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1
Nicholls, Felicity K. M. "Genetic analysis of the gene Additional sex combs and interacting loci." Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/29644.
Повний текст джерелаАнотація:
In order to recover new mutant alleles of the Polycomb group gene Additional sex combs (Asx), mutagenized chromosomes were screened over the putative Asx allele XT129. Thirteen new mutant strains that fail to complement XT129 were recovered. Unexpectedly, the thirteen strains sorted into four complementation groups. Recombination mapping suggests that each complementation group represents a separate locus. The largest group fails to complement a deletion of Asx and maps in the vicinity of 2-72, the published location of Asx. All new mutant strains enhance the phenotype of Polycomb mutant flies and are not allelic to any previously discovered second chromosome Polycomb group genes. Therefore, the new mutants may be considered putative new members of the Polycomb group. This study suggests that Asx belongs to a sub-group of genes displaying intergenic non-complementation.<br>Science, Faculty of<br>Zoology, Department of<br>Graduate
2
O'Keefe, Louise. "Genetic analysis of the role of pebble during cytokinesis in Drosophila." Title page, contents and abstract only, 2001. http://web4.library.adelaide.edu.au/theses/09PH/09pho415.pdf.
Повний текст джерелаАнотація:
Errata pasted onto back page. Bibliography: p. 133-149. The RhoGEF activity of PBL is shown to be acting predominantly by the activation of Rho1 and downstream signaling pathways required for contractile ring function during cytokinesis. Genetic evidence suggests this could be through the activation of Diaphanous (an FH protein) to reorganize the actin cytoskeleton, as well as through the activation of Rho-kinase which results in the phosphorylation, and activation of myosin. Highlights a possible role for PBL during contractile ring function at a later stage that previously thought. Genetic interaction screens were employed to identify regulators of PBL activity during cytokinesis. CDK1 was identified genetically as a candidate for regulating PFB activity, but functional studies in vivo showed that this regulation was not by direct phophorylation of the PBK consensus CDK1 suites tested. Further screening has identified other possible components pf PBL signaling pathways, but a role during cytokinesis for these interactors remains to be confirmed. The eye phenotypes described provide ideal systems for the identification of components of PBL signaling pathways in Drosophila. The high level of conservation in the mechanism of cytokinesis from yeast to mammals would also suggest that the identified interactors would most likely represent components of cytokinesis pathways in all eukaryotes.
3
Riddihough, Guy. "The Drosophila hsp27 promoter." Thesis, University of Cambridge, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.258159.
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4
Johnstone, Oona. "Characterization of the Vasa-eIF5B interaction during Drosophila development." Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=84265.
Повний текст джерелаАнотація:
Translational control is an important means of regulating gene expression. Development of the Drosophila germ line relies on translational regulation to differentially express maternal mRNAs, allowing it to develop distinctly from the soma. One of the critical factors required for germ cell development and function is the conserved DEAD-box RNA helicase Vasa (Vas). The research presented in this thesis examines the role of Vas in translational regulation during Drosophila germ line development. A two-hybrid screen conducted with Vas identified a translation initiation factor eIF5B (dIF2), as a direct interactor. Mutations were created in eIF5B and were found to enhance the vas mutant phenotypes of reduced germ cell numbers, and posterior segmentation defects, suggesting a functional interaction between these factors in vivo. In order to further understand the biological significance of the Vas-eIF5B interaction, the region of Vas required for eIF5B-binding was mapped and then specifically disrupted. Reduction of Vas-eIF5B binding using a transgenic approach, virtually eliminated germ cell formation, while having only a moderate effect on the somatic requirement of Vas in posterior segmentation. In addition, Vas-eIF5B interaction was found to be required for the establishment of polarity within the egg during oogenesis, likely through direct regulation of gurken (grk) mRNA. We concluded that through interaction with eIF5B, Vas plays a critical role in translational regulation in the germ line. In addition, another Drosophila DEAD-box protein, highly similar to Vas, called Belle (Bel) was characterized. Mutations in bel were found to also affect the germ line, leading to both female and male sterility. Like Vas, Bel is implicated in translation initiation, however bel is an essential gene, with a requirement for growth, whose function is not restricted to the germ line. Our data suggest that Bel may be a nucleocytoplasmic shuttling protein,
5
Zhang, Li. "DRMT4 (Drosophila arginine methyltransferase 4) : functions in Drosophila oogenesis." Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=80905.
Повний текст джерелаАнотація:
DRMT4 (Drosophila Arginine MethylTransferase 4) is an arginine methyltransferase in Drosophila (Boulanger et al. 2004). It shows the highest identities with mammalian PRMT4/CARM1 (Protein Arginine MethylTransferase 4) (59% identity, 75% similarity). HPLC analysis demonstrated that DRMT4 belongs to the type I class of methyltransferases (Boulanger et al. 2004), meaning that DRMT4 catalyzes asymmetrical dimethylarginine formation. A polyclonal antibody against DRMT4 was generated and used to study DRMT4 expression using western blots and immunostainings. In order to study DRMT4 function in Drosophila using genetic methods, we created three kinds of DRMT4 transgenes: a genomic DRMT4 under its own control, a genomic DRMT4-GFP fusion gene and a cDNA DRMT4 under UAS control. We investigated DRMT4 localization in wild type flies using the DRMT4-GFP transgenic line and immunostaining.
6
Lee, Michael James. "TACC proteins in Drosophila and Xenopus." Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.619794.
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7
McGurk, Leeane. "Drosophila lacking RNA editing." Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/2695.
Повний текст джерелаАнотація:
ADAR is an adenosine deaminase that acts on dsRNA. Once bound to dsRNA, ADAR deaminates specific adenosines into inosines. If this occurs within the coding region of a transcript the inosine will be read as a guanosine. This can lead to a change in the amino acid at this position and increase protein diversity. In mammals there are three ADAR genes: ADAR1, ADAR2 and ADAR3. However, only ADAR1 and ADAR2 have been shown to be enzymatically active. ADAR1 is widely expressed and can edit both coding RNA and non-coding RNA. ADAR2 is restricted to the CNS and the key transcript that it edits encodes the GluR-B subunit of the glutamate-gated ion channel receptor. Editing of the Q/R site in the GluR-B transcript occurs with an efficiency of more than 99.9% and changes the genomically encoded glutamine into an arginine. This results in an ion channel that is impermeable to calcium. The ADAR2 knock-out mice are viable, but suffer from epileptic seizures and die by day 20. This phenotype can be rescued by expressing the edited R isoform of GluR-B, suggesting that this site is the most important target for ADAR2. Drosophila has only one Adar gene and its product has been reported to edit more than one hundred adenosines in different transcripts. Many of these transcripts encode subunits of ion channels, and it has been hypothesised that lack of ion channel editing causes the behavioural defects and age-related neurodegeneration observed in Adar deletion mutants. In this thesis I investigate the function of ADAR in an uncharacterised Adar mutant, Adar5G1. To characterise the Adar5G1mutant I not only used standard histology but a 3D imaging technique, optical projection tomography (OPT), that had not been reported to be used with Drosophila before this work. OPT allows the internal organs to be imaged without any manual sectioning or dissecting. I used OPT to identify neurodegenerative vacuoles from within the intact head and present the data both in 2D and in 3D. In addition to this, I demonstrate that this technique can be used to image global expression patterns in the Drosophila adult and I relate the TAU-β galactosidase expression pattern to the Drosophila anatomy. The neurodegeneration observed by OPT was confirmed by detailed analysis of stained wax sections. Complete loss of Adar, in the Adar5G1 mutant revealed age-dependent vacuolisation of the retina and mushroom body calyces. The vacuolisation observed in the Adar5G1 mutant was rescued by expression of Drosophila Adar and human ADAR1 p110, and ADAR2. However the cytoplasmic form of ADAR1, ADAR1 p150, did not rescue the vacuolisation of the Adar5G1 mutant. ADAR3, a catalytically inactive ADAR, rescued the vacuolisation phenotype of the Adar5G1 mutant, suggesting that ADAR may have an additional function independent of editing activity. The vacuolisation of the Adar5G1mutant was found not to be associated with type I programmed cell death. However, it was associated with swollen nerve fibres and degrading ommatidia containing multilamellar whorls. Neurodegeneration in various Drosophila mutant models and human neuropathies has been associated with similar cellular structures, suggesting that loss of ADAR results in neurodegeneration common to many of the known neuropathies. Finally, I found that expression of edited isoforms of the nicotinic receptor channel 34E subunit (Nic 34E) failed to rescue the locomotion phenotype of the Adar mutant. However, I found preliminary evidence that one of the lines generated for an edited isoform of Rdl, a subunit of the GABA receptor ion channel, gave a partial rescue of both locomotion and neurodegeneration of the Adar1F4 and Adar5G1 mutant.
8
Ometto, Lino. "The selective and demographic history of Drosophila melanogaster." Diss., [S.l.] : [s.n.], 2006. http://edoc.ub.uni-muenchen.de/archive/00004942.
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9
Vermeulen, Cornelis Joseph. "Genetics of lifespan determination in Drosophila melanogaster /." [Wageningen] : Ponsen & Looyen, 2004. http://www.gbv.de/dms/goettingen/473006952.pdf.
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10
Gilchrist, Anthony Stuart. "Sperm displacement in drosophila melanogaster." Thesis, University College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.263252.
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11
Harbison, Diane T. "Male-specific transcripts from Drosophila melanogaster." Thesis, University of Glasgow, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337508.
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12
Von, Dassow George Robert Hartmann. "How dynamic networks animate living embryos /." Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/5237.
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13
O'Connell, Sinead. "Functional characterisation of the Polycomblike protein of Drosophila melanogaster." Title page, table of contents and abstract only, 1999. http://web4.library.adelaide.edu.au/theses/09PH/09pho1841.pdf.
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14
Garrido, Damien. "Etude de l’homéostasie lipidique chez Drosophila melanogaster." Thesis, Université Paris-Saclay (ComUE), 2015. http://www.theses.fr/2015SACLS030.
Повний текст джерелаАнотація:
Le métabolisme des acides gras (AG) est crucial dans le maintien de l’homéostasie. Son implication dans des processus tels que la signalisation, le stockage énergétique, l’isolation thermique, la régulation du comportement ne révèle qu’une fraction de la complexité et de la variabilité des rôles dans lesquels il peut être associé. En outre, ce métabolisme est dérégulé dans de nombreuses pathologies, diabète, obésité, cancers,... C’est pourquoi les enzymes de ce métabolisme constituent des cibles attractives pour développer de nouveaux traitements. Cependant les conséquences de ces dérégulations sur l’organisme sain sont encore mal connues, surtout à l’échelle de chaque organe.L’objectif de ma thèse était d’évaluer comment le métabolisme des AGs participe à la régulation de l’homéostasie au sein d’un organisme entier. Pour cela, j’ai utilisé les possibilités génétiques du modèle drosophile dont le métabolisme est comparable à celui des mammifères. J’ai ainsi montré que la synthèse d’AGs contribue à neutraliser les effets toxiques du sucre alimentaire. Ce processus se fait en coopération avec la voie de la détoxification du méthylglyoxal qui permet de prévenir la formation de composés issus de la glycation non enzymatique. J’ai aussi contribué à montrer que les précurseurs des hydrocarbures et phéromones ont une origine flexible, qui dépend du maintien de l’homéostasie et qui peut perturber les interactions entre individus. Je suis actuellement en train d’étudier la sensibilité à l’inhibition de la synthèse d’AG de différents modèles de croissance dérégulée. Enfin, dans un travail préliminaire, j’ai montré que le métabolisme des AGs est essentiel dans le tube digestif, possiblement en perturbant l’homéostasie hydrique de la larve.L’ensemble de ces résultats aidera à mieux cerner l’importance du métabolisme des AGs dans le maintien de l’homéostasie d’un organisme sain et dans des processus dérégulés<br>Fatty acid (FA) metabolism is crucial in maintaining homeostasis, but also in a numerous of processes including signaling, energy storage, protection to temperature loss, regulation of behavior... In addition, FA metabolism is deregulated in several pathologies including diabetes, obesity, and cancers... Therefore, the enzymes that catalyze the reactions of the FA metabolic pathways constitute attractive targets to develop novel therapies. However the consequences of these deregulations in healthy organism are still poorly known, in particular at the level of each organ.The aim of my PhD was to estimate how FA metabolism participates in the regulation of homeostasis within a whole body organism. To address these issues, I used the genetic possibilities of the Drosophila model, whose metabolism is similar to that of mammals.I showed that FA synthesis contributes to neutralize the toxic effects of dietary sugar. This process operates in cooperation with the methylglyoxal detoxification pathway, which prevents the formation of compounds resulting from the non-enzymatic glycation. I also contributed to a project showing that the precursors of hydrocarbons and pheromones have a flexible origin, which depends on lipid homeostasis and may affect sexual recognition between individuals. Currently, I’m studying the consequences of FA synthesis inhibition in various deregulated growth models. Finally, in a preliminary work, I showed that the FA metabolism is essential in the digestive tract, possibly by disrupting water homeostasis in larvae. Taken together, these results will help to characterize the importance of FA metabolism in healthy organism as well as in deregulated processes
15
Ayyar, Savita. "Analysis of TGIF function in Drosophila." Thesis, University of Cambridge, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.620360.
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16
Wang, Shu-Huei. "Regulation of vein, an activating ligand of the drosophila EGF receptor." Connect to this title online, 2003. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1054165285.
Повний текст джерелаАнотація:
Thesis (Ph. D.)--Ohio State University, 2003.<br>Title from first page of PDF file. Document formatted into pages; contains xv, 189 p.; also includes graphics (some col.) Includes bibliographical references (p. 168-189). Available online via OhioLINK's ETD Center
17
Gould, Alexander Paul. "Homeotic gene function during embryogenesis in Drosophila." Thesis, University of Cambridge, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.335101.
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18
Hemmat, Mortaza. "Genetic analysis of competition in Drosophila melanogaster." Thesis, University of Liverpool, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.257181.
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19
Tauber, Merav. "Molecular genetics of aggressive behaviour in Drosophila melanogaster." Thesis, University of Leicester, 2010. http://hdl.handle.net/2381/10224.
Повний текст джерелаАнотація:
Aggression is a key component of the normal repertoire of behaviours in a broad range of animals from insects to mammals. Although the genetic basis for aggression is widely accepted, only a few individual candidate genes have been studied. Recent studies have indicated that Drosophila melanogaster can serve as a powerful model system to study the genetics of aggression. The aim of this project was to identify genes associated with aggression by global profiling of the fly transcriptome using DNA expression microarrays. At the core of this study was a behavioural screen in which the aggression of 910 pairs of males was observed and scored. Microarray analysis revealed 350 genes that were differentially expressed between aggressive and nonaggressive flies. Several biological functions such as translation activity, immune response, ion transport, and sensory transduction were significantly over-represented. Analysis of the upstream region of these genes also suggested several shared motifs that might serve as transcription factor binding sites that drive the co-expression of these genes. One of the top differentially expressed genes was Dat, (dopamine-Nacetyltransferase), which was upregulated in aggressive flies. Dat has two isoforms generated by alternative splicing, DatA and DatB. QPCR analysis revealed that only DatB is upregulated in aggressive flies. In Datlo mutants that express only DatB, aggression is also increased, an effect that can be reverted by over-expressing the DatA transgene. Additional experiments over-expressing DatB indicate that the two isoforms effectively act in opposite ways to regulate aggression, suggesting that a balance between them is necessary for adaptive levels of aggression. Another candidate gene was CG6480, whose levels were reduced in aggressive flies. The function of this gene is unknown, but it does share a conserved motif called Fascin with its mammalian ortholog frg1. Silencing this gene by dsRNAi resulted in flies that show elevated levels of aggression.
20
Palmer, William Hunt. "Evolution and genetics of antiviral immunity in Drosophila." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31557.
Повний текст джерелаАнотація:
Virus-host interactions determine virus transmissibility and virulence, and underlie coevolution that shapes interesting biological phenomena such as the genetic architecture of host resistance and host range. Characterization of the virus factors that exert selective pressure on the host, and the host genes which underlie resistance and adaptation against viruses will help to define the mechanistic pathways embroiled in host-virus coevolution. In this thesis, I describe the viral causes and host consequences of host-virus coevolution. These include genomic signatures consistent with antagonistic coevolution in antiviral RNA interference pathway genes such as high rates of positive selection and polymorphism, loci that underlie genetic variation in resistance to virus infection, and apparent conflict between NF-κB signalling and DNA virus infection. The RNA interference (RNAi) pathway is the most general innate immune pathway in insects, underlined by the observation that many viruses encode suppressors of RNAi (VSRs). The relationship between RNAi and VSRs has garnered attention as a plausible battleground for host-virus antagonistic coevolution, and genomic patterns in Drosophila support this hypothesis. However, genomic patterns in the N-terminal domain of the key RNAi effector gene, Argonaute-2, have not been described. In Chapter 2, I sequence the Argonaute-2 N-terminal domain using PacBio long-read sequencing technology to describe variation within and across Drosophila species, and test whether this variation is associated with resistance to Drosophila C Virus. The RNAi pathway evolves adaptively in Drosophila, but this has not been formally extended across invertebrate species. In Chapter 3, I quantify rates of adaptive protein evolution and describe evidence for selective sweeps in RNAi pathway genes using population genomic data from 8 insect and nematode species. These analyses indicate that RNAi genes involved in suppression of transposable elements and defence against viruses evolve rapidly across invertebrates, and I identify genes with signatures of elevated adaptation in multiple insect species. Host genes that underlie host-virus interactions have been described in RNA virus infection of Drosophila, however substantially less attention has focussed on the host response to DNA viruses, primarily because no DNA viruses have been isolated from Drosophila. In Chapter 4, I describe the isolation of Kallithea virus, a Drosophila dsDNA nudivirus, and characterise the host response to infection and genetic variation in resistance. I find that Kallithea virus infection causes early male-specific lethality, a cessation of oogenesis, and induction of undescribed virus-responsive genes. Further, I describe genetic variation in resistance and tolerance to Kallithea virus infection, and identify a potential causal variant for virus-induced mortality in Cip4. Insect viruses commonly encode viral suppressors of RNAi, however there are a multitude of antiviral immune mechanisms besides RNAi which may select for viral-encoded inhibitors. In Chapter 5, I describe the requirement for RNAi and NF-κB in immunity against Kallithea virus, and map gp83 as a virus-encoded inhibitor of NF-κB signalling. I find that gp83 inhibits Toll signalling at the level of, or downstream of NF-κB transcription factors, and that this immunosuppressive function is conserved in other nudiviruses.
21
Brown, Elizabeth. "The Behavioral Genetics of Olfaction in Drosophila melanogaster." University of Cincinnati / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1490351166817714.
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22
Sun, Qi Zinn Kai George. "Molecular genetics of axon guidance in Drosophila melanogaster /." Diss., Pasadena, Calif. : California Institute of Technology, 2000. http://resolver.caltech.edu/CaltechETD:etd-03242005-130557.
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23
Jud, Molly Christine. "Jun signaling during Drosophila development." Thesis, The University of Utah, 2016. http://pqdtopen.proquest.com/#viewpdf?dispub=10130207.
Повний текст джерелаАнотація:
<p> Jun N-terminal kinase (JNK) signaling is a key modulator of development and disease in all multicellular organisms. One process in which the consequences of both gain and loss of JNK signaling can be monitored is embryonic dorsal closure (DC) in the fruit fly, <i>Drosophila melanogaster.</i> DC occurs midway through embryogenesis; it is the process by which the lateral epidermis expands bilaterally to meet and fuse at the dorsal midline, thereby encasing the entire embryo in epidermis. JNK signaling in leading edge (LE) cells (the dorsal-most row of epidermis) initiates closure. My studies of a novel but conserved JNK signaling antagonist, Raw, have provided several unique insights into: 1) Jun function as a component of the AP-1 transcription factor, and 2) the role of the epidermis as a signaling template mediating development of the epidermis and adjacent tissues.</p><p> My graduate work has built upon the demonstration that <i>raw</i> is required to prevent promiscuous JNK signaling in the embryonic epidermis just prior to DC. I have shown that <i>raw</i> is necessary for proper accumulation of Jun in LE cells required to define the LE, which functions as a signaling center required for epidermal closure as well as for underlying heart development. I have gone on to show that Jun accumulates at previously unrecognized sites in the embryonic epidermis, including tracheal pits and solitary epidermal cells lying directly above the peripheral nervous system (PNS). Jun activity is required for tracheal and nervous system defects observed in mutants of two JNK signaling antagonists, <i>raw</i> and <i> rib,</i> and indicates that cell signals within and to an adjacent tissue are integral to proper development. I have found that the epidermis plays an instructive role during development, and results from my work have led to insights into how JNK signaling centers in the epidermis coordinate morphological processes.</p><p> As Raw is a novel but conserved JNK signaling antagonist, I have built and tested models of its molecular mechanism of action as well. Bolstering conclusions of previous studies of mammalian c-Jun in cell culture, my data indicate that N-terminal phosphorylation is not an on/off switch, but rather it increases Jun stability for its activity as a component of the AP-1 transcription factor. <i>raw</i> mutants exhibit both high levels of Jun protein and an accumulation of phosphorylated Jun (P-Jun), and my data point to a role for Raw in effecting the Jun:P-Jun ratio via mediation of Jun degradation. In deciphering the mechanism of Raw function, we are gaining significant new insights into previously unrecognized mechanisms of JNK signaling regulation. Understanding these mechanisms will be important for dissecting the etiology of developmental abnormalities and diseases, such as cancer, which hinge on the Goldilocks effect, having just the right amount of signaling at just the right time.</p>
24
Aradhya, Rajaguru. "Characterization of quiescent state and reactivation of adult muscle precursor cells in Drosophila melanogaster." Thesis, Clermont-Ferrand 1, 2013. http://www.theses.fr/2013CLF1MM16.
Повний текст джерелаАнотація:
Pas de résumé disponible<br>Use of stem cells in regenerative medicine has attracted great interest in the past decade. Muscle stem cells such as satellite cells were shown to regenerate skeletal muscle tissue after injury and to contribute to muscle growth. These properties have raised an enormous interest in using satellite cells for the therapy of skeletal muscle wasting disorders where the intrinsic stem cell population is unable to repair muscle tissue. However, better understanding of the mechanisms controlling satellite cell lineage progression and self-renewal is crucial to exploit the power of these cells in combating myopathic conditions. In the studies described here, the mechanisms regulating the in vivo behavior and maintenance of quiescence of Drosophila Adult Muscle Precursors (AMPs) that share several properties with the vertebrate satellite cells are analyzed. We show that undifferentiated embryonic AMPs display homing behavior and that their survival depends on the somatic muscles. We observe that AMPs establish direct contact with muscle fibers by sending thin filopodia and that this AMP-muscle interaction is crucial for AMPs spatial positioning. Larval muscles also play an important role in promoting the AMP cell proliferation. They achieve this by secreting Drosophila Insulin like peptide 6 (dIlp6) that activate the AMPs from their quiescent state and induce proliferation during the end of the second larval instar. We also demonstrate that Notch acts downstream of Insulin pathway and positively regulates proliferation of AMPs via dMyc. In the second part of the thesis manuscript we report that the affected formation ofadult muscles impacts on persisting abdominal larval templates. In this section role of the Notch signaling pathway in specification of the Adult founder cells is also demonstrated. Finally, we report generation of new tools for the cell type specific genome wide approaches that can be applied to identify global gene expression profiles in quiescent versus activated AMPs. Together these studies identified several new features of AMPs and enhance our understanding on the processes regulating stem cells homing, quiescence and reactivation
25
Zecchini, Vincent. "A novel function of Notch regulates JNK activity and apoptosis in the Drosophila embryo." Thesis, University of Cambridge, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.621033.
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26
Shen, Shih-Pei. "Characterisation of Dichaete functions and targets during Drosophila embryonic development." Thesis, University of Cambridge, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612743.
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27
Coulson, Michelle R. "Characterisation of starvin' : a novel Drosophila melanogaster gene." Title page, abstract and contents only, 1999. http://web4.library.adelaide.edu.au/theses/09PH/09phc855.pdf.
Повний текст джерелаАнотація:
Bibliography: p. 133-141. A genetic and molecular characterisation of the Drosophila gene starvin', focussing on analysis of the sequence of starvin', characterisation of the embryonic localisation of starvin' protein, and the identification and phenotypic characterisation of starvin' mutants.
28
Łada, Karolina. "Tissue interactions and morphogenesis during Drosophila dorsal closure." Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611646.
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29
Liang, Lu. "Vasa function in Drosophila pole plasm." Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=42079.
Повний текст джерелаАнотація:
Pole plasm in Drosophila melanogaster, through the posteriorly localized determinant nanos, controls the formation of the abdominal segments and, through an unknown mechanism, controls the formation of the germline. oskor, vasa, and tudor are three critical genes in the pole plasm assembly pathway and their gene products, oskar RNA, Vasa protein and Tudor protein are localized in the pole plasm in a precise order. The localization of oskar and nanos mRNAs is closely related to their translational activation. We provide evidence here by in vitro biochemical assays that Vasa protein is an ATP-dependent RNA helicase, an ATPase and an RNA-binding protein, as was predicted from its sequence similarity to mammalian translation initiation factor eIF-4A. The enzymatic activities of Vasa protein are important for its function, but the initial localization of Vasa protein to the pole plasm is independent of its RNA helicase and RNA-binding activities. Further, we cloned Bruno, a Xenopus etr-1 homologue with three ribonucleoprotein-recognition-motifs (RRM), by far-western screening using Vasa protein as bait. Bruno is the product of the gene arrest, which was cloned independently by Webster and Macdonald at Stanford University. The localization of Bruno protein in S1-10 oocytes is similar to that of oskar and gurken RNAs. This is significant as both oskar and gurken RNAs contain Bruno-response-elements at their 3$ sp prime$UTRs. Bruno is mislocalized in vasa mutant ovaries, suggesting that the localization of Bruno protein requires Vasa function. As a translational activator of oskar and nanos RNAs and a regulator of Bruno protein. the participation and the importance of Vasa protein in pole plasm assembly and function is obvious. Whether Vasa acts directly or indirectly to activate translation of specific mRNAs will require further examination.
30
Peel, Nina. "Control of the centrosome cycle in Drosophila." Thesis, University of Cambridge, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612903.
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31
Aspland, Simon Eric. "Extradenticle and HOX gene function in Drosophila." Thesis, University of Cambridge, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.627253.
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32
Nanda, Shreeya. "Functional characterisation of the Drosophila Sox100B gene." Thesis, University of Cambridge, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.614283.
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Boisclair, Lachance Jean-François. "Mechanisms of epithelial patterning in the «Drosophila» ovary." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=96966.
Повний текст джерелаАнотація:
Patterning of the Drosophila eggshell requires the induction of dorsal fates in the follicular epithelium of the ovary, which will secrete this eggshell. These fates are induced by the localized activation of epidermal growth factor (Egfr) signaling mediated by its localized ligand Gurken (Grk), which restricts the acquisition of dorsal fates to the dorsal anterior domain of the epithelium. The generation of the complex pattern of fates along the dorsal-ventral (DV) axis has been proposed to be generated by the induction of a second round of Egfr signaling in the follicular epithelium by the late Grk-Egfr signaling. Along the anterior-posterior axis, the restriction of dorsal fates induction to the anterior of the epithelium has been proposed to be mediated by the restriction of Decapentaplegic (Dpp) signaling to the anterior of the tissue. However, some results from the literature cannot be explained by these two models, suggesting that the mechanisms leading to dorsal fates specification are not fully understood. Contrary to these two models, I have shown that a second round of Egfr signaling induced by Grk-Egfr signaling is not required to specify dorsal fates along the DV axis. Instead, my data support the hypothesis that the different levels of Egfr activity generated by the gradient of Grk are sufficient to generate the pattern of fates along the DV axis. Furthermore, my results show that Dpp signaling is not required to restrict dorsal fate acquisition to the anterior of the tissue. Rather, my results suggest that the restriction of competence to induce dorsal fates to the anterior of the epithelium depends on the generation of a posterior refractory fate. My results suggest that it is the absence of the expression of the transcription factor Mirror (Mirr) in response to ectopic Egfr signaling in the posterior domain that restricts dorsal fates acquisition to the anterior domain. Taken together, my results suggest that the competence to express Mirr in the posterior domain is dependent on the early induction of Egfr signaling in this domain. Since only the dorsal-anterior domain is exposed to late Grk-Egfr signaling, Mirr expression is restricted to this domain.<br>La formation des structures dorsales sur la coquille de l'oeuf de la drosophile requiert l'induction de destinées cellulaires dorsales dans l'épithélium folliculaire. L'induction de ces destinées cellulaires dans le domaine dorso-antérieur de l'épithélium folliculaire est médiée par la restriction de l'activation de la voie de signalisation du récepteur du facteur de croissance épidermal (Egfr) par son ligand Gurken (Grk). Un mécanisme a été proposé pour expliquer la génération du patron des destinées cellulaires dorsales sur l'axe dorso-ventral. Ce mécanisme requiert l'induction par la signalisation Grk-Egfr, d'une seconde ronde de signalisation par Egfr dans l'épithélium folliculaire. De plus, un autre modèle propose que la restriction de ces destinées cellulaires est médiée par la restriction de la signalisation Decapentaplegic (Dpp) à l'antérieur de ce tissu. Cependant, certains résultats décrits dans la littérature ne sont pas expliquées par ces deux modèles suggérant que les mécanismes menant à l'induction des destinées cellulaires dorsales ne sont pas bien compris. Mes résultats montrent que la seconde ronde de signalisation Egfr n'est pas requise pour la spécification des destinées cellulaires dorsales. Mes résultats supportent plutôt l'hypothèse que différentes intensités de la signalisation Egfr activée par le gradient de Grk contrôlent l'induction des différentes destinées cellulaires. De plus, mes résultats montrent que la signalisation Dpp n'est pas requise pour la spécification des destinées cellulaires dorsales à l'antérieur du tissu. Mes résultats montrent plutôt que la génération d'une destinée postérieure réfractaire à l'induction des destinées cellulaires dorsales par la signalisation Egfr est responsable de la restriction des destinées dorsales à l'antérieur. Mes résultats suggèrent que la compétence, pour induire les destinées cellulaires dorsales, dépend de l'habileté des cellules pour induire l'expression du facteur de transcription Mirror (Mirr) en réponse à la signalisation Egfr. Dans leur ensemble, mes résultats supportent un modèle où la signalisation Egfr précoce induite par Grk inhibe l'habileté d'induire l'expression de mirr dans le domaine postérieur. Puisque le domaine dorso-antérieur n'est pas exposé au signal précoce, l'induction tardive de la signalisation Egfr par Grk induit l'expression de mirr dans ce domaine.
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Jacinto, Antonio Alfred Coelho. "Analysis of hedgehog signalling in Drosophila melanogaster development." Thesis, Imperial College London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.313805.
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Standen, Graeme N. "Some aspects of genetic recombination in Drosophila melanogaster." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.282210.
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Finlayson, Andrew. "Characterisation of phosphodiesterase 11 in Drosophila melanogaster." Thesis, University of Glasgow, 2010. http://theses.gla.ac.uk/1954/.
Повний текст джерелаАнотація:
The PDE 11 family of dual specificity phosphodiesterases was first identified in 2000, and has not been well characterised, although mutations in the gene have been linked to multiple disorders, including major depressive disorder, and cancer. DmPDE11 is a dual specificity phosphodiesterase, which shows 96% similarity with the catalytic domain of HsPDE11A, and around 40% similarity along the length of the protein. The focus of this project was to characterise this important enzyme using the model organism Drosophila melanogaster. The resources available to Drosophila researchers are unrivalled, and include a sequenced genome, unparalleled transgenic technology, of which stocks are freely available, and Homophila, a database of human disease genes and their Drosophila orthologues. Drosophila is genetically tractable to an extent not seen in any other multicellular organisms. The genetic dissection of gene function in Drosophila has allowed the identification and characterisation of numerous cell signalling genes. For example, mutations to Dunce were shown to affect olfactory learning. This allowed the identification and cloning of the mammalian dnc homologue PDE4. cAMP (and cGMP) were subsequently shown to modulate learning and memory in mammals. The 5.8 kb expressed sequence tag (EST) SD13096 had previously been shown to contain sequence present in the incomplete PDE11 RA ESTs previously released by Flybase, but also incorporating a 5’ UTR, and an in-frame start codon within two novel 5’ exons. A Northern blot of DmPDE11 RA produced one band of approximately 5.8kb; as this matches the size of the DmPDE11 RA ORF, was accepted that SD13096 encodes the entire PDE11 RA ORF (Day, unpublished). Expression of this EST in S2 cells revealed that the construct produced a protein of the accepted size, and the protein localised to the cytoplasm. However, PDE assays of S2 cell lysate revealed that the enzyme did not appear to encode an enzyme with either cA- or cG-PDE activity. DmPDE11 RA was replaced on Flybase by the new isoforms DmPDE11 RB and DmPDE11 RC, which had two key changes to the RA isoform. Both new isoforms had different N termini, sharing a second exon, with distinct first exons. Furthermore, exon 11 of the RA exon is not present in the newly predicted isoforms. These new isoforms were verified by reverse transcriptase- polymerase chain reaction analysis. In the course of this verification, two further novel isoforms were identified, which shared the novel N termini with the RB and RC isoforms, but include a novel exon/exon boundary within the original exon 19, which results in a truncated isoform. As such the four isoforms were named DmPDE11 RB long, DmPDE11 RB short, DmPDE11 RC long, and DmPDE11 RC short. The open reading frames of these isoforms were cloned from Drosophila cDNA using high-fidelity DNA polymerase and sequenced for fidelity. The open reading frames were tagged with YFP, and this tag was used to verify expression of these isoforms. Each isoform expressed a protein of the predicted size when expressed in Drosophila. DmPDE11 B and C proteins show distinct localisation in the Malpighian tubule, where the long and short isoforms of each isoform display indistinguishable localisations. DmPDE11 B localises to the apical and basolateral membranes, and DmPDE11 C localises to an unknown organelle, or to vesicles. All 4 isoforms were verified as dual specificity cA- and cG- PDEs. The previous finding (Day, unpublished) that DmPDE11 co-immunoprecipitates with cGMP dependent protein kinase activity, and that cGMP dependent protein kinases co-immunoprecipitate with cG-PDE activity, and thus that cG-PDE(s) interact with at least one cGMP dependent protein kinase, directly or indirectly, was investigated. DmPDE11 C long and short were co-transfected in Schneider 2 cells with the cGKs DG1, DG2P1 and DG2P2. Co-immunoprecipitation of these showed that both the long and short isoforms of DmPDE11 C interact with every cGK screened. Time did not permit the application of this protocol to screen DmPDE11 B interaction with the cGKs. Whether this interaction is direct or indirect was screened by peptide array. Peptide arrays were generated representing the sequence of DmPDE11, DG1, and DG2, and proteins were generated fusing fragments of these proteins with HIS6 and Glutathione-S-Transferase tags. These were expressed in E. coli, and verified by western blotting. HIS6 tagged protein expression was shown to be of higher quality, and was thus affinity purified, and used to overlay and probe the peptide arrays for putative direct interactions. When the PDE11 array was overlaid with tagged protein representing the C terminal half of DG1, and the N and C terminal halves of DG2, a putative direct interaction was identified between DG1 and PDE11 on two separate regions of the PDE11 array, which both fell within the sequence of PDE11 represented by the Middle-HIS6 fragment. As such, this was used to probe the PDE11 array. A reciprocal putative interaction was identified on three regions of the DG1 array, representing sequence in both DG1N-HIS6 and DG1C-HIS6 fragments. Unfortunately, although DG1-HIS6 was verified by western blotting at the analytical stage, attempts to affinity purify the protein failed. Time did not permit the probing of the array with DG1N-GST fusion protein, and so further putative interaction sites on PDE11 may remain. The generation of alanine substitution arrays, and subsequent mutagenesis analysis with yeast two hybrid or co-immunoprecipitation would be necessary to confirm this direct protein-protein interaction as bona-fide. The investigation into a putative direct interaction between PDE11 and DG2 did not yield conclusive data, and so further investigation is required. The role of DmPDE11 in immunity was investigated by the use of DmPDE11 RNAi and deletion lines. The DmPDE11 deletion line showed a qualitative reduction in survival in individual survival assays, but when these data were merged a significant decrease in survival compared to controls was seen. However, fly numbers did not permit the inclusion of all of the necessary controls, and so these assays should be repeated with these. However, upon immune challenge, progeny from a DmPDE11 RNAi (line 9) x Act5c (a ubiquitous GAL4 driver line) cross did not show a decrease in survival compared to parental lines. Transgenic Drosophila expressing H. sapiens PDE11A3 were generated. The protein localised to the nucleus at low levels of protein; increased expression led to nuclear exclusion, and localisation to the basolateral and especially apical membranes, with cytosolic localisation also. The work has provided the tools needed to further research PDE11. The implication of this gene as a tumour suppressor gene, and its role in other processes, means that it is of the utmost importance that this enzyme is further characterised.
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Blackney, Michael James. "Characterising the Drosophila extracellular superoxide Dismutase gene." Thesis, University of Southampton, 2010. https://eprints.soton.ac.uk/179761/.
Повний текст джерелаАнотація:
The indiscriminate action of reactive oxygen species (ROS), if left unregulated, has long been considered contributory to a range of disease processes within the animal kingdom and is also a factor associated with ageing. Consequently modifying the molecular mechanisms that regulate ROS levels may prove therapeutic and could also positively affect longevity. One of the key components of this machinery is the superoxide dismutase (SOD) family of enzymes which regulate ROS levels by scavenging the ROS superoxide. Mammals have three distinct SOD enzymes each responsible for managing superoxide levels in different cellular compartments. In Drosophila homologues of two of the mammalian SODs, the intracellular (SOD1) and mitochondrial (SOD2) SODs, have been identified and studied extensively demonstrating a clear link between SOD and oxidative protection and survival. Recently the sequence of a third sod gene, homologous to both the relatively poorly characterised mammalian (sod3) and C. elegans (sod-4) extracellular sod, was identified in Drosophila and is also predicted to locate extracellularly (sod3). To date, no (published) work has been carried out to assess the role of sod3 within insects. This thesis reports the molecular and biochemical characteristics of sod3 in Drosophila. Detailed within are the steps taken to clone the sod3 gene which appears to be expressed as two gene products formed by alternative splicing. Furthermore, a combination of gene expression, proteomic and functional analysis of a number of sod mutants was used to: i) reveal sex specific sod gene expression; ii) validate a sod3 hypomorph mutant; iii) indicate a functional role for sod3 in protection against H2O2 induced oxidative stress; iv) suggest a SOD1-SOD3 co-dependency for maintaining Cu Zn SOD activity; v) demonstrate the appearance of genetic modifiers in the sod3 hypomorph. The findings of this report and further studies on the Drosophila sod3 gene should encourage the re-evaluation of the previous work concerning SOD’s influence on disease states and lifespan regulation.
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Tixier, Vanessa. "Identification et analyse fonctionnelle de nouveaux gènes impliqués dans la myogénèse chez la drosophile : et mise en évidence d'une transition métabolique nécessaire à la différenciation musculaire." Thesis, Clermont-Ferrand 1, 2011. http://www.theses.fr/2011CLF1MM19/document.
Повний текст джерелаАнотація:
Il existe de nombreuses similitudes au niveau des mécanismes génétiques et moléculaires qui contrôlent les différentes étapes de la myogenèse entre la drosophile et les vertébrés. Afin de mettre en évidence de nouveaux gènes impliqués dans ce processus, nous avons sélectionné des gènes conservés au cours de l’évolution afin de tester leur rôle dans la myogenèse. Des gènes candidats conservés entre le poisson zèbre et la drosophile et exprimés dans des compartiments musculaires ont été sélectionnés in silico à partir des bases de données du poisson-zèbre (Zfin) et de la drosophile (BDGP). Ainsi, 120 gènes ont été mis en évidence, dont plus de la moitié jouerait un rôle dans le métabolisme, et sur les 23 testés par ARNi, 20 donnent des phénotypes musculaires suite à la diminution de leur expression. Les défauts musculaires observés ont permis de replacer le rôle putatif de ces 20 gènes dans le processus myogénique, montrant l’efficacité de cette approche. L’analyse fonctionnelle du gène Pglym78 impliqué dans la glycolyse a ensuite été réalisée. Ce gène est exprimé spécifiquement dans les muscles somatiques et son atténuation donne des défauts de différenciation musculaire caractérisés par un blocage de la fusion des myoblastes et la formation de muscles plus fins. L’ensemble des autres gènes de la glycolyse s’exprime de la même façon et leur inhibition donne aussi des problèmes de différenciation. Ainsi, il existerait au moment de la différenciation musculaire un switch métabolique se traduisant par une augmentation de la glycolyse, similaire à celui mis en évidence dans les cellules cancéreuses, pouvant contribuer à former l’ATP ainsi que les molécules nécessaires pour la synthèse des protéines, le tout permettant la croissance musculaire. Enfin, l’inhibition de la voie insuline, connue pour stimuler la glycolyse mais également la croissance musculaire, diminue l’activité glycolytique et donne des phénotypes similaires à ceux observés lorsque l’on bloque la glycolyse. Nos résultats mettent en évidence l’existence d’un switch métabolique vers la glycolyse, médié au moins en partie par la voie insuline afin de permettre l’augmentation de la synthèse de biomasse dans le muscle, nécessaire à la poursuite de sa différenciation. Ce travail révèle ainsi l’existence d’un lien entre le métabolisme et le développement musculaires<br>A large number of genes involved in myogenesis has been described, but several gaps in comprehension of mechanisms giving rise to functional muscles are still remaining. To fill in these gaps, we selected conserved uncharacterized genes expressed in muscular compartments in drosophila and zebrafish and tested their functions by RNAi knockdown. We found that most of the candidate genes have a role in different steps of embryonic myogenesis in drosophila and interestingly more than a half of them are involved in metabolism. One of these candidates, Pglym78, encodes a glycolytic enzyme and gives rise to late muscle differentiation defects after knockdown in drosophila. Glycolysis is a major metabolic process providing energy and components for biomass synthesis to rapidly growing/proliferating cells such as cancer cells but its role in embryonic development remains unknown. Here we show that starting from midembryogenesis, drosophila Pglym78 and almost all the glycolytic genes display muscle specific expression and that, consistent with this, an important increase in glycolytic activity appears since embryonic stage 14, suggesting that glycolysis can play a role in late steps of myogenesis. This possibility is supported by the fact that attenuation of Pglym78 and other glycolytic genes results in affected muscle differentiation. As shown in Pglm78 knockdown embryos these phenotypes are due to myoblasts fusion arrest and formation of significantly smaller muscle fibres.In order to understand how glycolysis controls myogenesis, we analysed the insulin pathway known to control glycolytic activity and to positively regulate muscle growth by stimulating protein synthesis. Interestingly, inhibition of insulin pathway in differentiating embryonic drosophila muscles leads to the reduced activity of PyK and to phenotypes that are reminiscent of those of glycolytic genes such as fusion arrest and formation of smaller fibres. Thus, our data reveal that metabolic switch to glycolysis positively regulated by insulin pathway is required to support increased biomass synthesis in syncytial muscle cells, revealing direct link between metabolism and development
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Stevens, Naomi Rosalie. "The molecular regulation of centriole duplication in Drosophila." Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611818.
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Fiúza, Ulla-Maj. "Mechanisms of regulation of notch signalling in Drosophila." Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611170.
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McQuilton, Peter Andrew. "Identification of a neurotrophin sequence homologue in Drosophila." Thesis, University of Cambridge, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.615279.
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Sajjadi, Fereydoun G. "The sequence TNNCT modulates transcription of a Drosophila Melanogaster tRNA ₄ gene." Thesis, University of British Columbia, 1987. http://hdl.handle.net/2429/27522.
Повний текст джерелаАнотація:
The transcription efficiency of transfer RNA genes is
modulated by sequences contained in their 5'-flanking region. For a tRNA val₄ gene a pentanucleotide with the sequence TCGCT was identified between positions -33 and -38. I have previously proposed that this sequence may be involved in specifically determining the rate of transcription of this gene. A general form of this sequence, TNNCT was found associated with other Drosophila tRNA genes which showed high ill vitro transcription efficiency.
To further elucidate the role of TCGCT in tRNA transcription, single and double base-pair changes were created in the sequence TCGCT using site-specific mutagenesis. Mutations in the nucleotides -38T, -35C and -34T showed decreased levels of transcription whereas nucleotide changes at the nucleotides -37C and -36G did not reduce template activity. Therefore the sequence which modulates transcription of the tRNAVal₄ gene does have the general form TNNCT. Competition experiments between the
Val₄ mutant -38G.-35A and a tRNASer₇ gene showed the TNNCT mutant to be a better competitor for transcription than the wild type template. Experiments analyzing the time-course of transcription, the effects of temperature and the effects of ionic strength indicated that TNNCT was not involved in determining the efficiency of stable complex formation. It is proposed that the pentanucleotide is probably responsible for influencing the rate of initiation of transcription. A sequence TGCCT contained in the anticodon stem/loop region of the Val₄ gene was also mutagenized and shown to be involved in complex stability or the elongation of Val₄ tRNAs.
Using deletion analysis of the 5'-flanking sequences of a tRNASer₇ gene, a second positive transcription regulatory element was delimited. This sequence was also found in the 5'-flanks of the tRNAVal₄ and a tRNAArg gene.<br>Medicine, Faculty of<br>Medical Genetics, Department of<br>Graduate
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Sambandan, Deepa. "The Genetic Architecture of odor-guided behavior in Drosophila melanogaster." NCSU, 2008. http://www.lib.ncsu.edu/theses/available/etd-06032008-131124/.
Повний текст джерелаАнотація:
Understanding the genetic architecture of complex traits requires identification of the underlying genes and characterization of gene-by-gene and genotype by environment interactions (GEI). Behaviors that mediate interactions between organisms and their environment are complex traits that are especially sensitive to environmental conditions. Drosophila melanogaster presents an opportunity to systematically dissect epistasis and GEI, since large numbers of genetically identical individuals can be reared under defined environmental conditions. The olfactory system of Drosophila and its behavioral response to odorants have been well characterized. Previous studies on olfactory behavior have shown that the genetic architecture of this model behavior depends on epistatic networks of pleiotropic genes. I have used P-element mutagenesis in a co-isogenic background to identify genes that contribute to olfactory behavior. I have demonstrated that the effects of the transposon insertions are often dependent on developmental stage and that hypomorphic mutations in developmental genes can elicit profound adult behavioral deficits. I also assessed epistasis among these genes by constructing all possible double heterozygotes and measuring avoidance responses at two odorant concentrations. I observed enhancer and suppressor effects among subsets of these genes, and surprisingly, these epistatic interactions shifted with changes in the concentration of the olfactory stimulus. I then assessed variation in olfactory behavior in a population of 41 wild-derived inbred lines and asked to what extent different larval rearing environments would influence adult olfactory behavior and whether GEI is a minor or major contributing source of phenotypic variation. My results show that about 50% of phenotypic variation in adult olfactory behavior is attributable to GEI. In contrast, transcriptional analysis revealed that only 20 genes show GEI at the level of gene expression (FDR<0.05), some of which are associated with physiological responses to environmental chemicals. Quantitative complementation tests with piggyBac-tagged mutants for two of these genes (CG9664 and Transferrin 1) demonstrate that genes that show transcriptional GEI are candidate genes for olfactory behavior, and that GEI at the level of gene expression is correlated with GEI at the level of phenotype.
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Shuford, David Tice Jr. "THE GENETIC ANALYSIS OF NEGATIVE GEOTAXIS BEHAVIOR IN DROSOPHILA MELANOGASTER." NCSU, 2004. http://www.lib.ncsu.edu/theses/available/etd-12082004-160325/.
Повний текст джерелаАнотація:
Behaviors are complex traits, which exhibit continuous phenotypic variation in natural populations. The continuous variation is attributable to the segregation of multiple interacting loci with individually small effects on behavior, which are sensitive to the environment. In Drosophila, loci with small, environmentally sensitive effects on behavior can be identified by screening collections of P-element insertions that have been generated in a co-isogenic background. Here, we have used this approach to identify novel candidate genes affecting geotaxis. Drosophila melanogaster are negatively geotactic, i.e., flies move opposite the Earth?s gravitational vector when disturbed. We developed a rapid assay to quantify this geotactic behavior. Individual flies are placed in a 15cm tube, and lightly tapped to the bottom. The vertical distance traveled in 10s is the measure of behavior. Using this assay, we quantified the behavior of 475 co-isogenic P-element insertion lines, generated in co-isogenic Canton-S backgrounds as part of the Berkeley Drosophila Gene Disruption Project. The most extreme scoring lines were also assayed for locomotor activity to control for pleiotropic effects associated with this quantitative trait. We found 24 lines with increased, and 15 lines with decreased geotaxis. Four lines had sex-specific effects on geotactic behavior. Seventeen of the mutations are in known genes, many of which affect neurogenesis (e.g. Mushroom-body expressed and neuralized). The remaining are insertions in predicted genes of unknown function. We tested a subset of lines in the classic geotaxis maze. Of the ten lines chosen to be tested, eight lines showed a significant difference from the parental line, and of these, six lines showed a phenotype that corroborated our observations in the climbing assay. Thus, our approach identified new candidate genes that contribute to geotaxis in Drosophila melanogaster.
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Shannon, Roger. "Predictive adaptive responses in Drosophila melanogaster." Thesis, University of Southampton, 2011. https://eprints.soton.ac.uk/338975/.
Повний текст джерелаАнотація:
Predictive Adaptive Responses are changes in development made in the perinatal period in response to maternally transmitted information, and a mismatch between the diet selected during human evolution and the contemporary Western diet can produce an adult phenotype characterised by weight gain, cardiovascular disease, hypertension and diabetes. In humans, most evidence is epidemiological. Using Drosophila melanogaster, the problem can be approached from an adaptive phenotypic plasticity perspective. Health effects in humans stem from predictive adaptations made to enhance fitness and so it must first be shown that D. melanogaster make these responses. To model the human dietary transition, two equivalent fly diets were designed, one a human Palaeolithic diet and the other a contemporary Western diet. Using isofemale lines, flies were swapped between diets over three generations and fitness indicators measured in the offspring generation. Fitness indicator responses to a range of diets differing in protein: carbohydrate ratio and total macronutrient content were also investigated. There were adaptive, compensatory effects on survival rate and male thorax size from parental diet, and development time from grandparental diets, but also non-adaptive effects on development time and female thorax size from the parental diets. Higher dietary protein: carbohydrate ratios reduced development time and increased thorax size and survival rate, while increased macronutrient content increased weight, lipid content and survival. Diet had no effect on ommatidia number relative to fly size. Whether a response to diet is predictive and adaptive depends not only on diet composition, but whether offspring, parents or grandparents consumed the diet, the phenotypic character measured and the genotype of the fly. The variety of responses in relation to parental and grandparental diets show that intergenerational effects are complex, and D. melanogaster is a suitable model to help unravel the causes of human diseases.
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Carneiro, da Silva Joana Servulo Correia. "Population genetics of P transposable elements and their host species, with emphasis on Drosophila willistoni and Drosophila sturtevanti." Diss., The University of Arizona, 2000. http://hdl.handle.net/10150/284221.
Повний текст джерелаАнотація:
The evolution of the P element family was studied in members of the Drosophila willistoni and Drosophila saltans species groups (subgenus Sophophora). The transmission of P elements among species, their spread within species and the strength of selective constraints, as well as the level at which they are imposed on these elements, were investigated using DNA sequence data. Particular emphasis was placed on the evolution of the canonical P element subfamily. This subfamily includes the functional P element first isolated from Drosophila melanogaster, which was termed canonical. It includes also other P elements belonging to the saltans and willistoni groups that are closely related to it. Based on the divergence among canonical elements, it was estimated that they last shared a common ancestor 3 million years ago, and that a minimum of eleven horizontal transfer events among species have taken place since then. This indicates that horizontal transfer is more important than anticipated in the transmission of P elements among species. The evolution of P elements within species was studied in detail in Drosophila sturtevanti and Drosophila willistoni. First, the population structure of these species was inferred from nuclear (alcohol dehydrogenase) and mitochondrial (part of subunits 4 and 5 of NADH dehydrogenase, and the transfer RNA gene for histidine) markers. The results suggest that only peripheral populations of D. willistoni show significant genetic differentiation. In D. sturtevanti significant population subdivision was detected among populations in the central part of the distribution, as well as between these and peripheral populations. These results were used as a reference to which P element divergence among populations could be compared. No selective constraints were detected in the evolution of canonical P elements within these two species. However, those constraints are present when elements were compared between species. It is concluded that selection is mostly effective at the time of horizontal transmission between species. Furthermore, P elements are shown to spread faster among populations than do neutral markers. This suggests that the spread of P elements within species can be achieved quickly, and surpass barriers such as moderate levels of population structuring within a species.
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Loh, Samantha Hui Yong. "Molecular and genetic characterisation of Drosophila Sox50E and Sox100B." Thesis, University of Cambridge, 2000. https://www.repository.cam.ac.uk/handle/1810/251700.
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Knox, Andrea Lesley. "Characterisation of genes that modulate integrin function in Drosophila." Thesis, University of Cambridge, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.621668.
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SSEKIMPI, PUPULIO SSEMOMBWE NKUNA ABBY. "CHROMOSOME VARIATION IN DROSOPHILA SPECIES OF THE MULLERI COMPLEX." Diss., The University of Arizona, 1986. http://hdl.handle.net/10150/183809.
Повний текст джерелаАнотація:
Drosophila species in mulleri complex show five rod-shaped and one pair of dot-shaped chromosome. The sex-chromosomes represent the largest pair in the female, but are heteromorphic in the male, the Y-chromosome being shorter than the X-chromosome. The purpose of the research presented here is to determine whether chromosomes in the mulleri cluster species are longer than in the mojavensis cluster. The length of X-, Y-chromosomes and the rod-like autosomes were compared among the ten species studied. All the rod-like chromosomes were measured in 30 or more brain cells in each of the ten species. The length of the X-chromosomes were measured in hybrid female larvae. Also the metaphase chromosomes were stained for heterochromatin. The results of this study do not support the division of the mulleri complex into the two clusters. This study shows that the X-chromosome in mulleri complex can be divided into three categories; the long X-chromosome found in D.sp.A, D.aldrichi and D.wheeleri; the intermediate or medium X-chromosome found in D.mojavensis, D.mulleri, D.sp.S, and D.sp.S-5; and the short X-chromosome found in D.arizonensis, D.mayaguana, and D.sp.N. The intermediate and the short X-chromosome groups represent species from the two clusters. The Y-chromosome appears to be most variable of all. Based on overall chromosome lengths the ten species can be placed into three groups; (1) D.sp.A, D.aldrichi, D.wheeleri, D.sp.S, and D.sp.S-5 in the long chromosome group, (2) D.mojavensis and D.mulleri in the medium chromosome group and (3) D.arizonensis, D.sp.N and D.mayaguana in the short chromosome group. The differences in chromosome length seem to be due to heterochromatin. The results seem to suggest that the ancestral species had the mulleri-mojavensis chromosome length (i.e. medium) and the mulleri gene arrangement. The chromosomes of the species in the long chromosome group are a result of addition of heterochromatin. However the amount of heterochromatin gained varies from chromosome to chromosome within species and also from species to species among corresponding chromosomes. The sex chromosomes in the short chromosome group seem to have become shorter due to loss of heterochromatin while the autosomes generally remained unchanged. Heterochromatin seems to play a significant role in crosscompatibility among these species.
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Staller, Max V. "Measuring and Modeling Enhancers in Perturbed Drosophila Melanogaster Embryos." Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:14226046.
Повний текст джерелаАнотація:
The diversity of animal shapes and sizes, colors and textures, or behaviors and habitats all depend on specialized cells. A newly fertilized embryo must build all these specialized cell types, a process called differentiation. Much of differentiation depends on appropriately turning genes on and off in each cell type. Cell type specific control of gene expression is encoded in a type of regulatory DNA called enhancers. I am interested in how enhancers control the cell type specific gene expression that enables specialized cell functions.
Enhancers read in information from regulatory proteins and output a level of gene expression. This conversion from input regulator concentrations to output expression level is a computation. I use quantitative measurement and computational modeling to study how enhancers compute. In embryos, many regulatory proteins bind to enhancers, and some will turn an enhancer on, while others will turn it off. This complex process is greatly simplified by employing computational models. These models can test whether all regulators have been identified (and if not, find the missing ones) and quantify the relationships between regulators. The relationships between regulators reflect the underlying molecular mechanisms used in the cell; when several models can fit the data, perturbation experiments can be used to distinguish the models and underlying mechanisms. However, most computational models of gene expression in animals have not been rigorously validated by perturbation experiments. A major contribution of my thesis work was developing methods for testing models.
To test computational models for how enhancers compute gene expression patterns, I experimentally manipulated the concentrations of regulatory proteins and precisely measured output gene expression patterns. Using the Drosophila melanogaster blastoderm embryo, I first developed efficient and scalable techniques for making perturbations to regulatory protein concentrations. This technique revealed a postulated property of development: that embryos mitigate the impact of perturbations by preventing the creation of new cell types. I then used two perturbations to test computational models of an enhancer, finding they were incomplete and discovering new regulatory connections. My work illustrates how computational modeling and quantitative measurement are powerful tools for untangling how regulatory DNA operates in embryos.