Relevant bibliographies by topics / Variegation

Academic literature on the topic 'Variegation'

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Published: 4 June 2021
Last updated: 21 February 2023

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Journal articles on the topic "Variegation"

1

Lloyd, Vett K., David Dyment, Donald A. R. Sinclair, and Thomas A. Grigliatti. "Different patterns of gene silencing in position-effect variegation." Genome 46, no. 6 (December 1, 2003): 1104–17. http://dx.doi.org/10.1139/g03-070.

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Position-effect variegation (PEV) results when a fully functional gene is moved from its normal position to a position near to a broken heterochromatic-euchromatic boundary. In this new position, the gene, while remaining unaltered at the DNA level, is transcriptionally silenced in some cells but active in others, producing a diagnostic mosaic phenotype. Many variegating stocks show phenotypic instability, in that the level of variegation is dramatically different in different isolates or when out crossed. To test if this phenotypic instability was due to segregation of spontaneously accumulated mutations that suppress variegation, four different and well-characterized strains showing PEV for the white+ gene (wm4, wmMc, wm51b, and wmJ) and representing both large and small spot variegators were repeatedly out crossed to a strain free of modifiers, and the phenotypes of these variegators were monitored for 30 generations. Once free of modifiers, these variegating strains were then allowed to reaccumulate modifiers. The spontaneous suppressors of variegation were found to include both dominant and recessive, autosomal and X-linked alleles selected to reduce the detrimental effects of silencing white+ and adjacent genes. The time of peak sensitivity to temperature during development was also determined for these four variegators. Although large and small spot variegators have previously been attributed to early and late silencing events, respectively, the variegators we examined all shared a common early period of peak sensitivity to temperature. Once free of their variegation suppressors, the different variegating strains showed considerable differences in the frequency of inactivation at a cellular level (the number of cells showing silencing of a given gene) and the extent of variegation within the cell (the number of silenced genes). These results suggest that large and small spot variegation may be a superficial consequence of spontaneous variegation suppressors. The nature and number of these spontaneous variegation suppressors depends on the number of genes silenced in a given variegating rearrangement. These results are interpreted in the context of a model that proposes that the different underlying patterns of gene silencing seen in PEV can be attributed directly to the formation of heterochromatin domains possessing different properties of propagation during cell division.Key words: Drosophila melanogaster, position-effect variegation, spontaneous suppressors of variegation.
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Dorer, Douglas R., and Steven Henikoff. "Transgene Repeat Arrays Interact With Distant Heterochromatin and Cause Silencing in cis and trans." Genetics 147, no. 3 (November 1, 1997): 1181–90. http://dx.doi.org/10.1093/genetics/147.3.1181.

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Tandem repeats of Drosophila transgenes can cause heterochromatic variegation for transgene expression in a copy-number and orientation-dependent manner. Here, we demonstrate different ways in which these transgene repeat arrays interact with other sequences at a distance, displaying properties identical to those of a naturally occurring block of interstitial heterochromatin. Arrays consisting of tandemly repeated white transgenes are strongly affected by proximity to constitutive heterochromatin. Moving an array closer to heterochromatin enhanced variegation, and enhancement was reverted by recombination of the array onto a normal sequence chromosome. Rearrangements that lack the array enhanced variegation of white on a homologue bearing the array. Therefore, silencing of white genes within a repeat array depends on its distance from heterochromatin of the same chromosome or of its paired homologue. In addition, white transgene arrays cause variegation of a nearby gene in cis, a hallmark of classical position-effect variegation. Such spreading of heterochromatic silencing correlates with array size. Finally, white transgene arrays cause pairing-dependent silencing of a non-variegating white insertion at the homologous position.
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Talbert, P. B., C. D. LeCiel, and S. Henikoff. "Modification of the Drosophila heterochromatic mutation brownDominant by linkage alterations." Genetics 136, no. 2 (February 1, 1994): 559–71. http://dx.doi.org/10.1093/genetics/136.2.559.

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Abstract The variegating mutation brownDominant (bwD) of Drosophila melanogaster is associated with an insertion of heterochromatin into chromosome arm 2R at 59E, the site of the bw gene. Mutagenesis produced 150 dominant suppressors of bwD variegation. These fall into two classes: unlinked suppressors, which also suppress other variegating mutations; and linked chromosome rearrangements, which suppress only bwD. Some rearrangements are broken at 59E, and so might directly interfere with variegation caused by the heterochromatic insertion at that site. However, most rearrangements are translocations broken proximal to bw within the 52D-57D region of 2R. Translocation breakpoints on the X chromosome are scattered throughout the X euchromatin, while those on chromosome 3 are confined to the tips. This suggests that a special property of the X chromosome suppresses bwD variegation, as does a distal autosomal location. Conversely, two enhancers of bwD are caused by translocations from the same part of 2R to proximal heterochromatin, bringing the bwD heterochromatic insertion close to the chromocenter with which it strongly associates. These results support the notion that heterochromatin formation at a genetic locus depends on its location within the nucleus.
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Locke, J., M. A. Kotarski, and K. D. Tartof. "Dosage-dependent modifiers of position effect variegation in Drosophila and a mass action model that explains their effect." Genetics 120, no. 1 (September 1, 1988): 181–98. http://dx.doi.org/10.1093/genetics/120.1.181.

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Abstract Twelve dominant enhancers of position effect variegation, representing four loci on the second and third chromosomes of Drosophila melanogaster, have been induced by P-element mutagenesis. Instead of simple transposon insertions, seven of these mutations are cytologically visible duplications and three are deficiencies. The duplications define two distinct regions, each coinciding with a locus that also behaves as a dominant haplo-dependent suppressor of variegation. Conversely, two of the deficiencies overlap with a region that contains a haplo-dependent enhancer of variegation while duplications of this same region act to suppress variegation. The third deficiency defines another haplo-dependent enhancer. These data indicate that loci capable of modifying variegation do so in an antipodal fashion through changes in the wild-type gene copy number and may be divided into two reciprocally acting classes. Class I modifiers enhance variegation when duplicated or suppress variegation when deficient. Class II modifiers enhance when deficient but suppress when duplicated. From our data, and those of others, we propose that in Drosophila there are about 20 to 30 dominant loci that modify variegation. Most appear to be of the class I type whereas only two class II modifiers have been identified so far. From these observations we put forth a model, based on the law of mass action, for understanding how such suppressor-enhancer loci function. We propose that each class I modifier codes for a structural protein component of heterochromatin and their effects on variegation are a consequence of their dosage dependent influence on the extent of the assembly of heterochromatin at the chromosomal site of the position effect. It is further proposed that class II modifiers may inhibit the class I products directly, bind to hypothetical termination sites that define heterochromatin boundaries or promote euchromatin formation. Consistent with our mass action model we find that combining two enhancers together produce additive and not epistatic effects. Also, since different enhancers have different relative strengths on different variegating mutants, we suggest that heterochromatic domains are constructed by a combinatorial association of proteins. The mass action model proposed here is of general significance for any assembly driven reaction and has implications for understanding a wide variety of biological phenomena.(ABSTRACT TRUNCATED AT 400 WORDS)
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Eissenberg, J. C., G. D. Morris, G. Reuter, and T. Hartnett. "The heterochromatin-associated protein HP-1 is an essential protein in Drosophila with dosage-dependent effects on position-effect variegation." Genetics 131, no. 2 (June 1, 1992): 345–52. http://dx.doi.org/10.1093/genetics/131.2.345.

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Abstract Chromosome rearrangements which place euchromatic genes adjacent to a heterochromatic breakpoint frequently result in gene repression (position-effect variegation). This repression is thought to reflect the spreading of a heterochromatic structure into neighboring euchromatin. Two allelic dominant suppressors of position-effect variegation were found to contain mutations within the gene encoding the heterochromatin-specific chromosomal protein HP-1. The site of mutation for each allele is given: one converts Lys169 into a nonsense (ochre) codon, while the other is a frameshift after Ser10. In flies heterozygous for one of the mutant alleles (Su(var)2-504), a truncated HP-1 protein was detectable by Western blot analysis. An HP-1 minigene, consisting of HP-1 cDNA under the control of an Hsp70 heat-inducible promoter, was transduced into flies by P element-mediated germ line transformation. Heat-shock driven expression of this minigene results in elevated HP-1 protein level and enhancement of position-effect variegation. Levels of variegating gene expression thus appear to depend upon the level of expression of a heterochromatin-specific protein. The implications of these observations for mechanism of heterochromatic position effects and heterochromatin function are discussed.
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Lloyd, Vett K., Donald A. Sinclair, and Thomas A. Grigliatti. "Competition Between Different Variegating Rearrangements for Limited Heterochromatic Factors in Drosophila melanogaster." Genetics 145, no. 4 (April 1, 1997): 945–59. http://dx.doi.org/10.1093/genetics/145.4.945.

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Position effect variegation (PEV) results from the juxtaposition of a euchromatic gene to heterochromatin. In its new position the gene is inactivated in some cells and not in others. This mosaic expression is consistent with variability in the spread of heterochromatin from cell to cell. As many components of heterochromatin are likely to be produced in limited amounts, the spread of heterochromatin into a normally euchromatic region should be accompanied by a concomitant loss or redistribution of the protein components from other heterochromatic regions. We have shown that this is the case by simultaneously monitoring variegation of a euchromatic and a heterochromatic gene associated with a single chromosome rearrangement. Secondly, if several heterochromatic regions of the genome share limited components of heterochromatin, then some variegating rearrangements should compete for these components. We have examined this hypothesis by testing flies with combinations of two or more different variegating rearrangements. Of the nine combinations of pairs of variegating rearrangements we studied, seven showed nonreciprocal interactions. These results imply that many components of heterochromatin are both shared and present in limited amounts and that they can transfer between chromosomal sites. Consequently, even nonvariegation portions of the genome will be disrupted by re-allocation of heterochromatic proteins associated with PEV. These results have implications for models of PEV.
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Michailidis, John, Neil D. Murray, and Jennifer A. Marshall Graves. "A correlation between development time and variegated position effect in Drosophila melanogaster." Genetical Research 52, no. 2 (October 1988): 119–23. http://dx.doi.org/10.1017/s0016672300027488.

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SummaryPosition-effect variegation is a phenomenon in which cell-autonomous genes, normally expressed in all cells of a tissue, are expressed in some cells but not in others, leading to a mosaic tissue. Variegation occurs when a normally euchromatic gene is re-positioned close to heterochromatin by chromosome rearrangement. The extent of variegation is known to be influenced by a number of environmental and genetic factors. In the courss of investigations of the influence of the pH of larval medium on the extent of eye-colour variegation in In(1)ωm4 Drosophila melanogaster, we have found that the extent of variegation depends on development time. Flies reared at pH 2·6 develop slowly and show more extreme variegation than those reared at higher pH. This effect, as well as variations within the pH treatments, can be accounted for by differences in development time. The observed regression relationship between variegation and development time also appears to accommodate the influences of temperature on both variables. We suggest that development time may account causally for the reported influences of a number of environmental agents (temperature, crowding, chemicals) on variegation. Ways in which this might occur are discussed in the context of models of the molecular basis of differential gene activity.
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Hearn, M. G., A. Hedrick, T. A. Grigliatti, and B. T. Wakimoto. "The effect of modifiers of position-effect variegation on the variegation of heterochromatic genes of Drosophila melanogaster." Genetics 128, no. 4 (August 1, 1991): 785–97. http://dx.doi.org/10.1093/genetics/128.4.785.

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Abstract Dominant modifiers of position-effect variegation of Drosophila melanogaster were tested for their effects on the variegation of genes normally located in heterochromatin. These modifiers were previously isolated as strong suppressors of the variegation of euchromatic genes and have been postulated to encode structural components of heterochromatin or other products that influence chromosome condensation. While eight of the modifiers had weak or no detectable effects, six acted as enhancers of light (lt) variegation. The two modifiers with the strongest effects on lt were shown to also enhance the variegation of neighboring heterochromatic genes. These results suggest that the wild-type gene products of some modifiers of position-effect variegation are required for proper expression of genes normally located within or near the heterochromatin of chromosome 2. We conclude that these heterochromatic genes have fundamentally different regulatory requirements compared to those typical of euchromatic genes.
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Marcotrigiano, Michael, and Grant Hackett. "Quantifying Leaf Variegation." HortScience 28, no. 4 (April 1993): 344. http://dx.doi.org/10.21273/hortsci.28.4.344.

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Rodermel, Steven. "Arabidopsis Variegation Mutants." Arabidopsis Book 1 (January 2002): e0079. http://dx.doi.org/10.1199/tab.0079.

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Dissertations / Theses on the topic "Variegation"

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Hedrick, Amy L. "Characterization of a cluster of dominant suppressors of position effect variegation including effects on heterochromatic variegating rearrangements in Drosophila melanogaster." Thesis, University of British Columbia, 1989. http://hdl.handle.net/2429/27473.

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The mosiac, cell-autonomous expression of genes resulting from chromosomal rearrangement and relocation next to broken heterochromatin is termed position effect variegation (PEV). Since the gene is inactivated due to chromatin changes, this system allows the genetic study of chromatin structure and function using mutations which rescue the mosaic phenotype. These mutations called suppressors of variegation, Su(var)s, must influence chromatin structure. The genetic characterization of several groups of Su(var)s has been undertaken in this study using Drosophila melanogaster. Variegation of the light gene, located in heterochromatin, is enhanced by several Su(var) mutations on chromosome two. This opposite effect suggests that products of these Su(var)s are essential for functioning heterochromatin and deleterious for euchromatic environments. Other Su(var)s have slight or no effects on the same variegating rearrangements, demonstrating functional differences, among the Su(var)s tested. A group of Su(var)s located within 4 map units near the centromere of chromosome three was characterized using deficiency mapping, new compound autosome formation and inter se complementation based on newly established homozygous phenotypes. Two Su(var)s mapped to 87B on 3R, while one Su(var) maps to 3L according to compound mapping. Inter se complementation, in combination with mapping data, suggests that four seperate loci make up this group of Su(var)s. Eight of nine Su(var)s are extremely sensitive to heterochromatic deletions as shown by their responses to loss of 2R heterochromatin, as well as the Y chromosome. In contrast, Su(var)A130 is insensitive to both forms of heterochromatic deficiencies. Su(var)s show complicated reactions to maternal verses paternal source effects. Six of nine Su(var)s show a female-specific temperature sensitive maternal effect. Some maternal and paternal effects are observed at 22 C. Su(var)A57 is maternal semi-lethal and suppressed at 29 C. This characterization has better defined these mutants, making them ammenable to molecular study.
Science, Faculty of
Zoology, Department of
Graduate
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Liu, Huiying. "The study of the mechanism of Arabidopsis immutans variegation." [Ames, Iowa : Iowa State University], 2010. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3403816.

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Blattes, Roxane. "BASES MOLECULAIRES DE LA VARIEGATION D'EFFETDE POSITION CHEZ DROSOPHILA MELANOGASTER." Phd thesis, Université Paul Sabatier - Toulouse III, 2006. http://tel.archives-ouvertes.fr/tel-00107128.

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Les séquences satellites III (SATIII) représentent la majeure partie de l'hétérochromatine du
chromosome X de drosophile et jouent un rôle dans la variégation d'effet de position du gène
white dans l'inversion white-mottled. Leurs caractéristiques structurales dues à leur richesse en
dA•dT sont ciblées par des ligands synthétiques du petit sillon de l'ADN, outils qui ont permis de
caractériser la fonction des SATIII dans l'assemblage de l'hétérochromatine. Nous avons mis en
évidence un rôle de D1, qui reconnaît spécifiquement les SATIII, mais aussi de la topoïsomérase
II, dans l'initiation de l'assemblage de l'hétérochromatine. Nos résultats suggèrent que les
SATIII pourraient constituer un réservoir de protéines servant à la régulation de la transcription
du locus des gènes ribosomiques (rDNA) adjacent aux SATIII. Enfin, nous avons pu identifier un
élément frontière qui contrôle le cloisonnement de l'hétérochromatine et jouerait un rôle dans la régulation de l'expression du rDNA
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Sahasrabhojane, Pranoti. "Identification and characterization of the E(var)3-5 gene in Drosophila melanogaster." Morgantown, W. Va. : [West Virginia University Libraries], 2008. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=5853.

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Thesis (M.S.)--West Virginia University, 2008.
Title from document title page. Document formatted into pages; contains vii, 96 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 84-96).
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Uribe, Lewis Santiago. "Regulation of transgene variegation by modifiers of chromatin structure in mice." Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.429040.

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Hiragami, Kyoko. "Studies into the stability of gene silencing in mammalian position effect variegation." Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.439517.

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Sabl, Joy F. "Effects of repetitiveness, pairing and linkage on position-effect variegation in Drosophila /." Thesis, Connect to this title online; UW restricted, 1996. http://hdl.handle.net/1773/5204.

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Fan, Ngo-yin, and 樊傲賢. "Functional study of suppressor of variegation 3-9 homolog 1 in hepatocellular carcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B49617928.

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Hepatocellular carcinoma (HCC) is the major type of primary liver cancer which is well-known for its high heterogenicity and metastatic potential. Despite of the current advancement in surgical resection and the availability of targeted therapy, HCC remains a barely curable and fatal disease. We previously demonstrated that deregulation of epigenetic regulators is a common event in human HCC. Herein, we identified the frequent up-regulation of the prototype of H3K9 tri-methyltransferase SUV39H1 in clinical HCCs. SUV39H1 over-expression was also significantly associated with increased Ki67 expression and the presence of venous invasion. By using both SUV39H1 over-expression and knockdown model, we consistently demonstrated that SUV39H1 contributed to HCC tumor growth and migration. Most importantly, SUV39H1 knockdown drastically suppressed in vivo tumorigenicity and extra-hepatic metastasis of HCC cells in nude mice model. These findings evidently demonstrated the oncogenic role of SUV39H1 in HCC and implied potential therapeutic targeting of SUV39H1 for HCC treatment. Molecularly, SUV39H1 knockdown HCC cell underwent morphological changes and accompanied with increased lysosomal β-galactosidase activity and elevated p21 protein and γH2AX level. This data suggested senescence induction in SUV39H1 knockdown HCC cells. SUV39H1 has been implicated in telomere regulation and transcriptional control. However, neither telomere length nor expression of tumor suppressor genes was altered in SUV39H1 knockdown HCC cells. Interestingly, we demonstrated a novel observation that SUV39H1 may potentially methylate non-histone substrates that are yet to be identified, which may contribute to the pro-tumorigenic function of SUV39H1 in HCC. We also investigated the upstream regulation of SUV39H1 and identified miR-125b as the negative post-transcriptional regulator of SUV39H1. Ectopic expression of miR-125b abolished SUV39H1 3’UTR-coupled luciferase activity and suppressed endogenous SUV39H1 at both mRNA and protein level. Clinically, miR-125b level was found inversely correlated with SUV39H1 expression. We have previously reported the frequent under-expression of miR-125b in HCC. Collectively, our data suggested that SUV39H1 up-regulation in HCC may be the sequential outcome of miR-125b down-regulation. In conclusion, we demonstrated for the first time that SUV39H1 up-regulation contributed to HCC development and metastasis, potentially via senescence evasion. SUV39H1 elevation in HCC was attributed to the loss of its negative regulator, the tumor suppressive miR-125b.
published_or_final_version
Pathology
Doctoral
Doctor of Philosophy
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Bruxner, Timothy James. "Characterisation of mutants influencing epigenetic gene silencing in the mouse." University of Sydney, 2008. http://hdl.handle.net/2123/2238.

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Doctor of Philosophy (PhD)
The field of epigenetics emerged primarily from studies in Drosophila, and is now being studied intensively by mammalian biologists. In order to increase our knowledge of epigenetic gene control in the mouse, I have studied modifiers of epigenetic gene silencing. My main method of investigation involved the characterisation of mutants from a sensitised ENU mutagenesis screen performed previously in our laboratory. The screen was carried out in an FVB/NJ strain carrying a variegating GFP transgene expressed in erythrocytes. To date we have recovered 12 dominant (D) and seven recessive (R) mutant mouse lines from this screen that display altered transgene expression. We have named these Mommes (Modifiers of murine metastable epialleles). I investigated the phenotype and attempted to identify the underlying causative mutation of two of these Momme mutants. MommeD6 is a semi-dominant, homozygous lethal mutation that acts as a suppressor of variegation with respect to the GFP transgene. This mutation has a large effect on the level of expression of the transgene in expressing cells, but little effect on the percentage of cells expressing the transgene. MommeD6 is linked to a 2.5 Mbp interval on chromosome 14. MommeD9 is a semi-dominant, homozygous lethal mutation that acts as an enhancer of variegation with respect to the GFP transgene. Mutants have a tendency to become obese as they age, show abnormal haematology profiles, and females develop infertility. MommeD9 is linked to a 17.4 Mbp region on chromosome 7. I produced and studied a strain carrying the same GFP transgene but in a new strain background, C57BL/6J. This strain provided an opportunity to look for strain-specific modifiers of expression of the GFP transgene. Several regions were mapped to chromosomal locations. Further work will be needed to identify the genes involved. This mouse will be useful in future mutagenesis screens of this type.
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Festenstein, Richard. "Molecular analysis of the human CD2 Locus Control Region in transgenic mice." Thesis, Open University, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321311.

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Books on the topic "Variegation"

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Variegations. [Place of publication not identified]: Dorrance Pub Co, 2010.

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Daloiso, Michele, and Marco Mezzadri. Educazione linguistica inclusiva Riflessioni, ricerche ed esperienze. Venice: Fondazione Università Ca’ Foscari, 2021. http://dx.doi.org/10.30687/978-88-6969-477-6.

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Il volume raccoglie i contributi di numerosi studiosi di varie discipline, prevalentemente linguisti educativi, ma anche linguisti generali e neuroscienziati, che hanno accolto la proposta di riflettere su un possibile minimo comune denominatore di alcuni filoni delle proprie ricerche, riassumibile nel concetto di inclusività. Ne è nato un volume variegato ma coeso da cui si evince la volontà della Linguistica Educativa in Italia di proporre riflessioni scientifiche aggiornate ma al contempo fedeli ai paradigmi della disciplina, che vedono due degli assi portanti nella prospettiva interdisciplinare e nella ricerca di risposte alle molteplici sfide dell’educazione linguistica oggi.
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Rogari, Sandro, ed. Quale federalismo per l’Italia di oggi? Florence: Firenze University Press, 2013. http://dx.doi.org/10.36253/978-88-6655-433-2.

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In occasione dei 150 anni dell’Unità nazionale, la Facoltà di Scienze Politiche “Cesare Alfieri” ha promosso una serie di lezioni d’impianto interdisciplinare su temi cruciali della nostra costituzione unitaria. A conclusione di questo ciclo di letture, il 28 novembre 2011 la Facoltà ha promosso una giornata di studi sul tema Quale federalismo per l’Italia di oggi. A questo scopo sono stati chiamati a proporre le loro riflessioni studiosi che in prospettiva storica, costituzionalistica, sociologica, politologica ed economica facessero il punto sulla questione cruciale della ridefinizione in chiave federale dello Stato italiano. Ne è emerso un quadro variegato e complesso, dove le diverse prospettive disciplinari compongono un mosaico integrato, multiforme ma non contraddittorio del federalismo possibile oggi, volto a rigenerare le istituzioni della Repubblica ed il loro rapporto con i cittadini. Il volume raccoglie i risultati di quella giornata di studi e li propone alla lettura di studenti e studiosi.
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Rossi, Maddalena, and Claudio Saragosa, eds. I territori della contemporaneità. Florence: Firenze University Press, 2019. http://dx.doi.org/10.36253/978-88-6453-805-1.

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Il testo raccoglie la rielaborazione di alcune delle tesi di laurea più significative prodotte, dal 2011 al 2015, nei corsi di laurea triennale in Pianificazione della città, del territorio e del paesaggio e di laurea magistrale in Pianificazione e progettazione della città e del territorio dell’Università di Firenze, con sede a Empoli. Le tesi trattano un panorama attuale e variegato di problematiche interne alla disciplina urbanistica, utilizzando metodologie, chiavi di lettura e prospettive di analisi assai diverse. Il territorio che emerge come protagonista delle narrazioni dei giovani autori è un oggetto complesso e pluristratificato, fatto di cose e relazioni, adagiato sui tempi lunghi della storia, teso sul presente e proiettato nel futuro, che continua a sollecitare loro domande, dubbi, curiosità e anche alcune fruttuose risposte. In sintesi, più che campi di discussione di un sapere acquisito e valido una volta per tutte, i lavori qui presentati rappresentano campi di riflessione e di sperimentazione, occasioni di costruzione incrementale di soluzioni creative da parte degli autori.
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VERLAG, TENEUES. Variegation in the Triangle, Vasily K. Antique Collectors' Club, 2022.

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Calvert, Lee Alexander. Complementary DNA cloning and partial molecular characterization of Citrus tristeza and Citrus variegation viruses. 1987.

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Kolatan, Ferda, and Jenny Sabin. Meander - Variegating Architecture. Bentley Institute Press, 2010.

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Keenan, William. Variegations: 105 Poems of Feeling & Fancy. Terence Publishing, Michael, 2022.

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Mercer, Katie. Lemure Variegato: Immagini Bellissime e Fatti Interessanti Libro per Bambini Sui Lemure Variegato. Independently Published, 2021.

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Labirinti Colorati: Labirinti per Bambini - Ediz. a Colori - Libro Di Labirinti Divertenti, Variegati e Colorati. Independently Published, 2020.

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Book chapters on the topic "Variegation"

1

Murakami, Yota. "Position Effect Variegation." In Encyclopedia of Systems Biology, 1721. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_1574.

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Tilney-Bassett, Richard A. E. "Genetics of Variegation and Maternal Inheritance in Ornamentals." In Genetics and Breeding of Ornamental Species, 225–49. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-3296-1_12.

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Lev-Yadun, Simcha. "The Proposed Anti-herbivory Roles of White Leaf Variegation." In Progress in Botany, 241–69. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-08807-5_10.

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Walbot, Virginia. "Distinguishing Variable Phenotypes from Variegation Caused by Transposon Activities." In Methods in Molecular Biology, 11–20. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-568-2_2.

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Henikoff, Steven. "A Pairing-Looping Model for Position-Effect Variegation in Drosophila." In Genomes of Plants and Animals, 211–42. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-0280-1_15.

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Rosso, Dominic, Diego Saccon, Lori Schillaci, Shelly Wang, Wenze Li, Steven R. Rodermel, Denis P. Maxwell, and Norman P. A. Huner. "Excitation Pressure Regulates Variegation in the immutans Mutant of Arabidopsis thaliana." In Photosynthesis. Energy from the Sun, 1115–19. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6709-9_244.

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Cinquin, Bertrand, Joyce Y. Kao, and Mark L. Siegal. "i.2.i. with the (Fruit) Fly: Quantifying Position Effect Variegation in Drosophila Melanogaster." In Bioimage Data Analysis Workflows ‒ Advanced Components and Methods, 147–74. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-76394-7_7.

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AbstractMany of the methods developed for the analysis of bioimages focus on microscopy images on the cellular level. However, bioimages can also be used by biologists to assess non-cellular level morphological phenotypes. Collecting non-cellular images and developing image workflows for them is similar to working with microscopic images, but also has its unique challenges.
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Ho, Elaine Lynn-Ee, and Fang Yu Foo. "Debating Integration in Singapore, Deepening the Variegations of the Chinese Diaspora." In Contemporary Chinese Diasporas, 105–25. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-5595-9_5.

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"Variegation." In Encyclopedia of Genetics, 2103. Elsevier, 2001. http://dx.doi.org/10.1006/rwgn.2001.2070.

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"Variegation." In Brenner's Encyclopedia of Genetics, 273. Elsevier, 2001. http://dx.doi.org/10.1016/b978-0-12-374984-0.01619-3.

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Conference papers on the topic "Variegation"

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Sedkowski, Wiktor, and Karol Bierczynski. "Perceived severity of vulnerability in cybersecurity: cross linguistic variegation." In 2022 IEEE International Carnahan Conference on Security Technology (ICCST). IEEE, 2022. http://dx.doi.org/10.1109/iccst52959.2022.9896488.

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Johnson, Jason S. "Complexity as a Creative Force in Design Variegation, Heterogeneity, Diversity." In ACADIA 2006: Synthetic Landscapes. ACADIA, 2006. http://dx.doi.org/10.52842/conf.acadia.2006.510.

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Takahashi, Nozomi, and Rie Mori. "The Excessive Variegation of Nomenclature of Major Fields of Academic Degrees in Japan: Study of English Versions Based on 2017 Survey." In 2019 8th International Congress on Advanced Applied Informatics (IIAI-AAI). IEEE, 2019. http://dx.doi.org/10.1109/iiai-aai.2019.00203.

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N. R., Mr Jaswin Kumar. "A Conceptual View on Unifying God and Science through Variegating Perspective." In International Conference On Contemporary Researches in Engineering, Science, Management & Arts, 2020. Bonfring, 2020. http://dx.doi.org/10.9756/bp2020.1002/21.

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Rossi, Gabriele, Massimo Leserri, and Alma Benitez Calle. "Dry stone architecture: the survey as a tool to safeguard the risk of morphological or formal homologation." In HERITAGE2022 International Conference on Vernacular Heritage: Culture, People and Sustainability. Valencia: Universitat Politècnica de València, 2022. http://dx.doi.org/10.4995/heritage2022.2022.15606.

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Ci sono esempi unici e variegati di costruzioni in pietra a secco nella regione mediterranea, il cui interesse, in Puglia (Italia) e attestato negli ultimi decenni, ha determinato un atteggiamento speculativo che ha permesso a queste architetture vernacolari di acquisire un notevole valore economico. Di conseguenza, oltre alle azioni supportate dai regolamenti comunali e dagli strumenti di pianificazione sia locale che regionale, è necessario individuarne il valore culturale e le peculiarità, tutte necessarie per attuare politiche consapevoli per una corretta tutela e conservazione. Ci proponiamo in particolare di concentrarci sul rilievo di queste architetture all'interno di questo contributo, un argomento trascurato di una certa complessità, al fine di proporre una serie di riflessioni che supportino l'attività di coloro che intendono intervenire su questi manufatti. Infatti, la loro componente plastica e l'unicità morfologica permettono loro di fondersi con sculture che richiedono l'utilizzo di metodologie e tecnologie moderne e raffinate per la loro documentazione. Pertanto, il mancato riconoscimento su caratteristiche e peculiarità ha portato ad azioni riguardanti il loro restauro con un'omologazione formale generale e la perdita della singolarità morfologica originale durante gli interventi per la loro conservazione.
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