DNA Tranlession Polymerase in Prokaryotic Cells

DNA Tranlession Polymerase in Prokaryotic Cells DNA Tranlession Polymerase in prokaryotic cells: History, structures and function Soheil Malekpour DNA is one of the most important part of the cell that gives cell integrity and character. This part of the cell can be exposed to different kinds of damages that may put the cells integrity in jeopardy. The only part of the cell that has this ability to be repaired is DNA. Basically repairing should be done due to a reasonable reason. Repairing the other macromolecules are not profitable. For example, if a defective protein forms, the protein can be simply be replaced by another one. But defects in DNA can cause problem in the whole cell organisms and the character of cell [1]. Usually the whole repairing process is happening fast, although there are defects that persist against this process. The repairing process is done by special polymerases and the whole process of DNA repair is called translesion DNA synthesis (TLS) [2]. DNA can be damaged due to different reasons, such as base modification, elimination or addition of nucleotides, crosslinking of DNA strands and breakage of phosphodiester backbone [1]. These reasons can be due to some environmental conditions such as radiation or insertion of certain chemicals in to the body or due to malfunction of polymerases and enzymes in cellular process, such as putting wrong nucleotide in the DNA strand chain [1]. Up to now, it is known that there are three translesion DNA polymerases (TLS polymerases) in E. coli and about fifteen polymerases in eukaryotes that can run this process [2]. History For the first time it was in the early 1940s, that it was found agents causing mutational changes such as ionizing and radiation of UV, interact with cells and can damage their genome [3]. Also it was found that these cells can survive and recover from theses damages [4] and the term DNA repair was found. DNA repair is a biochemical term that defines biological processes during which alterations in the chemistry of DNA (DNA damage) are removed and the integrity of the genome is restored [3]. The first DNA repair mechanism to be discovered was enzymatic photo reactivation (EPR) [3]. This process is referred to the elimination of cyclobutane pyrimidine, which are generated by UV radiation and can block both DNA replication and transcription, from the genome [4]. This reaction can be catalyzed by photoreactivating enzyme in a reaction that needs a visible range light. The second mechanism found was excision repair [3]. This mechanism is referred to DNA damages cut out from genome that leaves some gaps in DNA duplex. These gaps are repaired by a non-semiconservative mode of DNA synthesis called repair synthesis [5]. By the end of the 1970s, it was known that cells are using various mechanisms for DNA repair process that focus around two basic principles: the excision of base damage or its direct reversal such as EPR [3]. In the mid1970s Miroslav Radman proposed a new hypothesis called SOS hypothesis [5, 6]. TheSOS hypothesis proposes an overall response to DNA damage in which thecell cycleis stopped andDNA repairis induced. Genetics experiments demonstrated that main players involved in damage-induced mutagenesis are lexA, recA along with umuD and umuC [2]. LexA cleavage from recA* and also umuD cleavage that form umuD use the same mechanism and is an absolute requirement for SOS mutagenesis. For showing that, E. coli because of its simple structure was used as a model for translesion DNA synthesis and mutagenesis. Later Harrison Echols proposed another model and suggested that in order to help the replication process against the lesions it is possible to reduce the fidelity of proteins so when DNA replication process is stopped at a location of unrepaired DNA damage, certain SOS-regulated genes can encode proteins that interact with the hindered replication process in a manner that reduces their fidelity [3]. In the late 1980s and early 1990s, it was demonstrated that Echols genes are in fact specialized low-fidelity DNA polymerases that enhance low-fidelity replication across the lesion, the so-called translesion DNA synthesis (TLS) [3]. Their highly reduced fidelity allows the replicative bypass of sites of DNA damage, but with a high chance of combining incorrect nucleotides [5]. Early TLS models and PolV Bridges and Woodgate were the first ones who defined the function of Umu proteins during UV-induced TLS in 1985 [7]. According to them, TLS happened in two steps. In the first step Pol III add a nucleotide opposite the first (3†²) T of a T-T cytidine diphosphate diacylgelycerol (CPD). Bounding a RecA protein to the template proximal to the lesion is a requirement for this step. In the second step, Pol III interacts with UmuDC proteins to incorporate another nucleotide at the second (5†²) T of the cytidine diphosphate diacylgelycerol (CPD). At least one of these two steps are non-WC, causing a mutation targeted at the site of the CPD [2]. Figure 1 shows the process schematically. Another model was proposed by Echols and Goodman in 1990 [3]. In this model they proposed that when Pol III encounters a template lesion, its holoenzymes (Pol III core, beta sliding clamp, gamma-clamp-loading complex) are completely blocked. This process follows by the assembly of a damage localized nucleoprotein complex involving RecA, UmuC, UmuD†², SSB, and Pol III holoenzyme, a mutasome, to copy past a template lesion [2]. The fact that RecA* simplifies the cleavage of UmuD to UmuD was used in this model [8]. Later, it was demonstrated that it was actually a dimeric UmuD2 that is cleaved to UmuD2 and that next interacts with UmuC to form a stable complex of UmuD2C [9]. This complex was named as Pol V in 1999 by Tang et al. [10]. It can be said that genome replication done on undamaged DNA by Pol III is rapid and error-free [11], the TLS process carried out by mutasome is slow and error-prone [2]. A key feature of the mutasome model is the assembly of RecA* on ssDNA proximal to the lesion (Fig. 1). When a replication fork encounters a lesion, an uncoupling of leading-and lagging-strand synthesis may ensue. Then, one of the TLS Pols can replace Pol III on the ÃŽ ²- clamp and copy the damaged DNA [2]. For both leading and lagging strands it be easily seen that RecA* can be assembled on the form of template strand, proximal to lesion. If the lesion occurred in the leading strand, RecA filaments can be formed on a region of ssDNA that is created by DNA unwinding by DnaB helicase downstream from the lesion but if lesions exist in lagging strand ssDNA is present as a result of Okazaki fragment synthesis [2]. Schlacher and Goodman [12] showed RecA* act in trans form on a non-template ssDNA strand and this transactivation of PolV by RecA* to perform TLS happens in-vitro. And this lead to the PolV mutasome model of TLS (Fig. 1). Jiang et al. [13] demonstrated this new PolV form as PolV Mut = UmuD2C-RecA-ATP. PolV Mut has this ability to copy both damaged and undamaged DNA (e.g. performs TLS) when RecA* is not present [2]. So, the straight role of RecA* in SOS-mediated TLS is to transfer a RecA molecule from the 3†²-filament tip with a molecule of ATP to convert into Pol V Mut, that can cross a different number of DNA lesions on its own. (Fig. 1) [2, 14]. PolV Mut can have two conformations. One is activated form that can copy DNA, the other one is deactivated form that is unable to copy the DNA. The activation of PolV Mut is depended on the location of RecA-ATP bond to the polymerase subunits UmuD2 and UmuC [13]. By representing the RecA* again, the deactivated form of PolV Mut can be activated. In this case, the old RecA-ATP is substituted by a new RecA-ATP from the 3-filament tip [13]. This type of switching on and off is unique to this kind of polymerase and has not been seen in other types of polymerases. This method can be useful specially preventing the undamaged DNA to go under mutation in E.Coli, and give the cell this power to activate Pol V Mut whenever replication fork have stuck at DNA template damage site [2]. PolII and PolIV in E.Coli TLS PolII discovered in 1970[15]. At first, it was thought that mutation is non-informative in PolII [16]. Pol II has an activity isolated from UV-irradiated cells that has this ability to replicate past abasic template lesions [2, 17]. This polymerase has some responses to UV radiation and this activity derives from that [2]. By purification it was proved that the induced lesion-copying protein was Pol II [17]. In 1980, Kenyon and Walker [18] discovered a DNA damage-inducible gene called dinA that can encode PolII. Also, one of the features of PolII is bypassing N2-deoxyguanosine-acetyl aminofluorene (AAF) adducts, this behavior can be error-free and produces 2-frame shift mutations [19]. AAF adducts are of family of aromatic amides that induce frame shift mutations within GpC sequences, such as the NarI sequences [19]. These adducts are able to increase the GC dinucleotide loss in NarI sequence (CGCGCC) by 107 times when they are bound to the G in middle of sequence [20]. PolII and Pol V can complement each other, but it does not mean that their activities are functionally unneeded [21]. As Pham et al. [21] mentioned PolV job is to copy UV-damaged DNA in an error-prone manner in TLS. But Pol II is able to copy chromosomal DNA in an error-free replication process. Kenyon and walker also introduced another gene called dinB gene that can be induced by cellular SOS response to DNA damage [18]. For many years, the function of this gene was unknown. After some year Ohmori et al. [22] found other gene, dinP gene, in the same section that dinB gene was found and Wagner et al. showed that they are able to encode Y-family DNA PolIV [23]. This kind of polymerases like other polymerases used in TLS are not crucial for life. Their role is to bypass certain N2-dG adducts (such as N2-furfuryl-dG) in an error-free manner [2]. Kumari et al. demonstrated they can copy past N2-N2-guanine interstrand cross-links in a high fidelity manner [24]. Regulation of TLS polymerases Different polymerases have this ability to traverse an extensive range of DNA lesions but this ability may cause in reducing the fidelity during replicating the undamaged DNA. Usually cells have several mechanisms to check and control the TLS polymerases because except PolII, all of them has this potential to delete errors made when duplicating an undamaged DNA [2]. Usually no regulation is needed for PolII. Because it has high fidelity derived by high intrinsic 3-5 exonucleolytic proofreading. On the other hand, the Y-family polymerases such as PolIV and PolV are exo-nuclease deficient and needed to be controlled [2]. PolV activity can be regulated by many proteins and many ways. First as said before the UmuD should be activated by UmuD. All UmuD, UmuC and UmuD proteins are all exposed to degradation by Lon and ClpXP protease. RecA* that forms PolV Mut can interact with UmuD2C complexes and active them. The PolV Mut itself activity can be enhanced by binding to the ÃŽ ²-clamp [2]. As Wagner et al. showed the PolIV activity can be stimulated by protein interaction with RecA, UmuD and ÃŽ ²-clamp [25]. Although the main mechanisms of DNA repair by various polymerases are known now, more studies can be conducted on E.Coli cells to find more details about the regulation and side reactions happening in this process. E.Coli cells as simple cells are an appropriate model to analyze these functions. Jarosz et al. proposed well questions about the future studies on Y-family DNA polymerases [26]: (1)How do Y-family polymerases gain access to an appropriate primer terminus and how is their action coordinated with that of replicative polymerases? (2)How do protein–protein interactions regulate the activity of Y-family polymerases? (3)Are there families of cognate lesions for each different Y-family polymerase? (4) Can mutations introduced by Y-family polymerases be corrected by exonucleolytic proofreading in trans? Different polymerases act in different paces after the damaged. For example PolII is induced immediately after DNA damage but PolV is induced about 50 min after the damage [21]. An area of interest could be study on how they can be regulated to be induced in shorter time. References Horton, R. H., Moran, L. A., Perry, M. D., Rawn, D. J. and Scrimgeour, G. K. (2006)Principles of biochemistry. 4th edn. United States: Pearson Education (US). Goodman, M. F. and Woodgate, R. (2013) ‘Translesion DNA Polymerases’,Cold Spring Harbor Perspectives in Biology, 5(10). doi: 10.1101/cshperspect.a010363. Friedberg, E. C. (2008) ‘A brief history of the DNA repair field’,Cell Research, 18(1), pp. 3–7. doi: 10.1038/cr.2007.113. Hollaender, A. and Duggar, B. M. (1938) ‘The effects of sublethal doses of monochromatic ultraviolet radiation on the growth properties of bacteria’,Journal of Bacteriology, 36(1): 17-37. Friedberg EC, Walker GC, Siede W, Wood RD, Schultz RA, Ellenberger T. DNA Repair and Mutagenesis. Washington DC, ASM Press, 2005 Friedberg EC. Correcting the Blueprint of Life. An Historical Accounting of the Discovery DNA Repairing Mechanisms. Cold Spring Harbor, NY: Cold Spring Harbor Laboratory Press, 1997. Ruiz-Rubio, M., Woodgate, R., Bridges, B. A., Herrera, G. and Blanco, M. (1986) ‘New Role for Photoreversible Pyrimidine Dimers in Induction of Prototrophic Mutations in Excision-Deficient Escherichia coli by UV Light’,Journal of Bacteriology, 166(3): 1141-1143. Burckhardt, S. E., Woodgate, R., Scheuermann, R. H. and Echols, H. (1988) ‘UmuD mutagenesis protein of Escherichia coli: overproduction, purification, and cleavage by RecA.’,Proceedings of the National Academy of Sciences, 85(6), pp. 1811–1815. doi: 10.1073/pnas.85.6.1811. Woodgate, R., Rajagopalan, M., Lu, C. and Echols, H. (1989) ‘UmuC mutagenesis protein of Escherichia coli: purification and interaction with UmuD and UmuD’,Proceedings of the National Academy of Sciences, 86(19), pp. 7301–7305. doi: 10.1073/pnas.86.19.7301. Tang M, Shen X, Frank EG, O’Donnell M, Woodgate R, Goodman MF. UmuD2†²C is an error-prone DNA polymerase, Escherichia coli, DNA pol V. Proc Natl Acad Sci. 1999; 96:8919–8924. Johnson A, O’Donnell M. Cellular DNA replicases: Components and dynamics at the replication fork. Annu Rev Biochem. 2005; 74:283–315 Schlacher K, Goodman MF. Lessons from 50 years of SOS DNA-damage-induced mutagenesis. Nat Rev Mol Cell Biol. 2007; 8:587–594 Jiang Q, Karata K, Woodgate R, Cox MM, Goodman MF. The active form of DNA polymerase V is UmuD2†²C-RecA-ATP. Nature. 2009; 460:359–363. Dutreix M, Moreau PL, Bailone A, Galibert F, Battista JR, Walker GC, Devoret R. New recA mutations that dissociate the various RecA protein activities in Escherichia coli provide evidence for an additional role for RecA protein in UV mutagenesis. J Bacteriol. 1989; 171:2415–2423. Knippers R. DNA polymerase II. Nature. 1970; 228:1050–1053. Foster PL, Gudmundsson G, Trimarchi JM, Cai H, Goodman MF. Proofreading-defective DNA polymerase II increases adaptive mutation in Escherichia coli. Proc Natl Acad Sci. 1995; 92:7951–7955. Bonner CA, Randall SK, Rayssiguier C, Radman M, Eritja R, Kaplan BE, McEntee K, Goodman MF. Purification and characterization of an inducible Escherichia coli DNA polymerase capable of insertion and bypass at abasic lesions in DNA. J Biol Chem. 1988; 263:18946–18952. Kenyon CJ, Walker GC. DNA-damaging agents stimulate gene expression at specific loci in Escherichia coli. Proc Natl Acad Sci. 1980; 77:2819–2823. Napolitano, R., Janel-Bintz, R., Wagner, J. and Fuchs, R. P. P. (2000)All three SOS-inducible DNA polymerases (Pol II,Pol IV and Pol V) are involved in induced mutagenesis, The EMBO Journal, 19(29), pp. 6259-6265. Koffel-Schwartz, N., Verdier, J.-M., Bichara, M., Freund, A.-M., Daune, M. P. and Fuchs, R. P. P. (1984) ‘Carcinogen-induced mutation spectrum in wild-type, uvrA and umuC strains of Escherichia coli’,Journal of Molecular Biology, 177(1), pp. 33–51 Pham, P., Rangarajan, S., Woodgate, R. and Goodman, M. F. (2001) ‘Roles of DNA polymerases V and II in SOS-induced error-prone and error-free repair in Escherichia coli’,Proceedings of the National Academy of Sciences, 98(15), pp. 8350–8354. Ohmori H, Hatada E, Qiao Y, Tsuji M, Fukuda R. dinP, a new gene in Escherichia coli, whose product shows similarities to UmuC and its homologues. Mutat Res. 1995; 347:1-7. Wagner J, Gruz P, Kim SR, Yamada M, Matsui K, Fuchs RPP, Nohmi T. The dinB gene encodes a novel Escherichia coli DNA polymerase, DNA Pol IV, involved in mutagenesis. Mol Cell. 1999; 4:281–286. Kumari A, Minko IG, Harbut MB, Finkel SE, Goodman MF, Lloyd RS. Replication bypass of interstrand cross-link intermediates by Escherichia coli DNA polymerase IV. J Biol Chem. 2008; 283:27433–27437. Wagner J, Fujii S, Gruz P, Nohmi T, Fuchs RP. The ÃŽ ² clamp targets DNA polymerase IV to DNA and strongly increases its processivity. EMBO Rep. 2001; 1:484–488. Jarosz, D. F., Beuning, P. J., Cohen, S. E. and Walker, G. C. (2007) ‘Y-family DNA polymerases in Escherichia coli’,Trends in Microbiology, 15(2), pp. 70–77.

The Role and Involvement of Senior Management

This essay will analyse the roles and involvement of senior management in determining and executing strategic information system in a global organisation. This will explain how organisation can beat the threat when competing in a global market and what strategy they needs to follow that will enable their business to stand out among other competitive market. Also this topic will states the paramount of information system in helping organisation in making strategic decision in all area of their business and what they need to put in place for them to be successful in their global business such as: like Geographical, their local business partners, the structure of the business, the business legislation in their desired area of location how all this is paramount will be discuss in the essay. I will argue about the assumption of universality of economic entrance and development which is incompatible the reality and development ways in the developing and developed countries. Role and involvement of senior management in global organisation The use and insight of Strategic Information System (SIS) was linked with IT and IS and is purpose is to assist the senior manager to control more effectively in order to improve the areas of communication and to progress in decision making. As the improvement in technology developed the focal point was motivated in the running performance of an organisation processes to a long term strategic view they desired. This was done by using an adopting technologies and systems which helps the management to redesign their existing ways of running and ensuring there is stability in their path. After seeing that there is a superior understanding of the organisation the management were able to be familiar with new ways of utilizing the technology which subsequently make it possible for them to be more effective of the use of information. In all organisations information system plays a vital role in the operation of the business which allows the organisation to process information using database, communication, system and many other applications. In the recent year Information system has become well-known as a means of absorption and the enabler of new competitiveness for today’s scheme in the global organisation. It is very important for senior managers to have a good understanding of the effective and responsible use of information system which will enable them to be successful in their area of businesses when operating in a global environment. When it comes to the aspect of processing decision senior management rely on information systems in making strategic outcome. As a senior management when introducing a strategic information system in Global organisation they must ensure that the importance of user must be involve when making the process and the mangers must provide a guide line which will allow them to maximize user or customer involvement in the design and implementation of a strategic information. Also when the management are making a determination and executing a strategic in a global organisation there are ways in which they can liked their business strategy to define the business needs and structure which will help them in driven into information system and one of the way they can use to do this is by looking into the competitive advantage. There are different types of strategies which the management can put into consideration in order for them to differentiate their product in a competitive market and they can use generic strategies which will help them in reducing their cost, differentiate their product in which they provide on market niche (porter, 1980). In addition, evidence shows that companies that globalize achieve better competitive and financial performance. But globalizing, in the sense of spreading activities around the world, is not enough. Companies also need to be globally integrated. They need globally coherent strategies, global networks, and the ability to maximize profits on a global basis. When considering the geographic and time that might stands like a barrier to promote the organisation in the global world information system can assist the senior management in this particular aspect and the way they can promotes the business is to provides an online electronic market place where customers can purchase any of their product at any particular hours of time. Also they need to understand the business language whenever the location of the business is situated. In looking for a way to develop an appropriate Information system strategies it is very usual to put some form of hole analysis which will help the management in identifying the hole of where the organisation are and where they want to progress to. Conclusion This essay are critically analyse the roles of management in executing strategic information system and has analyse the important of information system which will help them to make a development in their business and to be successful in the globalisation market or organisation environment. An important key factor of this essay is that the commitment of senior management in a global organisation is so essential which lead them to think of the effectiveness of technology and the way they can transform the business that will be different from other competitive market. The choices to be made in order to beat organisational boundaries such as : marketing, operations, finance, legal, business partners, location and other strategic decision can only be made by senior management.

Miss Essay

Unit Title: Unit sector reference: Level: Credit value: Guided learning hours: Unit accreditation number: Promote good practice in handling information in health and social care settings HSC 038 3 2 16 J/601/9470 Unit purpose and aim This unit is aimed at those working in a wide range of settings. It covers the knowledge and skills needed to implement and promote good practice in recording, sharing, storing and accessing information. Learning Outcomes The learner will: 1 Understand requirements for handling information in health and social care settings Assessment Criteria The learner can: 1.1 Identify legislation and codes of practice that relate to handling information in health and social care 1.2 Summarise the main points of legal requirements and codes of practice for handling information in health and social care 2.1 Describe features of manual and electronic information storage systems that help ensure security 2.2 Demonstrate practices that ensure security when storing and accessing information 2.3 Maintain records that are up to date, complete, accurate and legible 3.1 Support others to understand the need for secure handling of information 3.2 Support others to understand and contribute to records Other s may include: ï‚ · Colleagues ï‚ · Individuals accessing care or support Exemplification 2 Be able to implement good practice in handling information 3 Be able to support others to handle information  © OCR 2010 1 Assessment This unit needs to be assessed in line with the Skills for Care and Development QCF Assessment principles. This unit is competence based. This means that it is linked to the candidate’s ability to competently perform a range of tasks connected with their work. This unit may be assessed using any method, or combination of methods, which clearly demonstrates that the learning outcomes and assessment criteria have been met. This unit requires workplace assessment of occupational competence. Assessment decisions for competence based learning outcomes (eg those beginning with ‘Be able to’) must be made in a real work environment by an occupationally competent assessor. Any knowledge evidence integral to these learning outcomes may be generated outside of the work environment but the final assessment decision must be within the real work environment. Competence based assessment must include direct observation as the main source of evidence. For this unit, learning outco mes 2 and 3 must be assessed in a real work environment. Guidance on assessment and evidence requirements  OCR does not stipulate the mode of delivery for the teaching of the content of this unit. Centres are free to deliver this unit using any mode of delivery that meets the needs of their candidates. Centres should consider the candidates’ complete learning experience when designing learning programmes. National occupational standards (NOS) mapping/signposting This unit has been developed by Skills for Care and Development in Partnership with Awarding Organisations. It is directly relevant to the needs of employers and relates to national occupational standards developed by Skills for Care and Development. As such, the unit may provide evidence for the following national occupational standards in health and social care developed by Skills for Care and Development: HSC 31 Content recurs throughout HSC NOS knowledge requirements NOS can be viewed on the relevant Sector Skills Council’s website or the Occupational standards directory at www.ukstandards.co.uk Functional skills signposting This section indicates where candidates may have an opportunity to develop their functional skills. Functional Skills standards can be viewed at http://www.qcda.gov.uk/15565.aspx 2  © OCR 2010 Functional Skills Standards English Speaking and Listening Reading ïÆ' ¼ ïÆ' ¼ Mathematics Representing Analysing ICT Use ICT systems Find and select information Develop, present and communicate information ïÆ' ¼ Writing ïÆ' ¼ Interpreting Additional information For further information regarding administration for this qualification, please refer to the OCR document ‘Administrative Guide for Vocational Qualifications’ (A850). This unit is a shared unit. It is located within the subject/sector classification system 01.3 Health and Social Care.

Pride and Prejudice and A Midsummer Nights Dream

First Impressions Revisited â€Å"The course of true love never did run smooth.† -William Shakespeare, A Midsummer Nights Dream ‘Pride and Prejudice first appeared between 1796 and 1797 under the title, ‘First Impressions. At first, the novel was written anonymously; however, after Jane Austens death, the novel became publicly known to people. The novel itself is a comedy of manners set in a quiet and charming rural England, between 1796 and 1813; to be exact, Pride and Prejudice is set amidst Napoleonic Wars, dating from 1797 up to 1815. In Austens words, the novel was ‘light and bright and sparkling. The quote from William Shakespeare best describes the love stories of Jane Bennet and Charles Bingley; Elizabeth Bennet and†¦show more content†¦Darcy, the antagonist-turned-protagonist in the novel. His pride blinds his judgment of people. Darcy judges people through their manners hence, because of his dislike in Elizabeths family manners; he separated Charles and Jane away from each other, leaving Elizabeths sister heartbroken. Austens books are written with satirical humor best rep resented by Mr. Collins and Lady Catherine de Bourgh. Mr. Collins is a comical and pompous, snobbish clergyman living at Hunsford parsonage near Rosings, the home of Lady Catherine de Bourgh. According to the English law, since Mr. Bennet had no male children to inherit the state, Mr. Collins is the rightful heir of the estate since he is a distant relative of Mr. Bennet. Mr. Collins is a funny character in the novel due to his extremely long speeches and silly formalities of no clear meaning. He is very proud of Lady Catherine and her generosity in giving him the Hunsford parsonage. â€Å"A fortunate chance had recommended him to Lady Catherine de Bourgh when the living of Hunsford was vacant; and the respect which he had felt for her high rank, and his veneration for her as his patroness, mingling with very good opinion of himself and his authority as a clergyman, made him altogether a mixture of pride and obsequiousness, self-importance and humility.† (Austen and Jennings 67) Mr. Collins long speeches do not represent the truth in general; it is his only means of making people admire him.Show MoreRelatedComparing Shakespeare s Midsummer Night s Dream, Pride And Prejudice And The Great Gatsby2712 Words   |  11 PagesCompare and contrast the presentation of love and marriage in A Midsummer Night’s Dream, Pride and Prejudice and The Great Gatsby. 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