse. For example, the Tat trans-activator affects the ability of a cellular transcription complex to elongate and inhibits premature termination of the HIV transcript (1, 2, Chapter 4). The Rev gene product, on the other hand, does not affect the synthesis of viral RNA but acts with cellular factors on an RNA structure after formation of the primary transcript (3, 4, Chapter 5). For these trans-activators, an intimate association has evolved between host cell factors and viral gene products. These essential trans-activators are synthesized only after viral transcription has been initiated. The regulation of the initiation of HIV transcription also plays an important role in the viral life cycle.
Conference papers on the topic "Conflicts between DNA replication and transcription"
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Marinello, Jessica, Maria Delcuratolo, Yves Pommier, Monica Binaschi, Andrea Pellacani, and Giovanni Capranico. "Abstract B188: DNA topoisomerase-mediated transcription-replication conflicts cause DNA damage by a transient increase of R loops and proteasome activity." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; October 26-30, 2017; Philadelphia, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1535-7163.targ-17-b188.
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Young, Paul W. "Student-produced video of role-plays on topics in cell biology and biochemistry: A novel undergraduate group work exercise." In Learning Connections 2019: Spaces, People, Practice. University College Cork||National Forum for the Enhancement of Teaching and Learning in Higher Education, 2019. http://dx.doi.org/10.33178/lc2019.15.
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Group work or cooperative learning is a form of active learning that has potential benefits that extend beyond just being an alternative or improved way of learning course material. For example, Shimazoe and Aldrich (2010) identified six proposed benefits of active learning to students, namely (1) promoting deep learning, (2) helping students earn higher grades, (3) teaching social skills & civic values, (4) teaching higher order thinking skills, (5) promoting personal growth and (6) developing positive attitudes toward autonomous learning. There is evidence for the effectiveness of role-plays both in achieving learning outcomes (Azman, Musa, & Mydin, 2018; Craciun, 2010; Latif, Mumtaz, Mumtaz, & Hussain, 2018; McSharry & Jones, 2000; Yang, Kim, & Noh, 2010), but also in developing desirable graduate attributes such as teamwork, communication and problem solving skills [4]. The importance of such skills is widely touted by employers of science graduates, sometimes more so than discipline-specific knowledge, arguing in favour of the incorporation of role-plays and other forms of cooperative learning into undergraduate science curricula. Role-playing is probably not as widely used in the physical and life sciences as it is in other academic disciplines. In science the most obvious role-play scenarios in which students play the roles of people might be in examining historical figures at the centre of famous scientific discoveries or debates (Odegaard, 2003). In addition, role-plays fit well at the interface between science and other discipline when exploring ethical, legal or commercial implications of scientific discoveries(Chuck, 2011). However, to apply role-play to core topics in science or mathematics the roles that must be played are not those of people but rather of things like particles, forces, elements, atoms, numbers, laws, equations, molecules, cells, organs and so on. The learning scenarios for science-based roleplays in which the characters represented are not people are less obvious, probably explaining why the use of role-plays in science education is less common. Nevertheless, focusing on the life sciences, role-plays in which the characters are organelles in a cell or enzymes involved in fundamental cellular processes like DNA replication, RNA transcription and protein translation have been described for example (Cherif, Siuda, Dianne M. Jedlicka, & Movahedzadeh, 2016; Takemura & Kurabayashi, 2014). The communication of discipline-specific templates and successful models for the application of role-playing in science education is likely to encourage their wider adoption. Here I describe a videoed group role-play assignment that has been developed over a ten-year period of reflective teaching practice. I suggest that this model of videoed group role-plays is a useful cooperative learning format that will allow learners to apply their varied creativity and talents to exploring and explaining diverse scientific topics while simultaneously developing their teamwork skills.